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04/21/2304/21/23 11
2. SPECTRUM AND MANAGEMENT OF 2. SPECTRUM AND MANAGEMENT OF CHRONIC LIVER DISEASE CHRONIC LIVER DISEASE
(CLD)(CLD)
HSAR LELOSUTANHSAR LELOSUTAN
SUBDIVISION OF GASTROENTEROLOGY-HEPATOLOGY SUBDIVISION OF GASTROENTEROLOGY-HEPATOLOGY
DEPARTMENT OF INTERNAL MEDICINEDEPARTMENT OF INTERNAL MEDICINE
CENTRAL ARMY HOSPITAL (RSPAD) GATOT SOEBROTO - JAKARTACENTRAL ARMY HOSPITAL (RSPAD) GATOT SOEBROTO - JAKARTA
Mata Kuliah Pakar
04/21/2304/21/23 22
Diagram of Chronic Liver Diseases (CLD) :
04/21/2304/21/23 33
SPECTRUM OF CLD IN RSPAD GATOT SOEBROTO – JAKARTAINTO JANUARY 1 – DECEMBER 31, 2005.
NO SPECTRUM PATIENT
(n=409)
VISIT
(R=3012)EXPLANATION
1. a. Chronic in active hepatitis
b. Chronic active hepatitis
c. Steato-hepatitis
8
102
18
17
196
72
AST/ALT was NL
AST/ALT was increased
AST/ALT, g-GT, ALP were increased, Dislipidemia
2. Liver cirrhosisa. Compensated LC
b. Decompensated LC
c. Hepatoma
82
110
63
816
1290
621
3. Deaths 26 ---SUMBER : Medical Record RSPAD GS, Pav. Kartika, Pav Darmawan. 2005.
Child’s-Pugh Score A
CPS B or CAFP was inreased
ESHF
04/21/2304/21/23 44
04/21/2304/21/23 55
ANATOMI SISTIM DIGESTIVUS (The alimentary tract.)
Parotid gland
Salivary glands
04/21/2304/21/23 66
SIRRHOSIS HEPATISSIRRHOSIS HEPATISBerat hati : 1,2 – 1,5 kgFaal hati : metabolisma, RES,
sintesis, sistim koagulasi,
detoksifikasi,regulasi endokrin.
04/21/2304/21/23 77
• DEFINISI :Hepatitis = keradangan hati
• PENYEBAB :1. Infeksi : parasit (malaria, amoeba),
bakteri (tbc, banal), jamur, viral (hepatitis A, B, C, D, E, F, TT, CMV, EBV)
2. Kerusakan hati : alkohol, obat-obat (asetaminofen, metildopa, INH, fenitoin, valproat, CPZ, amiodaron, TMP-SMZ, eritromisin), bahan beracun
3. Autoimun4. Fibrosis kistik5. Penyakit Wilson : deposit Cu berlebihan dalam hati6. Sindroma Reye7. Sindroma Budd-Chiari
04/21/2304/21/23 88
Viral HepatitisViral Hepatitis
Source ofvirus
Route oftransmission
Chronicinfection
Prevention
Feces
Fecal-oral
No
Vaccine, immuneglobulin
A
Type of Hepatitis
Blood/body fluids
Yes
Vaccine,immuneglobulin,
Childbirth, needles,
sex, transfusio
n
B
Blood/body fluids
Yes
Blood donorscreening,
risk management,education
Needles, transfusio
n,sex,
childbirth
C
Feces
Fecal-oral
No
Ensure safedrinkingwater
E
Blood/body fluids
Yes
Needles, sex, transfusion
(requires HBV co-infection)
D
HBV vaccine
CDC fact sheets, available at www.cdc.gov
04/21/2304/21/23 99
PATOGENESIS PATOGENESIS HEPATITIS VIRALHEPATITIS VIRAL
Averett DR and Mason WS. Viral Hep. Rev. 1995; 1:129–42
Clinical hepatitis
HBV or HCV-infected
hepatocytes
Inflammationand cell death
HBV or HCV production
Hepatocyteregeneration
Uninfected hepatocyte
s
Infection
Immunerespons
e
Re-infection
Alcohol,co-infection
etc.
