Hepatitis Viral Akut

Introduction:
 Inflammation of Liver
 Viral, immune, drugs, toxins & other.
 Acute, Chronic & Fulminant - types
 Viral Hepatitis –
– Hepatitis A, B, C, D, E, & other
 Specific

 Systemic - CMV, EBV, other.

 Hepatitis-3

Hepatitis viruses:(A,B,C,D,E,G & other)

Virus Hep-A Hep-B Hep-C

Agent ssRNA dsDNA ssRNA

Transm. Feco-oral Parenteral Parenteral

Carrier None 0.1-1.0% 0.2-1.0%

state
Chronic None 5-10% >50%
Hepatitis
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 Phases of Hepatitis :
 Carrierstate / Asymptomatic phase
 Acute hepatitis
 Chronic Hepatitis
 Chronic Persistent Hepatitis
 Chronic Active Hepatitis

 Fulminant hepatitis
 Cirrhosis
 Acute Hepatitis:
1. Incubation phase.
2. Symptomatic pre-icteric / prodromal phase.
3. Symptomatic icteric phase.
4. Convalescence.
 Hepatitis-6

PRODROMAL :
3-4 HARI S/D 2-3 MGG,LELAH, ANOREKSIA,
MUAL, HIPERPIREKSIA RINGAN,NYERI PERUT
KANAN ATAS, SAKIT KEPALA, NYERI OTOT

IKTERIK :
1-4 MGG URIN GELAP, HEPATOMEGALI,
SPLENOMEGALI.

KONVASELEN :
MULAI MENGHILANGNYA IKTERUS,NAFSU
MAKAN BAIK.
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 Hepatitis-7

Acute Chronic
1. Ballooning deg.  Ground glass (B)
2. Cholestasis  Apoptosis
3. Apoptosis  Periportal Necrosis
4. Periportal Necrosis  Macrophages
5. Macrophages  Portal Lymphoid
6. Inflammation infiltrate
7. Portal inflammation  Bridging fibrosis

8. Fatty change(C)  Fatty change(C)

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 Hepatitis-8

HEPATITIS AKUT - A

. 1912 COCKAYNE = “ HEPATITIS INFEKSIOSA”.

. 1923 BLUMMER MENDESKRIPSI SEMPURNA.
. DIGOLONGKAN ENTERO VIRUS TIPE 72
( PICORNAVIRIDAE VIRUS FAMILY ).
. 27-28 nm.
. STABIL PADA 60 0C.
. INAKTIF PADA 85 0C DALAM 1 MENIT.
. HANYA 1 ( SATU ) JENIS SERO TIPE

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 Hepatitis-9

PATOGENESE :

. ORAL FECAL ROUTE INOKULASI

VIRUS HEPATOCYTE REPLIKASI
JUMLAH VIRUS AKAN MENURUN SETELAH
TIMBUL MANIFESTASI KLINIS MUNCUL
IgM ANTI HAV YANG SPESIFIK.

. KERUSAKAN SEL HATI OLEH KARENA VIREMIA

YANG SANGAT PENDEK.

. KERUSAKAN SEL HATI DISEBABKAN OLEH

AKTIFASI SEL T LIMFOSIT.
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 Hepatitis-10

. HISTOLOGIS :
NEKROSIS SEL HATI
DIIKUTI INFILTRASI LIMFOSIT, MAKROFAG,
SEL PLASMA, EOSINOFIL DAN NEUTROFIL.

. IKTERUS AKIBAT GANGGUAN ALIRAN EMPEDU

. KERUSAKAN SEL HATI MENYEBABKAN

PELEPASAN ENZIM TRANSAMINASE (SGPT)

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 Hepatitis-11

GEJALA KLINIS
-ASYMPTOMATIS
-SYMPTOMATIS  JAUNDICE SELF LIMITED
SEMBUH DALAM 8 MINGGU
-CHOLESTASIS JAUNDICE DALAM 10 MINGGU
ATAU LEBIH
-RELAPSE
-FULMINANT HEPATITIS (JARANG HIDUP)
-PENINGGIAN TRANSAMINASE > 10-20 KALI
-GEJALA KLINIS KLASIK TDD :
PRODROMAL (FLU LIKE SYNDROME)
FASE IKTERIK
FASE PENYEMBUHAN

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 Hepatitis-12

DIAGNOSTIK :
Gejala klinis, pemeriksaan fisik dan laboratorium.
Berdasarkan ditemuinya Ig M anti HAV

PENATALAKSANAAN :
- Tidak ada yang spesifik, bersifat :
- Suportif
- Simptomatis

Prognosis
- Prognosis baik, angka kematian akibat hepatitis
fulminan 0,1 - 0,2%.
- Dilaporkan terjadi 0,13 - 0,35% kasus hospitalisasi.
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 Hepatitis-13

PENCEGAHAN :
POLA HIDUP YANG BAIK DAN BERSIH.

