Transcript
ENDOKARDITIS INFEKTIF
Definisi : infeksi mikroorganisme pada endokard atau katup jantung
Vegetasi katup (khas) Juga pada endokard dan pembuluh darah
besar Biasanya pada jantung yang rusak P.J. Bawaan atau yang didapat
ENDOKARDITIS INFEKTIF
Prof.dr.H. Saharman Leman, DTM&H. SpPD-KKV
Etio : bakteri, jamur, virus dll Pada jantung normal, E.I. dapat terjadi
pada katup sebab : misalnya pada penyalahgunaan narkoba
Perjalanan penyakit : bisa hiper akut, sub akut, khronik
Sub akut (bulan-2 tahun), hiper akut / akut fatal
Khronik tak didiagnosa
EPIDEMIOLOGI
Umur rata-rata 39-50 tahun Pria > wanita Bertambah banyak Tanda-tanda khas jarang ditemukan Insiden 6-7 dalam 100.000 penduduk
FAKTOR PREDISPOSISI / PENCETUS
1. Kelainan jantung organik (PJR, PJ kongenital, ASHD dll)
2. Tanpa kelainan jantung (akibat obat imunosuppresif, sitostatik, hemodialisa, sirosis hati, PPOK, ginjal, LE, Pirai, obat-obat IV)
PENCETUS : ekstraksi gigi, kateter urine dll
ETIOLOGI
Sub akut : Strept. Viridans (terbanyak) Akut : Staphy. aureus, Staphy. Fecalis,
gram (-) aerob, anaerob, jamur, virus, ragi, kandida
PATOGENESIS DAN PATOLOGI ANATOMI Port d’entre : saluran nafas, saluran kemih,
genital, saluran pencernaan, vena dan kulit. Endokard tidak rata / yang rusak
vegetasi trombosit dan fibrin Katub, abses miokard, aneurisma miokard,
ruptur chorda tendinea Trombus + kuman
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IV Drug Use
Recurrent Polymicrobial Staph aureus accounts for the majority of
cases of endocarditis tricuspid valve, either alone or in
combination, us most often infected
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Predisposing Factors Polymicrobial
Infective Endocarditis
Iv drug use
Central line
Prosthetic valve
Previous IE
Murmur
Dental procedure
Rheumatic disease
Miscellaneous
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Polymicrobial Infective Endocarditisclinical features
IV drug use is the predominant risk factor younger age (mean 36.5 years) 2/3 were male right-sided cardiac involvement in > 60% streptococci more frequent than S. aureus 1/3 of patients died mortality rate is 4x higher for pure left-sides vs
pure right-sided endocarditis
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Diagnostic (Duke) Criteria
Definitive infective endocarditis– pathologic criteria
• microorganisms or pathologic lesions: demonstrated by culture or histology in a vegetation, or in a vegetation that has embolized, or in an intracardiac abscess
– clinical criteria (see below) • two major criteria, or one major and three minor
criteria, or five minor criteria
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Polymicrobial Infective Endocarditisclinical features
IV drug use is the predominant risk factor younger age (mean 36.5 years) 2/3 were male right-sided cardiac involvement in > 60% streptococci more frequent than S. aureus 1/3 of patients died mortality rate is 4x higher for pure left-sides vs
pure right-sided endocarditis
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Diagnostic (Duke) Criteria
Definitive infective endocarditis– pathologic criteria
• microorganisms or pathologic lesions: demonstrated by culture or histology in a vegetation, or in a vegetation that has embolized, or in an intracardiac abscess
– clinical criteria (see below) • two major criteria, or one major and three minor
criteria, or five minor criteria
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Diagnostic (Duke) Criteria
Possible infective endocarditis– findings consistent of IE that fall short of “definite”,
but not “rejected”
Rejected– firm alternate Dx for manifestation of IE
– resolution ofmanifestations of IE, with antibiotic therapy for 4 days
– no pathologic evidence of IE at surgery or autopsy, after antibiotic therapy for 4 days
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Diagnostic (Duke) Criteria
Major criteria– positive blood culture for IE
– evidence of endocardial involvement
Minor criteria– predisposition (heart condition or IV drug use)
– fever of 100.40F or higher
– vascular or immunologic phenomena
– microbiologic or echocardiographic evidence not meeting major criteria