04/21/2304/21/23 1010
Viral replication
Transplantor
Death
Immune response
Tissue damage
Scarring
HCC
Cirrhosis
Evidence of disease
PATOGENESIS PATOGENESIS HEPATITIS VIRAL KRONIKHEPATITIS VIRAL KRONIK
Adapted from Dr Z Goodman, Armed Forces Institute of Pathology, Washington, DC
Host and environmental
factors(e.g. alcohol, co-
infection)
04/21/2304/21/23 1111Chronic severe hepatitis
04/21/2304/21/23 1212
Adalah :Proses pengerasan parenkhim hati akibat nekro-inflamasi yang berlarut-larut/kronik
Cirrhotic = pengerasan, batu
PARENKHIM HATI
inflamasi nekrotik
HEPATOMA
CIRRHOSIS HEPATIS
BERBAGAI PENYEBAB
fibrotik
04/21/2304/21/23 1313
Drug Induced Hepatitis
Viral Hepatitis
Fatty Liver/Steato Hepatitis
Nodul-nodul
<-----------------------------------------------------------kronik<-----------akut6 bulan
Patologi Anatomi : Etiologi :
04/21/2304/21/23 1414
Definisi SHDefinisi SHIstilah “ kirrhos “
Laennec tahun 1826Kuning / ketengguli – tenggulian
WHO : proses difus yang dikarakteristik oleh adanya fibrosis dan perubahan struktur normal hepar mjd struktur nodul abnormal tanpa adanya organisasi lobular
04/21/2304/21/23 1515
Indonesia : Pria > wanita 2 – 4,5 : 1>> usia dekade ke-5
AS :Angka kematian 26.000 – 35.000
/tahunPenyebab kematian no.9
04/21/2304/21/23 1616
Patogenesis SHPatogenesis SH
Hepar InjuryNekrosis Hepatoseluler
JaringanKolagen / fibrotik
Nodul –nodul
Sirosis
Etiologi Patofisiologi Patologi Anatomi
04/21/2304/21/23 1717
• Klasifikasi Klinis (Patofisiologi)
• Klasifikasi Morfologi (Patologi Anatomi)
• Klasifikasi Penyebab (Etiologi)
04/21/2304/21/23 1818
Klasifikasi EtiologiKlasifikasi Etiologi
Penyebab tersering :
- hepatitis C (26 %)- alcoholic liver disease (21%)- hepatitis C dengan alcoholic liver disease (15%)- kriptogenik (18%)- hepatitis B yang koinsiden dgn hepatitis D (15%)- penyebab tidak diketahui (5%)
04/21/2304/21/23 1919
KLASIFIKASI KLINISKLASIFIKASI KLINIS
• SIROSIS HATI LATEN/TERKOMPENSASI (CPS A)
• SIROSIS HATI DEKOMPENSATA
(CPS B or C)
Berdasarkan : CHILD’s-PUGH Score
04/21/2304/21/23 2020
Klasifikasi CHILD’s-PUGHKlasifikasi CHILD’s-PUGHSKOR 1 2 3
Albumin (g/dL) > 3.5 2.8 - 3.5 < 2.8
Ascites None Mild Marked
Bilirubin (umol/dL) < 3.4 3.4 – 5.0 > 5.0
Ensefalopati None Mild Marked
PT (s prolonged) < 4 4 – 6 > 6
Nilai SKOR : Jika jumlah angka Child’s A : < 7 Child’s B : 7 – 9 Child’s C : > 9 the poorest prognostic group,
is less than 12 months
Hayes, et al. Churchill’s Pocketbook of Medicine, 3rd Edition. China, 2002.
