infektif endokarditis2

ENDOKARDITIS INFEKTIF

MIOKARDITIS

Masrul SyafriBagian Kardiologi dan Kedokteran VaskularFKUA/ RS Dr M Jamil Padang

Infective Endocarditis

Definitions

A microbial infection of a cardiac valve or theendocardium caused by bacteria, fungi, or chlamydia

Often categorized as acute or subacute based on therapidity of the clinical course

Infective Endocarditis

100% fatal if undiagnosed and untreated 20% fatal if diagnosed and treated uncommon primarily in adults commonly with underlying heart disease

Epidemiology of Endocarditis

Incidence the same or slightly increased 1.7-6.2/100,000 depending on the populationThe age of subjects with endocarditis has increased over the past 60 years (30-40 to 47-69) Among injecting drug users the incidence is as high as 150-2000/100,000 person yearsThere has also been a change in the microbiology of cases Increasing incidence of staphylococciThere has been an increasing incidence of nosocomialendocarditis - both native and prosthetic valveThere is an increased risk of IE among injecting drugusers, patients on long-term hemodialysis, patients withintravenous catheters, diabetics and HIV-infected patients

Incidence of Underlying Heart Diseasein Infective Endocarditis*

Pre-Antibiotic Era Present

Rheumatic ++++^ +Congenital + +Degenerative + ++Mitral valve prolapse + +++Normal valves + ++

*Incidence varies with population studied^ Relative incidence

Strom BL, Abrutyn E, Berlin JA, Kinman JL, Feldman RS, Stolley PD, et al. Ann Intern Med. 1998;129:761-9.IV drug users and nosocomial cases excluded.

Risiko tinggi : penyakit jantung bawaan sianotik, riwayat EI, penyakit katup terutama regurgitasi aorta dan mitralRisiko sedang : prolaps katup mitral disertai regurgitasi atau penebalan katup, stenosis katup mitral, trikuspid, pulmonal, kardiomiopati hipertropiRisiko rendah : defek septum atrium, penyakit jantung iskemik Pengguna obat intravena

Risk Factors for Infective Endocarditis

Dental procedures, poor dental hygiene - viridans streptococci, nutritionally variant streptococci, HACEKProsthetic valves Early: coagulase negative staphylococci, S. aureus Late: coagulase negative staphylococci, viridans streptococciGastrointestinal or genitourinary procedures - enterococci or S. bovis (colon carcinoma)Nosocomial - S. aureus (including MRSA), Gram negatives,Candida species

Brouqui and Raoult, Clin Microbiol Rev, 2001

Risk Factors for Infective Endocarditis

Nosocomial - S. aureus (including MRSA), Gram negatives, Candida speciesHIV - S. aureusAnimal or farm exposure: Coxiella, Chlamydia, BrucellaHistory of homelessness, alcoholism (body lice): Bartonella

Pathogenesis of Infective Endocarditis

Valvular endotheliumMucous membranes - otherperipheral tissueCongenital abnormalities,turbulent blood flowTrauma - damage attissue surfaceNonbacterial thrombus,Native valvesTransientbacteremia Adherence and colonizationPlatelet adherence, fibrin deposition vegetation formationElaboration of bacterial enzymes, proteases

Pathogenesis of Endocarditis

Inoculation of bacteria colonizing a mucosal (e.g., oral mucosa) or peripheral tissue site into the bloodstreamTransient bacteremia of a serum-resistant pathogen capable of adhering to a cardiac valvular surfaceTurbulent blood flow across the valveBacterial adherence to cardiac valvular surfacePathogen - host tissue interaction resulting in vegetation formation and local tissue damage Bacterial persistenceDissemination of infection to other tissue sites and elicitation of systemic findings

Most commonly of the valves, with vegetations = friable masses of infecting organisms and blood clot

Pathogenesis:1. Valvular endothelial injury2. Platelet + fibrin deposition3. Microbial seeding4. Microbial multiplication Up to 1010 bugs/gm (mature)

Gross Pathology

+ / - perforation of valve+ / - adjacent abscess+ / - fibrotic scarring+ / - calcification

Microscopic Pathology

Fibrin, platelets, masses of organisms, +/- necrosis, +/- neutrophils

Later: +/-lymphocytes, +/- macrophages, +/- fibroblasts, +/- fibrosis

Characteristic lesion vegetation containing : platelets, erythrocytes, fibrin, inflamatory cells and microorganisms.