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Duke’s Major Criteria
positive blood culture for IE– typical microorganism (strep viridans, strep bovis,
HACEK group, staph aureus or enterococci in the absence of a primary locus) for endocarditis from two separate blood cultures
– persistently positive blood culture from:• blood cultures drawn more than 12 hr apart, or
• all of 3 or a majority of 4 or more separate blood cultures, with first and last drqwn at least 1 hr apart
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Duke’s Major Criteria
Evidence of endocardial involvement– positive echocardiogram for endocarditis
• oscillating intracardiac mass on valve or supporting structure, or in the path of regurgitant jets, or on implanted material, in the absence of an alternate anatomic explanation
• abscess
• new partial dehiscence of prosthetic valve
– new valvular regurgitation (increase or change in pre-existing murmur not sufficient)
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Duke’s Minor Criteria
predisposition (predisposing heart condition or iv drug use)
fever of 100.40F or higher vascular phenomena (major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctive hemorrhages, Janeway lesions)
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Duke’s Minor Criteria
immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor)
microbiologic evidence (positive blood culture not meeting major criteria or serologic evidence of active infection with organism consistent with IE)
echocardiogram (consistent with IE but not meeting major criteria)
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Risk for Endocarditis
High risk– prosthetic cardiac valve– prior episodes of endocarditis– complex congenital cardiac defect– surgically constructed systemic-pulmonary
shunts or conduits
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Risk for Endocarditis
Moderate risk– patent ductus arteriosus– VSD, primum ASD– coarctation of the aorta– bicuspid aortic valve– hypertrophic cardiomyopathy– acquired valvular dysfunction– MVP with mitral regurgitation
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Risk for Endocarditis
Low risk– isolated secundum atrial septal defect– ASD, VSD, or PDA >6 months past repair– “innocent” heart murmur by auscultation in the
pediatric population– “innocent” heart murmur by echocardiography
in adult patients
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Treatment
Pre-antibiotic era - a death sentence Antibiotic era
– microbiologic cure in majority of patients
KLASIFIKASI E.I
1.a. Endokarditis infektif bakterial sub akut (SBE)
1.b. Endokarditis infektif akut (ABE)2.a. Native valve endokarditis (NVE)2.b. Endokarditis katup prostetik (PVE)
KLASIFIKASI KLINIS :I. S.B.EII. A.B.E
S B E
KELUHAN Tak jelas kapan timbul, Sesudah cabut gigi,
Infeksi saluran nafas, Tindakan lain Demam, lemah, letih, lesu, keringat malam
banyak, anereksia, BB turun, sakit sendi Bila emboli (+) : paralisis, sakit dada, sakit
perut, hematuria, buta mendadak, sakit jari kaki
S B E
GEJALA
1. Gejala umum toksemia : demam remitten, intermitten, menggigil, keringat banyak, anemia, hepatosplenomegali
2. Gejala jantung : penting, kelainan katup dll (SM, IM, IA, PDA, VSD), dispneu, takikardi, aritmia, sianosis, perubahan bising penting
S B E
GEJALA
3. Gejala emboli dan vaskular : ptekhie, Roth’s spot, splinter hemorrhage, Osler’s nodes, abses kulit, aneurisma mikotik, GNA, GG, splenommegali
ENDOKARDITIS INFEKTIF AKUT
Pada jantung normal Akut, panas tinggi Splenomegali, clubbing finger, osler’s node,
ptekhie dll Dst = SBE
PEMERIKSAAN PENUNJANG
LABORATORIUM Leukositosis (neutrofilia), Ig serum , g
globulin (+), C3 , total hemolitik
Biakan mikroorganisme : tiap hari (2-5 hari), dalam media serum, sebelum antibiotik
EKG
PEMERIKSAAN PENUNJANG
EKOKARDIOGRAFI
1. Vegetasi
2. Dilatasi / hipertrofi
3. Katup-katup
RADIOLOGI
1. Gagal jantung
2. Infiltrat paru
DIAGNOSIS
Tidak mudah Kelainan katup, kelainan jantung Demam, biakan darahD/ SBE : Septikemia Kelainan jantung bawaan dll Demam lama + bising +/- Respon pengobatan (+)
DIAGNOSIS
DD/ Demam rematik Pneumonia Sepsis lain ; thromboplebitis, meningitis TBC milier LE GNA, PNA Reaksi Obat
KOMPLIKASI