04/21/2304/21/23 2121
PATOFISIOLOGI : PATOFISIOLOGI : Sitokin & Hepatic Growth Sitokin & Hepatic Growth
FactorsFactorsHepar sitokin pro inflamasi :
- TNF - æ- IL 1- IL 6- IFN – æ
Hepatic Growth Factors HGFEGFTGF – æTGF - ß
04/21/2304/21/23 2222
Klasifikasi MorfologiKlasifikasi MorfologiI . Sirosis MikronodularDitemukan pada :
- hemokromatosis- sirosis hati akibat alkohol- nutritional cirrhosis- obstruksi bilier- obstruksi aliran vena hepatik- jejunoileal bypass- indian chillhood cirrhosis
04/21/2304/21/23 2323
Sirosis MikronodularSirosis Mikronodular
04/21/2304/21/23 2424
II. Sirosis MakronodularDitemukan pada :
- hepatitis C kronis- hepatitis B kronis- defisiensi alpha – 1 anti tripsin- sirosis bilier primer
III. Sirosis Campuran
04/21/2304/21/23 2525
Sirosis MakronodularSirosis Makronodular
04/21/2304/21/23 2626
FibrogenesisFibrogenesis
04/21/2304/21/23 2727
Pola Histologis FibrosisPola Histologis Fibrosis
• Fibrosis Portal• Fibrosis Periportal• Fibrosis Periseluler• Fibrosis Perivenular
• Fibrosis Septal• Fibrosis Bentuk Lain
04/21/2304/21/23 2828
Fibrosis PeriduktalFibrosis Periduktal
04/21/2304/21/23 2929
Fibrosis PeriportalFibrosis Periportal
04/21/2304/21/23 3030
Fibrosis PeriselulerFibrosis Periseluler
04/21/2304/21/23 3131
Fibrosis PerivenularFibrosis Perivenular
04/21/2304/21/23 3232
Fibrosis SeptalFibrosis Septal
04/21/2304/21/23 3333Liver cirrhosis
04/21/2304/21/23 3434
KOMPLIKASI SIROSIS HATIKOMPLIKASI SIROSIS HATI
• HIPERTENSI PORTAL :- Varises Esofagus (VE), - Pecahnya VE (HEMETEMESIS MELENA)- Asites : SBP
• HEPATOMA• ENSEFALOPATI HEPATIKUM• GAGAL HATI TAHAP AKHIR (ESHF):
- Sindroma Hepatorenal- Sindroma Hepatopulmoner- Koma Hepatikum
04/21/2304/21/23 3535
04/21/2304/21/23 3636
Epidemiologi :Epidemiologi :
• Kanker hati banyak didapatkan di daerah Timur Jauh dan Afrika.
• Penyebab utama : infeksi Hepatitis B dan C
• Di Indonesia sering disertai oleh Sirosis Hati
04/21/2304/21/23 3737
Hepatocellular carcinoma (large size)
04/21/2304/21/23 3838
Hepatocellular carcinoma(small size)
04/21/2304/21/23 3939
04/21/2304/21/23 4040
04/21/2304/21/23 4141
04/21/2304/21/23 4242
ENSEFALOPATI ENSEFALOPATI HEPATIKUMHEPATIKUM
04/21/2304/21/23 4343
When the Liver When the Liver fails, the Brain fails, the Brain
failsfailsR Butterworth
2000
04/21/2304/21/23 4444
CapillaryCapillary
NHNH33
Astrocyte
GSGS
GLNGLNGLNGLN
GLGLUUGLGLUU
Astrocyte
GSGS
GLNGLNGLNGLN
GLGLUUGLGLUU
AstrocyteGLNGLNGLNGLN
GLNGLNGLNGLN
GLNGLNGLNGLN
GLNGLNGLNGLNGLNGLNGLNGLN
GLNGLNGLNGLNGLNGLNGLNGLN
GLNGLNGLNGLN
H2OH2O
H2OH2OAstrocyte
GLNGLNGLNGLN
GLNGLNGLNGLN
GLNGLNGLNGLN
GLNGLNGLNGLNGLNGLNGLNGLN
GLNGLNGLNGLNGLNGLNGLNGLN
GLNGLNGLNGLN
H2OH2O
H2OH2O
GLNGLNGLNGLN
H2OH2O
H2OH2O
Ammonia makes the Ammonia makes the Brain Swell!!!Brain Swell!!!
