Spectrum and Management CLD

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

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