Factors Contributing to the Pathogenesis of Endocarditis

Hemodynamics - blood flow patternsBacterial propertiesHost factors

HEMODYNAMICS OF ENDOCARDITIS

Serum resistance - i.e. complement Bacterial adhesins mediate binding to the nonbacterial thrombus and to endothelial cells:dextran, fibrinogen- binding proteins Invasive potential of bacteria Ability to elaborate extracellular proteases Capacity for metastatic seeding Stimulation of tissue factor activityBacterial Factors Involved in thePathogenesis of Infective Endocarditis

Host Factors Involved in thePathogenesis of Infective Endocarditis

Valvular surfaces Nonbacterial thrombus forms on damaged valves Direct adherence to the endovascular surface of normal valves Suture line, valve surface of prosthetic valvesPlatelets dual role Platelet microbicidal proteins (-granules) Bacteria induce platelet aggregation Part of nonbacterial thrombus surfaceLeukocytes, complement, cytokines

The Pathogenetic Basis for the ClinicalManifestations of Infective Endocarditis

Valvular destruction and local intracardiaccomplicationsBland or septic embolization of vegetationsSustained bacteremiaImmunologic phenomena

Osler, Gulstonian Lectures, Lancet, 1885Weinstein and Schlesinger NEJM, 1974

Incubation period - NVE 2 weeks - PVE 2-5 weeks or more Signs and symptoms Symptoms % Signs % Demam 80-85 % Demam 80-90 % Menggigil 42-75 % Murmur 80-85 % Keringat 25 % Changing/new murmur 10-40 % Anoreksia 25-55 % Abnormalitas syaraf 30-40 % Penurunan BB 25-35 % Kejadian emboli 20-40 % Malaise 25-40 % Splenomegali 15-50 % Dyspnea 20-40 % Clubbing 10-20 % Batuk 25 % Manifestasi perifer Stroke 13-20 % Oslers node 7 -10 % Sakit kepala 15-40 % Splinter haemorrhage 5-15 % Mual/muntah 15-20 % Petechiae 10-40 % Myalgia/arthralgia 15-30 % Janeway lesion 6-10 % Nyeri dada 8-35 % Retinal lesion/Roth spot 4-10 % Nyeri perut 5-15 % Nyeri punggung 7-10 % Confusion 10-20 %Karchmer AW. Infective endocarditis. In : Braunwald E,editor, Heart Disease. 5th edn Philadelphia:Saunders;1997 Clinical features

Janeway Lesions:erythematous, macular, non tender.septic emboli?Oslers Nodes:Tender, subcutaneous nodules.4 Ps:PinkPainfulPea-sized Pulp of the fingers/toes.Immunologic origin?

Subungual (splinter) hemorrhageConjunctival hemorrhageRetinal hemorrhage: Roth Spot

Clinical featuresJaneways lesionSplinter haemorrhageMylonakis E, Calderwood SB. Infective endocarditis in adults.NEJM 2001;345:1318-29.

Conjuctival petechiaeOslers nodeMylonakis E, Calderwood SB. Infective endocarditis in adults.NEJM 2001;345:1318-29.Clinical features

30-65% of native valve endocarditisNormal oral commensalsA group, composed of several species:S. mitior, S. sanguis, S. mutans,etc.Alpha-hemolytic, non-typableTypical agents of classic SBEStrep. viridans

S. bovisLancefield group DGut flora: associated with GI pathologyS. pneumonia1-3% of cases of IE with predilection for AVUsually, in those with immune suppressionDM and EthanolismGroup B StreptococciElderly with chronic disease

Normal inhabitant of GI tract.Frequently encountered in UTIs.Up to 40% of cases without identified underlying predisposition to IE.Difficult to treat due to drug resistance.

Coagulase Positive (Staph. aureus)a major causative agent in all populations of IEtypically produces acute IEfulminant, rapidly progressive with few immunologic signs.CNS complications in 30-50%Coagulase Negative (Staph. epi, et al)Major cause of PVE. 3-8% of NVE.

Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, KingellaGram negative inhabitants of the upper airways.Large vegetations, high likelihood of embolization.Slow growing: hold cultures for 3 weeks.Traditionally sensitive to beta lactams, now some produce beta lactamase.

Commonly encountered agents:Candida, Torulopsis, AspergillusPredispositionsProsthetic valvesIVDAImmunosupressionHyperalimentationProlonged abx treatmentLarge vegetations and frequent embolic events.

PseudomonasBrucellaDiphtheroidsListeriaBartonellaCoxsiellaChlamydia

Accounts for 25% of cases of IE in US.5:1 male:femalePre-existing valvular diseases uncommon.Variable microbiology.Mortality

Affects 3% of prosthesis patients.Highest risk in first 6 months post op.Accounts for 10-20% of all IE cases.Increased risk inMalesBlacksProlonged pump timeMultiple valve replacement

Early (

KRITERIA DUKE

A. Endokarditis infektif definitif : 1. Kriteria patologi Mikroorganisme : dibuktikan dengan hasil biakan atau histologi vegetasi atau pada vegetasi yang mengalami emboli atau pada abses dalam jantung atau Lesi patologi : abses dalam jantung dan vegetasi yang diperjelas oleh histologis yang memperlihatkan EI aktif

2. Kriteria klinik : 2 kriteria mayor atau 1 kriteria mayor dan 3 minor atau 5 kriteria minorDIAGNOSIS

B. Kemungkinan endokarditis infektif (possible) Hasil sesuai dengan EI tetapi tidak cukup definitive, maupun rejected C. Endokarditis infektif ditolak (rejected ) - Terdapat bukti kuat yang menunjang gejala yang disebabkan penyakit lain - Perbaikan manifestasi EI dengan pengobatan antibiotik dalam waktu 4 hari atau kurang - Tidak ditemukan bukti EI pada operasi atau otopsi setelah pengobatan antibiotik 4 hari atau kurang