Jalan et al. Int J Biochem Mol Biol 2003, Jalan Gut 2000.
Brain
<0.1 mM<0.1 mM<0.1 mM<0.1 mM
0.5-5 mM0.5-5 mM0.5-5 mM0.5-5 mM
NN
LFLF
04/21/2304/21/23 4545
The pathogenesisThe pathogenesis
• Ammonia
• False neurotransmitter
• Endogenous toxin: Mercatan
• GABA
• Benzodiazepam
• Zn. Mg
04/21/2304/21/23 4646
BRAIN
LIVER
Glutamine KIDNEY
MUSCLEGUTNH3
Urea
CIRRHOSIS
Ammonia in Ammonia in Liver FailureLiver Failure patients patients
Shawcross and Jalan, Lancet 2005Shawcross and Jalan, Lancet 2005
04/21/2304/21/23 4747
Clinical Signs of Hepatic Encephalopathy
Mental status disorders
04/21/2304/21/23 4848
Flapping tremor
Clinical Signs of Hepatic Encephalopathy
04/21/2304/21/23 4949
04/21/2304/21/23 5050
04/21/2304/21/23 5151
04/21/2304/21/23 5252
04/21/2304/21/23 5353
Encephalohepatic stageEncephalohepatic stage
• Minimal
• Grade 1 : confused
• Grade 2 : drowsy
• Grade 3 : Stuporous
• Grade 4 : Coma
04/21/2304/21/23 5454
Spectrum of hepatic encephalopathySpectrum of hepatic encephalopathy
ComaComa
Manifest Manifest HEHE
Minimal HEMinimal HE
Precipitated (85-90%)BleedingDehydrationSepsis
Spontaneous (10-15%)40-70% cirrhotics
04/21/2304/21/23 5555
Manifest HE Manifest HE
• Definition - not precise, no good tests (psychometric test, number connection test)
• Impact on the patient - minimal, if any– quality of life– ability to work– prognosis
04/21/2304/21/23 5656
04/21/2304/21/23 5757
PENATALAKSANAAN.PENATALAKSANAAN.
• Diagnostik :
Klinis, Laboratorium dan Biopsi Hati.
• Terapeutik :
Pencegahan.
Pengobatan / medikamentosa.
• Edukasi :
04/21/2304/21/23 5858
KLINISLABORATORIUM BIOPSI HATI
04/21/2304/21/23 5959
Prevalence of HBV and Incidence of Prevalence of HBV and Incidence of Hepatocellular Carcinoma (HCC)Hepatocellular Carcinoma (HCC)
World prevalence of HBV carriers
HBsAg carriers–prevalence
<2%2–7%>8%Poorly documented
Annual incidence of primary HCC
Cases/100,000 population
1–33–1010–150Poorly documented
WHO 1999
04/21/2304/21/23 6060
Faktor risiko dan GejalaFaktor risiko dan Gejala
04/21/2304/21/23 6161
FAKTOR RISIKO HEPATITIS FAKTOR RISIKO HEPATITIS VIRAL KRONIKVIRAL KRONIK
1. IDU (pemakai obat suntik), Tatoo2. Overdosis asetaminofen, alkohol atau obat lain3. Kebiasaan seksual risiko tinggi / freesex4. Terkontaminasi : family, travel, eating, living5. Resipien : - transfusi darah sblm th. 1990,
- transplantasi organ6. AIDS7. Bayi dengan ibu pengidap Hepatitis B atau C8. Pekerja Kesehatan, Dentists and Dental Hygienists
04/21/2304/21/23 6262
Perjalanan Klinis HEPATITIS :Perjalanan Klinis HEPATITIS :
• Penyakit Hepatitis akut kronik FAILURE • Komplikasi kegagalan hati :
Sirosis hati :hipertensi portal varises esofagus :
pecah HEMATEMESIS – MELENAhipoalbuminemia asites : SBP
Hepatoma : HCC (diffuse parenchymal) Lobulated hepatoma
Ensefalopati hepatikum Sindroma hepatorenal
04/21/2304/21/23 6363
Diagnotic of Hepatitis B
• Viral markersHBV-DNA, HBsAg, HBeAg, Anti-HBs, Anti-HBe and Anti-HBc.
