INFECTIVE ENDOCARDITIS Definition Infective endocarditis is due to microbial infection of a heart valve (native or prosthetic), the lining of a cardiac

chamber or blood vessel, or a congenital anomaly (e.g. septal defect). Types 1)Acute endocarditis 2)Subacute endocarditis- ollo!s an indolent course,rarely causes metastatic infection typically caused by viridans streptococci. Pathophysiology Infective endocarditis typically occurs at sites of pre-e"isting endocardial damage. Infection !ith particularly virulent or aggressive organisms (e.g. Staphylococcus aureus) can cause endocarditis in a previously normal heart. #any ac$uired and congenital cardiac lesions are vulnerable to endocarditis, particularly areas of endocardial damage caused by a high-pressure %et of blood, such as ventricular septal defect, mitral regurgitation and aortic regurgitation, many of !hich are haemodynamically insignificant In contrast, the ris& of endocarditis at the site of many haemodynamically important lo!-pressure lesions (e.g. a large atrial septal defect) is negligible. 'he diagnostic pathologic lesion of S() is the development of a vegetation !hich is either sessile or a polypoidal mobile mass situated on the heart leaflets defects. A vegetation is formed !hen platelets and fibrin get deposited on the diseased valves forming small masses. 'he microbes then gain access to these sterile fibrin platelet masses producing localised inflammation and more platelet and fibrin deposition occurs enmeshing the microbes, resulting into gro!th of the vegetation'he bacteria gain entry into the circulation by !ay of an untreated or partially treated septic focus (abscess, pneumonia, urinary tract in%ection) or by diagnostic or therapeutic instrumentation (different types of endoscopies, operative procedures, dental surgery) or along ind!elling venous and arterial cannulae or intravenous catheters used for long-term feeding. Infection tends to occur at sites of endothelial damage because these areas attract deposits of platelets and fibrin, !hich are vulnerable to colonisation by blood-borne organisms. 'he avascular valve tissue and presence of fibrin aggregates help to protect proliferating organisms from host defence mechanisms. *hen the infection is established, vegetations composed of organisms, fibrin and platelets gro! and may become large enough to cause obstruction+ they may also brea& a!ay as emboli to the central nervous system or the abdomen or to the e"tremities resulting in digital gangrene.

 ,egetations can cause damage to surrounding structures li&e chordae or can cause perforation of valve. )"tracardiac manifestations such as vasculitis and s&in lesions are due to emboli or immune comple" deposition. #ycotic aneurysms may develop in arteries at the site of infected emboli. Microbiology 'he viridans group of streptococci (Strep. mitis, Strep. sanguis) are commensals in the upper respiratory tract are common causes of subacute endocarditis Enterococcus faecalis, E. faecium and Strep. bovis, may enter the blood from the bo!el or urinary tract. Staph. aureus is a common cause of acute endocarditis, originating from s&in infections, abscesses or vascular access sites. Other common organisms are -ram-negative bacteria of the .A/)0 group (Haemophilus spp+ Actinobacillus actinomycetem-comitans; Cardiobacterium hominis; Ei enella spp. and !ingella ingae" Co#iella burneti $rucella ungi -Candida, Aspergillus .Abscesses and emboli are common, therapy is difficult Prosthetic al e en!ocar!itis )arly (!ithin 2 months of valve surgery)- coagulase-negative staphylococci, S. aureus 1ate 2212 months after surgery- coagulase-negative staphylococci 312 months after surgery- similar to those in community-ac$uired native valve infection. Ris" of IE In ario#s car!iac lesions $igh ris" Mo!erate ris" %o& ris" 4rosthetic heart valves #itral valve prolapse !ith #itral valve prolapse !ithout (aortic, mitral) mitral regurgitation mitral regurgitation allot 'ricuspid stenosis #itral regurgitation Atrial septal defect 'ricuspid regurgitation 4atent ductus arteriosus 4ulmonic stenosis Aortic regurgitation #itral stenosis Aortic stenosis /oarctation of aorta ,entricular septal defect