DIAGNOSISESC guidelines

Blood cultures critical for specific diagnosis 3 sites 30-60 minutes apart before starting antibiotics. 86 96% of 1st cultures positive 98 100% of 1st 2 cultures positive

Blood cultures may be negative if the patienthas already received antibiotics; a few casesof infective endocarditis are culture-negative

lebih dianjurkan sampel darah arterisaat suhu tubuh meningkat ?dilakukan paling sedikit 3 kali, jarak 1 jam tusukan langsungsampel : 2 tabung (aerob dan anaerob) berisi 50 ml media + 10 ml darah dibiakkan suhu 37o c selama 5-6 harikeadaan khusus : - sepsis antibiotik empiris setelah ambil sampel - terapi antibiotik jangka pendek stop 3 hari - terapi antibiotik jangka panjang stop 6-7 hari

BIAKAN DARAHESC guidelines

Kriteria mayor

1. Biakan darah positif a. Mikroorganisme tipikal untuk EI dari 2 biakan darah terpisah : - S. viridans, S. bovis, HACEK - S. aureus atau enterokokus tanpa ditemukan fokus primer b. Biakan tetap positif, apabila - > 2 sampel positif dengan jarak pengambilan 12 jam atau - Tiga sampel atau mayoritas dari 4 sampel atau lebih hasil positif, dengan jarak waktu pengambilan pertama dan terakhir paling sedikit 1 jamDIAGNOSIS

2. Bukti keterlibatan endokardium

a. Ekokardiogram positif apabila : - Massa dalam jantung pada katup atau struktur yang menunjang katup atau pada aliran regurgitasi - Abses atau - Tonjolan baru dari katup buatan atau regurgitasi katup yang baru (perburukan atau perubahan bising yang sebelumnya tidak ada)

b. Regurgitasi katup yang baru

DIAGNOSIS

Kriteria Minor

a. Adanya faktor predisposisi (kelainan jantung atau penyalahguna obat) b. Demam > 38 celcius c. Fenomena vaskuler : emboli arteri mayor, infark paru septik, anuerisma mikotik, perdarahan intrakranial, lesi Jeneway, perdarahan konjungtiva d. Fenomena imunologi : glomerulonefritis, nodus osler, bintik roth e. Bukti mikrobiologi : biakan positif tetapi tidak memenuhi kriteria mayor atau kelainan serologis sesuai EI. f. Hasil ekokardiografi yang sesuai dengan endokarditis infektif tetapi tidak memenuhi kriteria mayor.

DIAGNOSIS

ALGORITME PEMERIKSAAN EKOKARDIOGRAFIGAMBARAN EKOKARDIOGRAFIKECURIGAAN EISEGERA TTEBILA MELIBATKAN ALAT/ KATUP BUATANKUALITAS GAMBAR BAIKTTE POSITIFDICURIGAI ATAU DIDOKUMENTIR KOMPLIKASI ATAU BEDAH SELAMA FASE AKTIF EIKECURIGAANRENDAHTINGGITEE+--++--+ESC guidelines

GAMBARAN EKOKARDIOGRAFIPotongan tranesofagus dan transgaster gambaran ventrikel kanan dan kiri, atrium kanan dan kiri, katup mitral, katup trikuspid, septum interventrikular dan interatrial, serta aorta.Eur Heart J 1995

Principles of Therapy

Bactericidal antibiotics must be usedProlonged therapy is necessary (weeks)Treatment is best started after multiple sets of bloodcultures have been taken.Urgency in the initiation of therapy is required for acute but not subacute endocarditis.Synergistic combinations of antibiotics are used when available.

EVALUASI : - DEMAM MENETAP ULANGAN BIAKAN DARAH (8 MGG SETELAH DARAH I)- BERHASIL : BIAKAN DARAH NEGATIF SETELAH 7 HARI PENGOBATAN- GAGAL : BIAKAN DARAH POSITIF SETELAH 10 HARI PENGOBATANPENATALAKSANAAN

1. Medikamentosa Terapi endokarditis oleh karena streptokokus Penisilin G : 12 20 juta IU/ 24 jam iv, dibagi dalam 4-6 dosisCeftriakson : 2 gr i.v dosis tunggal (infuse cepat). Bila diberikan secara intramuskular, sebaiknya hanya 1 gram dalam satu lokasi suntikan.Vankomisin : 30 mg/kg/hari iv dibagi dalam 2 dosis (lama pemberian tidak kurang dari 45 menit).Teicoplanin : 10 mg/kg i.v 2 kali sehari dalam 9 dosis pertama, dilanjutkan dengan 10 mg/kg hari dosis tunggal.Aminoglikosid : diberikan dalam 2 dosis perhari. Merupakan terapi kombinasi dengan obat tersebut di atas, selama 2 minggu perawatan pertama.PENATALAKSANAAN