• SECARA UMUM :
HIGIENE PERORANGAN, LINGKUNGAN
SANITASI YANG BAIK,PEMAKAIAN AIR BERSIH,
PEMBUANGAN EKSKRETA, PEMBUATAN
SUMUR YANG MEMENUHI STANDAR.

• MENCEGAH KONTAMINASI MAKANAN,

MEMASAK DENGAN BAIK.

VAKSINASI
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 Hepatitis-14

IMUNISASI PASIF :

a. PENCEGAHAN SEGERA SETELAH KONTAK.

(KELUARGA SERUMAH).

b. PENCEGAHAN SEBELUM KONTAK (BERPERGIAN KE

DAERAH ENDEMIS).

HBIG( HUMAN NORMAL IMUNO GLOBULIN ), 0,02 ml / kg

BB, TIDAK LEBIH SATU MINGGU SETELAH KONTAK.

SEBELUM KONTAK 0,02ml/kg BB UNTUK PERJALANAN <

2 BULAN, 0,08ml/kg BB > 4 BULAN.

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 Hepatitis-15

IMUNISASI AKTIF :

VAKSIN LIVE ATTENUATED YANG BERASAL

DARI GINJAL MONYET HIJAU AFRIKA
STRAIN HM -175

1993 DIIJINKAN PENGGUNAANNYA OLEH

REPORT OF COMMITTEE ON INFECTIOUS
DISEASE.

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 Hepatitis-16

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 Hepatitis-17
Hepatitis B - Clinical
Features
• Incubation period: Average 60-90 days
Range 45-180 days
• Clinical illness (jaundice): <5 yrs, <10%
5 yrs, 30%-50%
• Acute case-fatality rate: 0.5%-1%
• Chronic infection: <5 yrs, 30%-90%
5 yrs, 2%-10%
• Premature mortality from
chronic liver disease: 15%-25%

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 Hepatitis-18

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 Hepatitis-19

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 Hepatitis-20

Typical Serologic HepB Course

Symptoms

HBeAg anti-HBe

Total anti-HBc
Titer

HBsAg IgM anti-HBc anti-HBs

0 4 8 12 16 20 24 28 32 36 52 100
Weeks after Exposure
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 Hepatitis-21
Outcome of Hepatitis B Virus Infection
100 by Age at Infection 100

Symptomatic Infection (%)

Chronic Infection (%)

80 80

60 60
Chronic Infection

40 40

20 20

Symptomatic Infection
0 0
Birth 1-6 months 7-12 months 1-4 years Older Children
and Adults
Age at Infection
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 Hepatitis-22

Hepatitis B Virus
Modes of Transmission

• Sexual
• Parenteral
• Perinatal

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 Hepatitis-23

Risk Factors for Acute Hepatitis B

United States, 1992-1993
Heterosexual*
(41%)

Injecting
Drug Use
(15%)

Homosexual Activity (9%)

Household Contact (2%)
Health Care Employment (1%)

Unknown (31%)
Other (1%)
* Includes sexual contact with acute cases, carriers, and multiple partners.
Source: CDC Sentinel Counties Study of Viral Hepatitis
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 Hepatitis-24
Elimination of Hepatitis B Virus
Transmission United States
Strategy
• Prevent perinatal HBV transmission
• Routine vaccination of all infants
• Vaccination of children in high-risk groups
• Vaccination of adolescents
– all unvaccinated children at age 11-12
– “high-risk” adolescents at all ages
• Vaccination of adults in high-risk groups
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 Hepatitis-25

Concentration of Hep B Virus

in Various Body Fluids

Low/Not
High Moderate Detectable

blood semen urine

serum vaginal fluid feces
wound exudates saliva sweat
tears
breastmilk

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 Hepatitis-26

Fulminant Hepatitis:
 Hepatic failure with in 2-3 weeks.
 Reactivation of chronic or acute hepatitis
 Massive necrosis, shrinkage, wrinkled
 Collapsed reticulin network
 Only portal tracts visible

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 Hepatitis-27

GAMBARAN KLINIS
IKTERUS PROGRESIF

BILIRUBIN > 20MG%

GANGGUAN KESADARAN PROGRESIF,

MUAL DAN MUNTAH, HATI MENGECIL, MASA
PROTROMBIN MEMANJANG,
TRANSAMINASE NAIK CEPAT DAN SANGAT
MENINGGI SERTA ALBUMIN MENURUN.