Sy'pto's ( Signs ever 2 most common presenting symptom. Subacute endocarditis5 typically lo!-grade, rarely e"ceeds 67.89/ (1:69 ) . /an present as 4;<. Acute endocarditis5 onset is more acute and can be more high grade than subacute endocarditis. Anore"ia, !eight loss, malaise #us&ulos&etal symptoms li&e %oint pain, body ache -lomerulonephritis Signs 4allor /lubbing 4eripheral manifestations -<sler=s nodes, subungual hemorrhages, >ane!ay lesions, ?oth=s spots. 4etechiae, subcon%uctival hemorrhages Splenomegaly /ardiac signs and symptoms o .eart murmur5 - #ost of the patients have murmur. /hanging murmur can be important feature. o /ongestive heart failure5 develops in most of patients+ usually related to valvular dysfunction o /onduction abnormalities can be present. @eurologic manifestations-#ost often result from embolic stro&es S#bac#te en!ocar!itis Should be suspected !hen a patient &no!n to have congenital or valvular heart disease develops a persistent fever. /lubbing and immune mediated signs are late signs. Ac#te en!ocar!itis) It usually presents as a severe febrile illness !ith prominent and changing heart murmurs and petechiae. /linical stigmata of chronic endocarditis are usually absent. )mbolic events are common, and cardiac or renal failure may develop rapidly Differential Diagnosis @oninfective valvular disease (e.g., atrial my"oma, marantic endocarditis, 1ibman2Sac&s endocarditis) Rheumatic fever /onnective tissue diseases In estigations 1) #icrobiologic diagnosis (lood cultures - 6 blood culture sets should be obtained from different venipuncture sites over 28 h.

 'issueAemboli -Special stains and polymerase chain reaction for microbial B@A can assist in identifying an organism. Serology - or culture-negative patients, serologic tests can be used to identify C. burnetii and $rucella can be used. 2) )chocardiography Allo!s anatomic confirmation of infective endocarditis, siCing of vegetations, detection of intracardiac complications, and assessment of cardiac function 'ransthoracic echocardiography ('')) -@oninvasive and e"ceptionally specific 'ransesophageal echocardiography ('))) Safe ,Significantly more sensitive than '') Betects vegetations in 3 7:D of patients !ith Bu&e criteria2defined definite endocarditis <ptimal method to diagnose prosthetic valve endocarditis or myocardial abscess, valve perforation, or intracardiac fistulae 6)<ther investigations /omplete blood count5 sho!s anemia , leu&ocytosis )rythrocyte sedimentation rate5 elevated in 3 7:D of patients Serum complement levels !ill be decreased /-reactive protein level is high ?heumatoid factor5 present in E:D of patients ;rinalysis5 microscopic hematuria )lectrocardiography ()/-)5 sho!s conduction delays D#"e criteria for en!ocar!itis .ighly sensitive and specific for endocarditis Ma*or criteria 1) 4ositive blood culture 'ypical organism from t!o cultures 4ersistent positive blood cultures ta&en 3 12 hours apart 'hree or more positive cultures ta&en over more than 1 hour 2) )ndocardial involvement by )/.< cardiogarm 4ositive echocardiographic findings of vegetations @e! valvular regurgitation Minor criteria 4redisposition5 predisposing heart condition or in%ection drug use ever F 6G.:9/ (F1::.89 ) ,ascular phenomena5 ma%or arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, con%unctival hemorrhages, >ane!ay lesions Immunologic phenomena5 glomerulonephritis, <sler=s nodes, ?oth=s spots, rheumatoid factor