2. BedahINDIKASI :NVE : - gagal jantung - demam menetap - destruksi jaringan sekitar katup - kuman penyebabnya adalah jamur, Brucella spp, Coxiella spp - emboli berulang - destruksi katup - komplikasi neurologi PENATALAKSANAAN

Jamur Candida spp CNE (Culture Negative Endocarditis )PENATALAKSANAANTerapi empiris terhadap Culture Negative Endocarditis pada NVE atau PVENVE

Vankomisin 15.0 mg/kg iv setiap 12 jam 4-6 minggu + gentamicin 1.0 mg/kg i.v setiap 8 jam 2 minggu

PVE

Vankomisin 15.0 mg/kg i.v setiap 12 jam 4-6 minggu + Rifampisin 300-450 p.o setiap 8 jam 4-6 minggu + Gentamisin 1.0 mg/kg i.v setiap 8 jam 2 minggu

Gram negatifEnterobacteriaceae : beta laktam dosis tinggi + gentamisin 3 mg/kg hari dalam 2-3 dosis selama 4-6 mingguPseudomonas : beta laktam dosis tinggi dengan antipseudomonas + tobramisin 3 mg/kg/hari dalam 2-3 dosis selama 6 mingguHACEK : generasi III cephalosporin, misalnya ceftriakson 2 gr/hari iv dosis tunggal selama 3-4 minggu pada NVE dan 6 minggu pada PVE. Selain itu Ampisilin sampai 12 gr/hari dalam 3-4 dosis + gentamisin (3 mg/kg/hari dalam 2-3 dosis)Coxiella burnette : Doksisiklin 100 mg iv setiap 12 jam + Rifampin

PENATALAKSANAANTerapi endokarditis oleh karena kuman jenis lain

Terapi endokarditis karena enterokokus dan streptokokus resistens terhadap penisilinPENATALAKSANAANPenisilin MIC < 8 mg/l dan Penisilin G 16-20 juta IU terbagi 4-6 dosis + gentamisin MIC < 500 mg/l gentamisin 3 mg/ kg /24jam terbagi 2 dosis selama 4 mgg

Alergi penisilin dan enterococal yang Vankomisin 30 mg/kg/24 jam iv dosis terbagi 2suseptibel terhadap penisilin/ + gentamisin seperti di atas selama 6 mggGentamisin

Resisten terhadap penisilin Vankomisin 30 mg/kg/24 jam iv dosis terbagi 2 + gentamisin seperti di atas selama 6 mgg

Terapi pada NVE dan PVE oleh karena Streptokokus PENATALAKSANAANRegimen A NVE : suseptibilitas penuh terhadap penisilin (MIC < 0,1 mg/l)

Usia < 65 th, Penisilin G 12-20 juta UI/24 jam iv terbagi 4-6 dosis selama serum kreatinin normal 4 mgg + gentamisin3 mg/ kg 24jam (max 240mg/hr), terbagi 2-3 dosis selama 2 mgg Kondisi sama dg di atas Penisilin G 12-20 juta UI/24 jam iv terbagi 4-6 dosis selamatanpa komplikasi dan 2 atau 4 mgg dilanjutkan terapi ambulatoarsetelah 7 hari respon terapi cepat perawatan di rumah sakit

Usia > 65 th dan atau Penisilin G sesuai fungsi ginjal selama 4 mgg atau serum kratinin meningkat ceftriaxon 2 g/ 24 jam dosis tunggal selama 4 mggatau alergi penisilin

Alergi penisilin atau Vankomisin 30 mg/kg/24 jam iv dosis terbagi 2 selama 4 mgg Sepalosprorin Regimen B :suseptibiliti terhadap penisilin (MIC 0,1 mg/l-0,5 mg/l) atau PVE Penisilin G 12-20 juta UI/24 jam iv terbagi 4-6 dosis atau Ceftriaxon 2 gr / 24 jam dosis tunggal selama 4 mgg + gentamisin 3 mg/ kg /24jam terbagi 2-3 dosis selama 2 mgg Regimen C resisten terhadap penisilin, MIC > 0,5 mg/l Terapi sama dengan enterokokus

Terapi Endokarditis oleh karena StaphylococcusPENATALAKSANAANRegimen A NVE MSSA tidak alergi penisilin MSSA alergi penisilin MRSA Oksasilin 8-12 gr/24 jam iv,terbagi 4 dosis selamaminimal 4 mgg + gentamisin 3 mg/ kg /24jam (max 240mg/hr), terbagi 3 dosis pada 3-5 hari pertama Vankomisin 30 mg/kg/24 jam iv dosis terbagi 2 selama 4-6 mgg + gentamisin 3 mg/ kg /24jam ( maksimal240mg/hr), terbagi 3 dosis pada 3-5 hari pertama Vankomisin30 mg/kg/24 jam iv dosis terbagi 2 dosis selama 6 mgg