• Other markersALT (SGPT), Liver histology.
• Clinical examination, Ultrasound.
04/21/2304/21/23 6464
Importance of Serum Markers
04/21/2304/21/23 6565
Diagnostic of Hepatitis CDiagnostic of Hepatitis C
• HCV antibody tests– enzyme immunoassays (EIA)– recombinant immunoblot (RIBA)
• HCV-RNA tests– Qualitative: AMPLICOR HCV Test [50 IU/mL]– Quantitative: AMPLICOR MONITOR Test [600
IU/mL]
04/21/2304/21/23 6666
Assessing Predicting Length Response Sustained
Method Screen Confirmation of Therapy to Therapy Response
ALT/AST X
Enzyme Ximmunoassay (EIA)
Supplemental assay X(RIBA*)
HCV RNA qualitative X Xassay
HCV RNA quantitative X Xassay
HCV genotype X
NIDDK. Chronic hepatitis C: current disease management.
Utility of HCV Diagnostic TestsUtility of HCV Diagnostic Tests
*No longer widely used.
04/21/2304/21/23 6767
GEJALA DAN TANDA SHGEJALA DAN TANDA SH
• GEJALA : Cepat lelah, mengantuk siang hari, tidak bisa tidur malam hari. Ngomong ngaco.
• TANDA-TANDA :Badan kurus, perut membuncit (ascites),muntah darah (hematemesis), tremor,berak darah warna hitam/coklat marun (melena), kesadaran berkabut (encefalopati)
• LABORATORIUM :Hiperglobulinemia (rasio Alb/Glob terbalik)Trombositopenia
04/21/2304/21/23 6868
• Sirosis hepatis selalu diawali dengan proses nekrosis hepato seluler. Pembentukan jaringan parut / fibrosis merupakan dampak dari peningkatan pembentukan serta penurunan degradasi matriks ekstra seluler. Yang kemudian diikuti oleh kematian sel – sel hati sehingga memicu pembentukan nodul – nodul abnormal.
• Fibrosis merupakan marker penting dari distribusi perlukaan hati yang luas , dan berdasarkan gambaran – gambaran ini , beberapa pola histologis dapat dibedakan. Dalam beberapa kasus , penentuan pola histologis ini dapat sangat membantu dalam melakukan diagnosa , mempersempit diagnosa banding , memperkirakan kemungkinan etiologi serta mempertimbangkan prognosis.
04/21/2304/21/23 6969
Gejala dan Tanda HEPATOMA:Gejala dan Tanda HEPATOMA:
• Bervariasi
• Berlangsung perlahan-lahan
• ikterus
• Nyeri epigastrium
• Rasa tidak enak pada perut kanan atas
• BB menurun
• Asites hemorrhagik
04/21/2304/21/23 7070
Diagnosis HEPATOMA:Diagnosis HEPATOMA:
• Laboratorium : AFP (alfa feto protein)
• USG Abdomen
• CT-scan
• Angiografi
• Biopsi hati
04/21/2304/21/23 7171
Role of Liver Role of Liver Biopsy Biopsy
Confirm clinical diagnosis
Assess severity of fibrosis and
necroinflammation1,2
Evaluate possible concomitant disease
processes (eg, alcoholic liver disease,
NASH)1,2
Assess therapeutic intervention1
1. NIH Consensus Statement Online. Management of hepatitis C. 2. British Liver Trust Information Service. A guide to liver function tests.