1. GAGAL JANTUNG
2. EMBOLI
3. ANEURISMA NEKROTIK
4. GANGGUAN NEUROLOGI
PENGOBATAN Antibiotika, sesuai uji kuman Penisilin G ²,4 – 6 juta unit/hari, selama 4
minggu, parenteral 2 minggu, kemudian oral penisilin
+ Streptomisin 2 x 0,5 gr, 2 minggu Pada orang tua (+), gentamisin 3-5 mg /
kgBB, ²-3 dosis/hari, 4-6 minggu Sefalotin, oksasilin, vankomisin,
aminoglikosid Gagal jantung
PROGNOSIS
Buruk pada : Gagal jantung Resistensi mikroorganisma Pengobatan terlambat Bakteremia Orang tua Penderita dengan katup buatan
ENDOKARDITIS INFEKTIF PADA PENYALAHGUNAAN OBAT INTRA VENA
Def. End. Inf. : infeksi mikrobial pada lapisan endotel jantung dengan vegetasi pada daun katup dan dapat meluas ke chorda tendinea, muskulus papilaris, bahkan endokardium ventrikel dan atrium
Terbanyak di katup trikuspid dan pulmonal, jarang pada mitral dan aorta
PATOGENESIS Tidak jelas Diduga kerusakan mekanik karena obat-
oatan tercampur dengan partikel kontamisasi
ETIO Akut : S. aureus Sub akut : S. epidermis, S. viridans
MANIFESTASI KLINIS :
Demam 80-100% Lelah Anoreksia BB menurun Sesak nafas, sakit nkepala, mialgia, mual,
muntah
PEMERIKSAAN FISIK
Lesi ptekhie Osler’s node Lesi Janewey, abnormalitas kulit, emboli
septik, deposisi komplek immunTANDA SPESIFIK Murmur pada katup Di trikuspid : holosistolik. Blowing Kk : gagal jantung kongestif, splenomegali,
emboli paru
PEMERIKSAAN PENUNJANG
Kultur darah : 3 x terpisah Ekokardiogradfi T.E.E 98% (+)
DIAGNOSIS
KRITERIA DUKE UNIVERSITY 1994
1. EI DEFINITE
2. EI POSSIBLE
3. EI REJECTED
E.I. DEFINITE
KRITERIA PATOLOGIS Mikrorganisme : kultur darah, histologis vegetasi
emboli Ditemukan vegetasi diatas, abses intrakardial
histologis
KRITERIA KLINIS 2 kriteria mayor 1 mayor dan 3 kriteria minor 5 kriteria minor
E.I. POSSIBLE
DIANTARA DEFINITE DAN REJECTED
E.I. REJECTED
DIAGNOSIS ALTERNATIF TIDAK DITEMUKAN :
1. MANIFESTASI ENDOKARDITIS SELAMA 2-4 HARI
2. BAKTERI PATOLOGIS EI PADA SPESIMEN / OTOPSI KURANG DARI 4 HARI
KRITERIA MAYOR
1. KULTUR DARAH (+) UNTUK EIa. Mikroorganisme khas EI dari kultur darah
terpisah1. Strep. Viridans, Bovis / HACEK2. Staph. Aureus, enteerococci, tanpa vokus primer
b. Mikroorganisme konsisten EI dari kultur darah (+) persisten sebagai :
1. > 2 kultur darah yang diambil terpisah > 12 jam2. Semua dari 3 atau 4 kultur darah terpisah (atau
sampel awal dan akhir lebih dari 1 jam)
KRITERIA MAYOR
2. BUKTI KETERLIBATAN ENDOKARDIAL
a. EKOKARDIOGRAM1. Massa intrakardial oscilating pada katup atau
struktur lain pada aliran regurgitasi2. Abses3. Tonjolan pada katup prostetik
b. REGURGITASI VALVULAR YANG BARU ATAU MEMBURUK / BERUBAH DARI SEMULA
KRITERIA MINOR
PREDISPOSISI : KONDISI JANTUNG ATAU PENGGUNAAN OBAT IV
DEMAM LEBIH DARI 38 C FENOMENA VASKULAR
– Emboli arteri besar– Infark pulmonal septik– Aneurisma mikotik, perdarahan intra kranial,
konjungtiva dan lesi Janeway
KRITERIA MINOR
FENOMENA IMUNOLOGIS :– Glomerulonefritis, nodul Osler, Roth spots
dan faktor rematoid
BUKTI MIKROBIOLOGIS– Kultur darah (+)– Serologis infektif akut
TEMUAN EKOKARDIOGRAFI– Konsisten dengan EI tetapi tidak yang diatas
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New Treatments
Prosthetic valve endocarditis due to fluconazole-susceptible Candida species– many are due to bloodstream invasion
– chronic oral suppressive therapy with fluconazole for inoperable disease
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SBE Prophylaxis
Standard general prophylaxis amoxicillin
Unable to take oral meds ampicillin
Allergic to penicilin clindamycin
cephalexin
azithromycin
clarithromycin
Allergic to penicillin and unable clindamycin
to take oral medications cefazolin
TERAPI
EMPIRIS SAMBIL MENUNGGU KULTUR DARAH
PERTIMBANGAN AKUT ATAU SUB AKUT
Gram (-) (M.SSA)– Penisilin 6 x 3 juta U IV atau Ampisilin 6 x 2
gram + Gentamisin 3 x 50 mg– Terapi lain Seftriakson 1 x 2 gram– Semuanya diberikan minimal 4 minggu
TERAPI
Bila M.RSA– Vankomisin 2 x 1 gr IV– Terkoplamin 2 x 400 mg IV dibagi 3 dosis– Selama 4 minggu
TERAPI SURGICAL
INDIKASI
1. VEGETASI MENETAP
2. DISFUNGSI KATUP AI, MI AKUT GAGAL JANTUNG YANG TIDAK
RESPON DENGAN MEDIS PERFORASI / RUPTUR KATUP
3. EKSISTENSI PERIVALVULAR
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