Regimen B PVE MSSA MRSA, CONS Oksasilin 8-12 gr/24 jam iv,terbagi 4 dosis + rifampicin 900 mg/24 jam iv terbagi 3 dosis, selama 6-8 minggu, +gentamisin 3 mg/ kg /24jam (max 240mg/hr), terbagi 3 dosis selama 2 mgg opertama pengobatan Vankomisin30 mg/kg/24 jam iv dosis terbagi 2 selama 6 minggu, + rifampisin 300 mg/ 24 jam iv terbagi 3 dosis, + gentamisin 3 mg/ kg /24jam ( maksimal 240 mg/hari) terbagi 3 dosis, seluruhnya selama 6-8 mgg ESC guidelines

Circulation 2005;111;e394-e433* Ceftriaxone alone could be administrated for 4 weeks instead of Penicillin G

BacterialSusceptible/ResistantRegimenDosage and routeDurationViridan StreptococciPenicillin susceptiblePenicillin G Sodium1218 million U/24 h IV either continuously or in 4 or 6 equally divided doses4 wkStreptococcus bovisCeftriaxone Sodium* + Gentamicin2 g/24 h IV/IM in 1 dose + 3 mg/kg per 24 h IV/IM in 1 dose2 wkVancomycin hydrochloride30 mg/kg per 24 h IV in 2 equally divided dose4 wkViridan StreptococciRelatively Penicillin ResistantPenicillin G Sodium24 million U/24 h IV either continuously or in 46 equally divided doses4 wkStreptococcus bovisCeftriaxone Sodium + Gentamicin2 g/24 h IV/IM in 1 dose + 3 mg/kg per 24 h IV/IM in 1 dose2 wkVancomycin hydrochloride30 mg/kg per 24 h IV in 2 equally divided dose4 wkStaphylococciOxacillin-susceptible strainsNafcillin or oxacillin12 g/24 h IV in 46 equally divided doses6 wkOptional addition of gentamicin3mg/kg/24h IV/IM in 2 or 3 equally divided doses3-5 d For penicillin allergicCefazolin6 g/24 h IV in 3 equally divided doses6 wkOptional addition of gentamicin3 mg/kg per 24 h IV/IM in 2 or 3 equally divide doses3-5 dOxacillin-resistant strainsVancomycin30 mg/kg per 24 h IV in 2 equally divided doses6 wk

Circulation 2005;111;e394-e433

BacterialSusceptible/ResistantRegimenDosage and routeDurationViridan StreptococciPenicillin susceptiblePenicillin G Sodium24 million U/24 h IV either continuously or in 4 or 6 equally divided doses6 wkStreptococcus bovisCeftriaxone Sodium + Gentamicin2 g/24 h IV/IM in 1 dose + 3 mg/kg per 24 h IV/IM in 1 dose6 wk + 2 wkVancomycin hydrochloride30 mg/kg per 24 h IV in 2 equally divided dose6 wkViridan StreptococciRelatively Penicillin ResistantPenicillin G Sodium24 million U/24 h IV either continuously or in 46 equally divided doses6 wkStreptococcus bovisCeftriaxone Sodium + Gentamicin2 g/24 h IV/IM in 1 dose + 3 mg/kg per 24 h IV/IM in 1 dose6 wkVancomycin hydrochloride30 mg/kg per 24 h IV in 2 equally divided dose6 wkStaphylococciOxacillin-susceptible strainsNafcillin or oxacillin + Rifampin12 g/24 h IV in 6 equally divided doses+900 mg per 24 h IV/PO in 3 equally divided doses > 6 wkGentamicin3 mg/kg per 24 h IV/IM in 2 or 3 equally divide doses2 wkOxacillin-resistant strainsVancomycin+Rifampin30 mg/kg per 24 h IV in 2 equally divided doses+900 mg/24 h IV/PO in 3 equally divided doses >6 wkGentamicin3 mg/kg per 24 h IV/IM in 2 or 3 equally divide doses2 wk


BacterialSusceptible/ResistantRegimenDosage and routeDurationEnterococciPenicillin, Genytamycin, Vancomycin SusceptibleAmpicillin sodium12 g/24 h IV in 6 equally divided doses4-6 wkPenicilin G sodium+Gentamicin1830 million U/24 h IV either continuously or in 6 equally divided doses+3 mg/kg per 24 h IV/IM in 3 equally divided doses4-6 wkVancomycin+Gentamicin30 mg/kg per 24 h IV in 2 equally divided doses+3 mg/kg per 24 h IV/IM in 3 equally divided doses6 wkPenicillin, Streptomycin, Vancomycin Susceptible, Gentamicin ResistantAmpilin sodium12 g/24 h IV in 6 equally divided doses4-6 wkPenicillin G +Streptomycin24 million U/24 h IV continuously or in 6 equally in divided doses+15 mg/kg per 24 h IV/IM in 2 equally divided4-6 wkVancomicin+Streptomycin30 mg/kg per 24 h IV in 2 equally divided doses+15 mg/kg per 24 h IV/IM in 2 equally divided doses6 wkVancomycin, aminoglycoside Susceptible, Penicillin ResistantAmpicillin-Sulbactam+Gentamicin12 g/24 h IV in 4 equally divided doses+3 mg/kg per 24 h IV/IM in 3 equally divided doses6 wk Intrinsic Penicillin resistantVancomycin+Gentamicin30 mg/kg per 24 h IV in 2 equally divided doses+3 mg/kg per 24 h IV/IM in 3 equally divided doses6 wkPenicillin, Aminoglycoside,Vancomycin Resistant E faeciumLinazolid1200 mg/24 h IV/PO in 2 equally divided doses> 8 wkQuinupristin-dalfopristin22.5 mg/kg per 24 h IV in 3 equally divided doses> 8 wkPenicillin, Aminoglycoside,Vancomycin Resistant E faecalisImipenem/cilastatin+Ampicillin 2 g/24 h IV in 4 equally divided doses+12 g/24 h IV in 6 equally divided doses> 8 wkCeftriaxone Sodium + Ampicillin2 g/24 h IV/IM in 1 dose+12 g/24 h IV in 6 equally divided doses> 8 wk