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 Hepatitis-28
IMUNOPATOGENESE DARI FULMINAN HEPATITIS

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PATOGENESE
Hepatitis-29 FULMINAN HEPATITIS OLEH VIRUS

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 Hepatitis-30
ETIOLOGI
VIRAL HEMORAGIC FEVER VIRUS
HEPATITIS VIRUS SITOMEGALOVIRUS
HEPATITIS A HERPES SIMPLEX VIRUS
HEPATITIS B EPSTEIN BARR VIRUS
HEPATITIS C PARAMIXOVIRUS
HEPATITS E ADENOVIRUS
HEPATITIS G

DRUG/ TOXIN NEOPLASTIK

DOSE RELATED LIMFOMA
ACETAMINOFEN METASTASE HATI,
CCI 4 MELANOMA , PARU
AMANITA POISONING
YELLOW PHOSPORUS
BACILLUS CEREUS EMETIC TOXIN

PREGNANCY RELATED
ACUTE FATTY LIVER OF PREGNANCY
HELLP SINDROME
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Hepatitis-31
IDIOSINKRINASI METABOLIC
HALOTHANE INBORN METABOLISM ERROR
ISONIAZID GALACTOSEMIA
RIFAMPISIN FRUCTOSE INTOLERANCE
VALPROIC ACID TYROSINEMIA
DISULFIRAM NEONATAL IRON STORAGE
NSAID DISEASE
NORTRIPTYLINE WILSON DISEASE
REYE SYNDROME ALFA 1 ANTITRIPSIN DEFF.
HERBAL MEDICINE
MISC
BUDD CHIARI SYNDROME
VENO OCCLUSIVE DISEASE
AUTOIMUNE HEPATITIS
ISCHEMIC SHOCK LIVER
PRIMARY GRAFT NON FUNCTIONIN LIVER
TRANSPLANTED PATIENT
HEAT STROKE
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ADULT ONSET STILL’S DISEASE
 Hepatitis-32

TATALAKSANA
N-ASETIL SISTEIN
PENDEKATAN
FARMAKOLOGI PROSTAGLANDIN

HAEMOPERFUSI ARANG
KOLOUMN HEPATOSIT
PENDEKATAN REGULASI SITOKIN
MOLEKULER
REGULASI KASKADE KOAGULASI

INHIBISI APOPTOSIS
HEPATOSIT GROWTH FACTOR

HEPATOSIT TRANSPLANT
TRANSPLANTASI
LIVER TRANSPLANT

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 Hepatitis-33

Features of Hepatitis C Virus

Infection

Incubation period Average 6-7 weeks

Range 2-26 weeks
Acute illness (jaundice) Mild (<20%)
Chronic infection 60%-85%

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 Hepatitis-34

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 Hepatitis-35

Chronic Hepatitis C
Factors Promoting Progression
or Severity
 Increased alcohol intake
 Age > 40 years at time of infection
 HIV co-infection
 Other
 Male gender
 Chronic HBV co-infection

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 Hepatitis-36

Serologic Pattern of Acute HCV Infection

with Recovery
anti-
HCV
Symptoms +/-

HCV RNA
Titer

ALT

Normal
0 1 2 3 4 5 6 1 2 3 4
Months Years
Time after exposure
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 Hepatitis-37

Estimated Incidence of Acute HCV

Infection
United States, 1960-2001
140
New Infections/100,000

120
100 Decline in injection
80 drug users
60
40 Decline in
transfusion recipients
20
0
1960 1965 1970 1975 1980 1985 1989 1992 1995 1998 2001
Year
Source: Hepatology 2000;31:777-82; Hepatology 1997;26:62S-65S;
CDC, unpublished data
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 Hepatitis-38

Exposures Known to Be Associated With

HCV Infection in the United States

 Injectingdrug use
 Transfusion, transplant from infected donor
 Occupational exposure to blood
 Mostly needle sticks
 Iatrogenic (unsafe injections)
 Birth to HCV-infected mother
 Sex with infected partner
 Multiple sex partners

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 Hepatitis-39 HCV Prevention and Control

Reduce or Eliminate Risks for

Acquiring HCV Infection
 Screen and test donors
 Virus inactivation of plasma-derived
products
 Risk-reduction counseling and services
 Obtain history of high-risk drug & sex behaviors
 Provide information on minimizing risky
behavior, including referral to other services
 Vaccinate against hepatitis A and/or hepatitis B

 Safe injection and infection control practices

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 Hepatitis-40

HCV Testing Routinely

Recommended
Based on increased risk for infection
 Ever injected illegal drugs
 Received clotting factors made before 1987
 Received blood/organs before July 1992
 Ever on chronic hemodialysis
 Evidence of liver disease
Based on need for exposure management
 Healthcare, emergency, public safety workers
after needle stick/mucosal exposures to HCV-
positive blood
 Children born to HCV-positive women
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 Hepatitis-41