 #icrobiologic evidence5 positive blood culture but not meeting ma%or criterion, or serologic evidence of active infection !ith organism consistent !ith infective endocarditis. )/.< cardiogram not meeting ma%or criteria Diagnosis of en!ocar!itis is re*ecte! if+ Alternative diagnosis is established Symptoms resolve and do not recur !ith H 8 days of antibiotic therapy Surgery or autopsy after H 8 days of antimicrobial therapy yields no histologic evidence of endocarditis Definite en!ocar!itis+ t!o ma%or, or one ma%or and three minor, or five minor Possible en!ocar!itis+ one ma%or and one minor, or three minor Treat'ent ,- Anti'icrobial therapy )mpirical treatment depends on the mode of presentation, the suspected organism, and !hether the patient has a prosthetic valve andAor penicillin allergy. /ommon empirical therapy - 4enicillin - I, 8 million units I hourly J -entamicin I, 1 mgA&g (ma" G: mg) G hourly <nce organism is isolated specific therapy should be started. Al!ays drugs should be given by parenteral route Nati e Prosthetic Organis' Anti'icrobial Dose al e al e Viri!ans streptococci an! Strep. bovis #I/ H:.1 mgAml (enCyl penicillin 1.2 g 8-hourly 8 !ee&s1 I !ee&s i.v. 1 mgA&g G-12- 2 !ee&s 2 !ee&s and gentamicin hourly i.v. #I/ 3 :.1 to K :.E (enCyl penicillin 1.2 g 8-hourly 8 !ee&s I !ee&s mgAml i.v. 1 mgA&g G-12- 2 !ee&s 8-I !ee&s and gentamicin hourly i.v. #I/ F:.E mgAml (enCyl penicillin 1.2 g 8-hourly 8 !ee&s I !ee&s i.v. 1 mgA&g G-12- 8 !ee&s 8-I !ee&s and gentamicin hourly i.v. Enterococci Ampicillin-sensitive Ampicillin i.v. 2 g 8-hourly 8 !ee&s I !ee&s and 1 mgA&g G-12- 8 !ee&s I !ee&s gentamicin i.v. hourly

Ampicillin-resistant

,ancomycin i.v. 1 g 12-hourly and 1 mgA&g G-12gentamicin i.v. hourly (enCyl penicillin 1.2 g 8-hourly i.v. luclo"acillin 2 g 8-hourly (K i.v. GE &g I-hourly) ,ancomycin i.v. 1 g 12-hourly and 1 mgA&g Ggentamicin i.v. hourly

8 !ee& I !ee&s 8 !ee&s I !ee&s

Staphylococci 4enicillin-sensitive 4enicillin-resistant #eticillin-sensitive 4enicillin-resistant #eticillin-resistant

8 !ee&

I !ee&s

8 !ee&s I !ee&s6 8 !ee&s I !ee&s6 8 !ee&s

S#rgical therapy In!ications for s#rgery in infecti e en!ocar!itis 1) .eart failure due to valve damage 2) ailure of antibiotic therapy (persistent or uncontrolled infection) 6) 1arge vegetations on left-sided heart valves !ith evidence orLhigh ris&L of systemic emboli 8) Abscess formation Surgery should not be delayed to permit additional antibiotic therapy, because this course increases the ris& of death. Co'plications 1)/ardiac /ongestive heart failure (6:28:D) 4erivalvular abscesses .eart bloc& Arterial emboli -/ommonly involve e"tremities, spleen, &idneys, bo!el, or brain 2)Splenic abscess 6)?enal Biffuse glomerulonephritis and renal dysfunction and )mbolic renal infarcts causing flan& pain and hematuria 8) @eurologic Intracranial hemorrhage due to hemorrhagic infarcts or ruptured mycotic aneurysms #icroabscesses in brain and meninges in S. aureus endocarditis #ycotic aneurysms Prophyla.is Antibiotic prophyla"is is recommended for any cardiac condition !here the increased ris& of infective endocarditis

En!ocar!itis prophyla.is is reco''en!e! for 1) 4rosthetic cardiac valve 2) 4revious I) 6) /ongenital heart disease (/.B)-/ompletely repaired congenital heart defect !ith prosthetic material orBevice 8) /ardiac transplantation recipients !ho develop cardiac valvulopathy

Infecti e en!ocar!itis prophyla.is

Proce!#re 4rophyla"is for dental, oral and upper respiratory procedures Regi'en Oral regi'en Amo"ycillin 4< 6 g orally, one hour prior to procedure or penicillin allergic patients i. )rythromycin 4< 1 g 2 hours prior to procedure and :.E g I hours after first dose. or ii. /lindamycin 6:: mg 1 hour before procedure and 1E: mg I hours later Parenteral regi'ens Ampicillin I, 2 g 6: minutes before procedure and 1 g I hours later or /lindamycin I, 6:: mg 6: minutes before procedure and 1E: mg I hours later 4rophyla"is for Ampicillin I, 2 g genitourinary and J gastrointestinal procedures -entamicin I, 1.E mgA&g 6: minutes before procedure follo!ed by one dose G hours later of amo"ycillin 4< 1.E g or (or penicillin allergic patients ,ancomycin I, 1 g J -entamicin I, 1.E mgA&g 1 hour prior to procedure, both to be repeated after G hours