RegimenDosage and routeDurationHACEKCeftriaxone sodium2 g/24 h IV/IM in 1 dose4 wkAmpicillin- sulbactam12 g/24 h IV in 4 equally divided doses4 wkCiprofloxacin1000 mg/24 h PO or 800 mg/24 h IV in 24 wk


BacterialValvesRegimenDoseDurationCulture NegativeNative ValveAmpicillin-sulbactam+Gentamicin12 g/24 h IV in 4 equally divided doses+3 mg/kg per 24 h IV/IM in 3 equally divided doses4-6 wkVancomycin+Gentamicin30 mg/kg per 24 h IV in 2 equally divided doses+3 mg/kg per 24 h IV/IM in 3 equally divided doses4-6 wkplus ciprofloxasin1000 mg/24 h PO or 800 mg/24 h IV in 2 equally divided doses4-6 wkBacterialValveRegimenDosage and routeDurationCulture NegativeProsthetic ValveVancomycin+Gentamicin30 mg/kg per 24 h IV in 2 equally divided doses+3 mg/kg per 24 h IV/IM in 3 equally divided doses6 +2 wkplus Cefepim+Rifampin6 g/24 h IV in 3 equally divided doses+900 mg/24 h PO/IV in 3 equally divided doses6 wk

Anti Bacterial Therapy for Culture negativeCirculation 2005;111;e394-e433

BacterialBartonellaRegimenDosage and routeDurationCulture NegativeSuspectedCeftriaxone+Gentamicin2 g/24 h IV/IM in 1 dose+3 mg/kg per 24 h IV/IM in 3 equally divided doses6 + 2 wkwith/without Doxycycline200 mg/kg per 24 h IV/PO in 2 equally divided doses6 wkDocumentedDoxycycline+Gentamicin200 mg/24 h IV or PO in 2 equally divided doses+3 mg/kg per 24 h IV/IM in 3 equally divided doses6+2 wk

TIMING OF SURGERY

Prosthetic cardiac valves, including bioprosthetic and homograft valvesPrevious bacterial endocarditisComplex cyanotic congenital heart disease (eg, single ventricle states, transposition of the great arteries, tetralogy of Fallot)Surgically constructed systemic pulmonary shunts or conduits

Most other congenital cardiac malformations (other than above and below)Acquired valvular dysfunction (eg, rheumatic heart disease)Hypertrophic cardiomyopathyMitral valve prolapse with valvular regurgitation and/or thickened leaflets

Isolated secundum atrial septal defectSurgical repair of atrial septal defect, ventricular septal defect, or patent ductus arteriosus (without residua beyond 6 mo)Previous coronary artery bypass graft surgeryMitral valve prolapse without valvular regurgitation *

Physiologic, functional, or innocent heart murmurs Previous Kawasaki disease without valvular dysfunctionPrevious rheumatic fever without valvular dysfunctionCardiac pacemakers (intravascular and epicardial) and implanted defibrillators

Respiratory TractET intubationFlexible bronchoscopyPE tubesGI TractTEEEGD

GU TractVaginal hysterectomyVaginal deliveryC - sectionIn uninfected tissue:D and C/AbUrethral cathSterilizationIUDsCircumcision

Prophylaxis RecommendedDental procedures - extractions, cleaning withbleeding, periodontal proceduresRespiratory tract - tonsillectomy, rigidbronchoscopyGastrointestinal - schlerotherapy, biliary tractsurgeryGenitourinary - C-section, cystoscopy, prostatesurgery

JAMA 277:1794, 1997

ESC guideline; European Heart J 2004;00, 1-37

Dental, Oral, Oesophageal procedure

Not alergic PenicillinAlergic PenicillinRouteTime2 g Amoxicillin 600 mg ClindamycinOral/ IV1/2-1 h before(Child: 50 mg/kg)(Child: 20 mg/kg)