Postexposure Management for HCV

 IG, antivirals not recommended for
prophylaxis
 Follow-up after needlesticks, sharps, or
mucosal exposures to HCV-positive blood
 Test source for anti-HCV
 Test worker if source anti-HCV positive
 Anti-HCV and ALT at baseline and 4-6 months later
 For earlier diagnosis, HCV RNA at 4-6 weeks

 Confirm all anti-HCV

 Refer infected worker to specialist for medical
evaluation and management

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 Hepatitis-42 HCV Counseling

Preventing HCV Transmission to Others

Avoid Direct Exposure to Blood
 Do not donate blood, body organs,
other tissue or semen
 Do not share items that might have
blood on them
 personalcare (e.g., razor, toothbrush)
 home therapy (e.g., needles)

 Cover cuts and sores on the skin

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 Hepatitis-43 HCV Counseling
Mother-to-Infant Transmission of HCV

 Postexposure prophylaxis not available

 No need to avoid pregnancy or
breastfeeding
 Consider bottle feeding if nipple cracked/
bleeding
 No need to determine mode of delivery
based on HCV infection status
 Test infants born to HCV-positive women
 >15-18 months old
 Tests any children born since mom infected
 Evaluate infected children for CLD

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 Hepatitis-44 HCV Counseling

Other Transmission Issues

 HCV not spread by kissing, hugging,

sneezing, coughing, food or water, sharing
eating utensils or drinking glasses, or
casual contact
 Do not exclude from work, school, play,
child-care or other settings based on HCV
infection status

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 Hepatitis-45

Diagnostik :
• Ditemuinya anti HCV. (minggu 5-6 setelah terpapar)
• Peninggian transaminase pada minggu ke-2 s/d 26,
puncaknya minggu ke-5 s/d 12.
• Kadar ALT biasanya meninggi pada ¾ pasien lebih dari
15 kali dari batas atas normal.
• RNA HCV (+) menetap pada yang terinfeksi.

Gejala :
• Banyak kasus asimtomatik
• Flu-like sindrome, anoreksia, BB menurun, nyeri
abdominal, mialgia, atralgia dan fatigue.
• Simptom yang jarang : demam dan rash.
• Jaundice < 1/3 pasien.

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 Hepatitis-46

HEPATITIS AKUT - D
• Terdeteksi bersamaan dengan virus Hepatitis B.
• HDV (+) diseluruh dunia berhubungan dengan
prevalensi infeksi HBV (+).
• Lebih dominan didaerah tropikal dan subtropikal.
• Infeksi HDV di negara berkembang lebih besar dari
pada di negara maju (Barat).
• Manifestasi klinis dari coinfeksi atau super infeksi
bervariasi dari asimptomatis sampai yang berat
• 80% kasus kronik hepatitis D  menjadi sirosis dalam
5-10 tahun.
• Gold standard diagnosis : HDV RNA (+) atau HDAg (+)
liver.
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 Hepatitis-47

Transmisisi :
• Melalui parenteral, seksual, transfusi, jarum suntik,
haemodialisis.
• Infeksi HDV dapat berupa koinfeksi atau superinfeksi
dengan HBV.

Prevalensi Geografis :
+ 5% carier HbsAg terinfeksi dengan HDV

Diagnosa :
HDV (+) di serum dan liver, HDV RNA dan HDAg (+)
Diagnosa dini dengan IgM anti HD

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 Hepatitis-48

Gambaran Klinis :
Biasanya berat dan ikterus
Amino transferase meningkat

Pencegahan :
Dengan cara vaksinasi HBV

Therapi :
Tidak banyak bermanfaat dengan pemberian
antivirus dan immunodulator

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 Hepatitis-49

HEPATITIS AKUT –E
• Tidak berkapsul, sporadis , bersifat akut.
• Terdistribusi di Asia, Timur Tengah, sebagian Afrika, dan
Meksiko.
• Transmisi fecal – oral route.
• Paling sering pada dewasa muda.
• Masa inkubasi 2 - 10 minggu.
• Mortalitas : 25 %.
• Bersifat asimptomatis dan anikterik

Diagnosa :
HEV (+) , anti HEV (+) dan HEV RNA (+)
Tidak ada yang spesifik untuk terapi hepatitis E

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 Hepatitis-50

HEPATITIS AKUT – G
• Termasuk Flava virus.
• Terdistribusi secara luas.
• Ditularkan melalui parenteral, seksual
dan perinatal.
• HGV RNA dideteksi dengan PCR.
• HGV tidak mempengaruhi respon untuk
terapi antiviral.

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