04/21/2304/21/23 7272
Minimal HE and fitness to drive
Schomerus et al. Dig Dis Sci 1981;26:62260-85% of cirrhotic patients are unfit to drive
Watanabe et al. Metab Brain Res 1995; 10:23931-44% of cirrhotic patients are unfit to drive
Srivistava et al. J Hepatol 1994; 21:1039No deficits in real driving
Wein et al. Neurol Rehabil 2001, 7:242-262Driving deficits in SHE
Risk alertness ?Epidemiological studies required
Behaviour in risky traffick situations
04/21/2304/21/23 7373
HE and fitness to drive
Preliminary results withSHE patients:
• reduced reaction time
• Problems with track-keeping
• correlation to HE severity and age
Test ?
04/21/2304/21/23 7474
NUMBER CONNECTION TEST
04/21/2304/21/23 7575
Diagnosis of hepatic encephalopathyDiagnosis of hepatic encephalopathy
Manifest HE:
Clinical picture
West Haven Criteria
Laboratory test: No diagnostic value
Imaging:No diagnostic value
Subclinical HE:
Gold-standard:Computerpsychometry
Routine:Paper-Pencil-Tests
Paper-Pencil-Tests:
low sensitivityand specifity
Training effects
Age dependence
Subjective classification
for HE grade I-II
04/21/2304/21/23 7676
KRITERIA PENILAIAN “WEST HAVEN” KRITERIA PENILAIAN “WEST HAVEN” UNTUK UJI MENGHUBUNGKAN ANGKAUNTUK UJI MENGHUBUNGKAN ANGKA
L-ornithin-L-aspartate in the Therapy of Hepatic Encephalopathy, Merz PharmaL-ornithin-L-aspartate in the Therapy of Hepatic Encephalopathy, Merz Pharma
Frankfurt, Germany, 1995:9-Tab.4)Frankfurt, Germany, 1995:9-Tab.4)
Grade 0 15 - 30 sec.
Grade 1 31 - 50 sec.
Grade 2 51 - 80 sec.
Grade 3 81 - 120 sec.
Grade 4 > 120 (unable to do test)
04/21/2304/21/23 7777
Flimmerfrequenz Analyzer- Hepatonorm Analyzer-
04/21/2304/21/23 7878
Cause of EncephalohepathicCause of Encephalohepathic
• Liver cirrhosis
• Acute Hepatitis
• Hepatitis Chronic
• Fatty Liver
• NASH
04/21/2304/21/23 7979
PENCEGAHANMEDIKAMENTOSAMINIMAL INTERVENSI
04/21/2304/21/23 8080
Terapi Pencegahan :Terapi Pencegahan :
• Menjaga dan meningkatkan Daya Tahan Tubuh.
• Menghindari :- pemakaian jarum suntik berulang-
ulang.- seks bebas- transfusi darah sembarangan
• Memelihara higiene-sanitasi.• Imunisasi / Vaksinasi (untuk HBV).
04/21/2304/21/23 8181
Terapi Medikamentosa :Terapi Medikamentosa :
Averett DR and Mason WS. Viral Hep. Rev. 1995; 1:129–42
Block HBV or HCV production and/or re-
infectionwith antiviral,Therapy N.A
Clinical hepatitis
HBV or HCV -infected
hepatocytes
Inflammationand cell death
HBV or HCV production
Stimulate immune response with IFN-
Hepatocyteregeneration
Uninfected hepatocyte
s
Infection
Lysis of infected hepatocytes and
regulation of viral replication
Immunerespons
eAlcohol,
co-infectionetc.