500mg Azithromycin/ClarithromycinOral1 h before

Prophilaxis RegimenESC guideline; European Heart J 2004;00, 1-37

Genitourinary or Gastrointestinal Tract. Procedure Not allergic Penicillin

High riskRouteTimeModerate riskRouteTime2 g Amoxicillin+1.5mg/kg gentamicin I.V. or I.M.1/2-1 h before2g Amoxicillin/AmpicillinI.V./p.o.1/2-1 h before1g Amoxicillin/Ampicillinp.o.6 h laterAllergic PenicillinHigh riskRouteTimeModerate riskRouteTime1g Vancomycin+1.5mg/kg GentamicinI.V./I.M.over 1-2 h before1g VancomycinI.V./I.M.over 1-2 h before

Emboli Komplikasi paru Gagal jantung Miokarditis, Acute Renal Failure Gangguan konduksi KOMPLIKASI

Congestive Heart Failure:

Greatest impact on prognosis. Moderate to severe: 20% of case. Develop acutely from perforation, rupture, valve obstruction, progressive worsening of valve dysfunction 2/3may progress to severe CHF within the first month of therapyCirculation 2005;111;e394-e433

Risk of Embolization:

Occurs in 22%- 50% of Cases. The highest incidence seen in mitral and aortic valve. Most emboli occur within the first 1-2 week of therapy. Increased risk in staphylococcal, streptococci, fungal cause or increasing vegetation size during therapy

Periannular extension of InfectionSplenic AbscessMycotic Aneurysms


Myocarditis

Uncommon (1% at autopsy) (but 5% of patients in influenza, polio, Coxsackie virus epidemics)

Slight male predominance (male : female ratio 6 : 4)

Usually with pericarditis (hence the term myopericarditis)

Myocarditis is clinically and pathologically definedas inflammation of the myocardium.

Despite this unambiguous definition, the classification, diagnosis, and treatment of myocarditis continue to prompt considerable debate among clinicians.

*THE POSTVIRAL AUTOIMMUNITY HYPOTHESIS*ANTIGENIC MIMICRY HYPOTHESIS*DIRECT VIRAL INJURY HYPOTHESIS*DIRECT IMMUNE INJURY HYPOTHESIS

Myocarditis

Requires cardiac biopsy (generally transvenous right ventricular) for the diagnosis

Most commonly viral (Coxsackie B2, B3, B4 and B5 cause up to 44% of sporadic cases in adults)

Viral Myocarditis

Commonly in young, healthy individuals

Usually disseminated infection in neonates (with 50% mortality)

May have 2 phases:1. early direct viral infection of myocytes2. later auto-immune attack on myocytes

Viral Myocarditis

Manifestations

Fever, chest pain, dyspnea, malaise, myalgias, tachycardia, pericardial friction rub and electrocardiographic findings

(May cause sudden death due to arrhythmia)

Viral Myocarditis: Pathology

Pale mottled flabby dilated heart

multifocal interstitial, usually mononuclear (primarily lymphocytic) inflammation

associated with myocyte injury and necrosis (cytoplasmic hypereosinophilia, loss of cross-striations, nuclear degeneration and lysis)

Viral Myocarditis

90% recovery,10% chronic dilated cardiomyopathy,death rare (in adults)

Parvovirus B19, hepatitis C virus, adenovirus, cytomegalovirus, Coxsackie virus or otherenteroviruses in some dilated cardiomyopathy

Steroids and immunosuppressive drugs dont improve prognosis

Bacterial Myocarditis

Staphylococcus aureus (abscesses, part of disseminated infection)

Lyme disease (10%, AV block common)

Rocky Mountain Spotted Fever (50%)

Diphtheria (exotoxin)

Fungal Myocarditis

1. Candida- in immunocompromised patients- causes abscesses or granulomas- part of disseminated infection

2. Aspergillus- ditto

Protozoal Myocarditis

1. Toxoplasmosis primarily in immunocompromised patients, with foci of necrosis, chronic inflammation, intra-myocyte cysts (containing bradyzoites) and free tachyzoites

2. Trypanosomiasis Chagas disease, in Latin America (esp. Brazil)

endovascular microbial infection of cardiovascular structures including endarteritiris of the large intrathoracic vessels or of intracardiac foreign bodies facing the blood stream.ESC Guidelines,2004Definition of Infective Endocarditis

(This is not all patients with fever or positive blood cultures).Circulation 1997; 95: 1686-1784

Native Valves-ACC Guidelines:Detection/characterization of valvular lesionsDetection of vegetations and characterization of lesions in patients with CHDDetection of associated abnormalitiesReevaluation studies in complex IEEvaluation of patients with high suspicion of culture-negative IE

Prosthetic Valves-ACC Guidelines:Detection/characterization of valvular lesionsDetection of associated abnormalitiesReevaluation in complex IEEvaluation of suspected IE and negative culturesEvaluation of persistent fever without known source

TEE:Prosthetic valvesPoor visualization on TTE and high suspicionDetection of associated complicationsPreoperativeReevaluation in complex IE

DIAGNOSISDUKES CRITERIA

Pemberian obat untuk profilaksis ditujukan pada pasien-pasien yang mempunyai risiko tinggi dan sedang Probabiliti terjadinya EI tertinggi pada tindakan terhadap gigi dan mulut