CAM
with Hepatoprotektor/stimulator
Anti Encephalopathic
04/21/2304/21/23 8282
Pilihan Obat :Pilihan Obat :
• INTERFERON : IFN StandarPeg-IFN
• ANTIVIRAL : Ribavirin• NUKLEOSIDA
ANALOGUE : LamivudineAdevofir dipivoxil
• IMMUNE SUPPORT : Glicirrhizine, SST (TJ-9),Thymosin α
• HEPATO-PROTEKTOR : PPC 95,
• ANTI ENSEFALOPATIK : LOLA
04/21/2304/21/23 8383
Treatment of hepatic Treatment of hepatic encephalopathy encephalopathy
• TREATMENTS BASED UPON THE AMMONIA HYPOTHESIS • Reduction in ammoniagenic substrates - Enemas - Dietary protein reduction • Inhibition of intestinal ammonia production and absorption - Oral antibiotics - Lactulose and lactitol - Modification of colonic flora TREATMENTS BASED UPON THE FALSE NEUROTRANSMITTER HYPOTHESIS • BCAA infusions • Oral BCAA supplements
TREATMENTS BASED UPON THE GABA HYPOTHESIS
MISCELLANEOUS TREATMENTS • Zinc • Melatonin
04/21/2304/21/23 8484
continue intensive careparenteral nutritioniv. Antibiotics, BCAA infusion
+Flumazenil (antidotum CSE)
Lactulose oralBCAA oral
Stepwise approach to treatment of Stepwise approach to treatment of hepatic encephalopathy in cirrhoticshepatic encephalopathy in cirrhotics
Initial treatment:correct precipitating factorsiv.fluids, REDUCED NH3 serumrestricted protein, neomycinlactulose oral
-
++ -
Protein intolerance < 50 gProtein intolerance < 50 g
Suplementation BCAASuplementation BCAA
Lactulose oral, TJ-9Lactulose oral, TJ-9
+
04/21/2304/21/23 8585
No Drug for Hepatic No Drug for Hepatic Encephalopathy? There is Encephalopathy? There is
……..……..
NeomycinNeomycin
LactuloseLactulose
BCAABCAA
04/21/2304/21/23 8686
1. LOLA,vs. 1. LOLA,vs. Retriction protein-intakeRetriction protein-intake
2. 2. Anti-bioticsAnti-bioticsXX
3. Lactulose3. LactuloseXX
4. Branch4. Branch Chain Amino AcidsChain Amino AcidsXX5. Flumazenil5. Flumazenil
(Porto-Systemic Encephalopathy as a Complication of Liver Cirrhosis, Dr. Falk Pharma GmbH, Germany, 1995)
TERAPI ENSEFALOPATI HEPATIK
04/21/2304/21/23 8787
• If drug treatment is needed only treatments with proven efficacy should be used:– flumazenil (only in case of BZD-induced HE)– lactulose enemas (in pts. with GI hemorrhage or
constipation)
– ornithine-aspartate iv. (hymerammonemia)
– BCAA (longterm therapy in severe protein intolerance)
04/21/2304/21/23 8888
INTERVENSION OPTIONS :INTERVENSION OPTIONS :
• MINIMAL INTERVENSION :
1. PHLEBOTOMY
2. TACE
• LIVER TRANSPLANTATION
04/21/2304/21/23 8989
Kapan dinyatakan sembuh dari Kapan dinyatakan sembuh dari serangan infeksi Hepatitisserangan infeksi Hepatitis
• Serangan akut HBV : HBsAg (+),IgM anti HBc (+).
HCV : sulit diidentifikasi.
• Kondisi kronis HBV : Anti HBc total (HBc + Hbe) neg(-)HBsAg (+)HBeAg (+) replikasi aktif
HCV : Anti HCV (+).Fatty liver : Dislipidemia, USG hati : FL (+)Steato-hepatitis : Fatty liver, g-GT me , ALP me
• Keadaan sembuh HBV : HBsAg (-),Anti HBs / Anti Hbe (+)/(+), HBV DNA (-)
HCV : Anti HCV (-), HCV RNA (-)Steat-hep: Lipid profil DBN, g-GT dan ALP DBN
04/21/2304/21/23 9090
04/21/2304/21/23 9191
Qur’an Ch 94 Ver.7-8ALAM NASYRAH
Selesai satu urusan, kerjakanlah urusan lain
Dan hanya kepada Tuhanmulah Hendaknya kamu berharap.