Profilaksis terhadap kuman enterokokus, streptokokus bovis dan enterobacteriaceae PENCEGAHAN

risiko morbiditi dan mortaliti diagnosa cepat, terapi efektif serta penemuan dini terjadi komplikasi perkembangan risiko, klasifikasi dan terminologi, kuman penyebab, kriteria diagnosis, pencegahan, serta jenis antibiotika PENDAHULUAN

Historical Perspective.. A concretion larger than a pigeons egg; contained in the left auricle. Burns, 1809Oslers Gulstonian lectures provided the 1st comprehensive overview of the diseaseLewis and Grant (1923) were the first to link a transient bacteremia with deformed valves as the two predominant risk factors for infectionThe introduction of penicillin marked the first successful therapy for this otherwise lethal infection

Oslers Gulstonian

EPIDEMIOLOGI Insidens Endokarditis Infektif 1,7 6,2 kasus dalam 100.000 org /tahun - Laki-laki : perempuan 1,7:1 - Faktor : jumlah penduduk, infeksi, protese di bidang jantung dan pembuluh darah, imunosupresif, obat-obatan intravena

EI memberi risiko morbiditas dan mortalitas yang tinggi..Terminologi EI berdasarkan aktifiti, rekurensi, anatomi, mikrobiologi.Faktor risiko penting untuk mencegah terjadinya EI diantaranya dengan cara memberikan obat profilaksis sebelum tindakan diagnosis dan terapi.Gambaran klinis secara umum sama, akibat proses kardiak dan non kardiakDiagnosis berdasarkan klinis, pemeriksaan ekokardiografi terutama TEE, dan biakan darah, kemudian ditentukan dengan kriteria Duke.Penatalaksanaan : medikamentosa dan atau bedahKomplikasi harus diperhatikan selama masa perawatan KESIMPULAN

Immunologic Manifestations of Infective Endocarditis

Hypergammaglobulinemia; both antigen specific andpolyclonal B cell activation (e.g., rheumatoid factor) May block IgG opsonic response, accelerate microvascular damage or stimulate phagocytosisVasculitis Circulating immune complexes HypocomplementemiaClinical syndromes: Lumpy-Bumpy glomerulonephritiswith deposition of complexes plus complement, Oslers nodes

Patologi NVE - Kardiak - Non kardiakEndokarditis sisi kanan Endokarditis sisi kiri

Patologi PVE

PATOGENESIS

TRAUMA MEKANIK, IMUNOLOGIS ENDOKARDIUM TIDAK INTAK PERLEKATAN MIKROTROMBUS

MIKRORGANISME KE DALAM SIRKULASI MELEKAT PADA ENDOKARDIUM

BERTAMBAH BANYAK DAN MERANGSANG FORMASI TROMBUS SELANJUTNYA

VEGETASI

IVDA ?

PATOGENESIS

Berdasarkan : (a) aktifiti penyakit dan rekurensi, (b) status diagnosa, (c) patogenesis, (d) letak anatomi, dan (e)mikrobiologi Terminologi baru : - active mitral valve IE due to Enterococcus faecalis - healed recurrent PVE due Staphylococcus epidermidis - suspected culture negative late mitral valve endocarditis KLASIFIKASI DAN TERMINOLOGIESC guidelines

KLASIFIKASI DAN TERMINOLOGIaktifitirekurensTerminologidiagnosispatologianatomimikrobiologiEpisode 1aaktifsembuhrelapsrekurenssuspectedpossibleEarly PVELate PVEIVDAbKatup mitral, Aorta, trikuspiddsbMikroorganismeKultur negatifSerologis negatifPCR negatifHistologis negatifdefiniteanativeaa bila kolom rekurens, terminologi diagnosis, dan atau patologi tanpa teks, menunjukkan episode pertama (bukan relaps atau rekurens), definite IE (bukan suspected atau possible) dan keterlibatan katup asli (native valve)b intravenous drug abuseTerminologi Endokarditis InfektifESC guidelines

PVE : - early PVE - late PVE PENATALAKSANAAN

Prevention of Infective Endocarditis

High risk Prosthetic valve Complex congenital heart disease Previous endocarditisModerate risk Acquired valvular dysfunction (e.g. rheumatic valve) Mitral valve prolapse with regurgitationNegligible risk Mitral valve prolapse without regurgitation Rheumatic fever without valvular dysfunction

AHA Recommendations, JAMA 277:1794, 1997

Respiratory TractTonsillectomyViolation of respiratory mucosa.Rigid bronchoscopy.Gastrointestinal TractEsophageal sclerotherapy or stricture dilationERCPBilliary surgeryViolation of intestinal mucosaGU TractProstate surgeryCystoscopyUrethral dilatation

Microbiology of Native Valve Endocarditis in Urban Hospitals

Organisms Percent Cases

Streptococcus spp. 34Enterococcus spp. 6Staphylococcus aureus 40Coagulase-negative staphylococci 5Gram negative bacilli 6Fungi 2Misc. / Polymicrobial 3Culture negative 4

Karchmer, Scientific American Medicine, 1999

infektif endokarditis2

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