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Complication
Siti Nurdjanah
Introduction
Cirrhosis represents a late stage of
progressive hepatic fibrosis
characterized by distortion of the
hepatic architecture and the
formation of regenerative nodules.
The Actiology of LC
1. Viral hepatitis types B + Delta; C
2. Alcohol
3. Metabolic, e.g. haemochromatosis,
Wilsons diseases Alpha1 Anti trypsin
deficiency; NAS, Intestinal bypass
4. Prolonged cholestasis, intra and extra
hepatic
5. Hepatic venous ouobstruction e.g. veno
occlusive disease, contrictive pericatditis;
Budd-chiari Syndrome
6. Autoimmune hepatitis
7. Toxin and therapeutic agents
8. Indian chilhood cirrhosis
Comparison of the hepatitis viruses
Hepatiti
Hepatiti Hepatitis Hepatitis Hepatiti
sC
s A virus B virus D virus s E virus
virus
Virus class Picorna- Hepadna- Flavivirus Deltavirus Calcivirus
virus virus
Genome RNA DNA RNA RNA RNA
Hepatocellular Decompensated
carcinoma cirrhosis
Death
Natural History of HBV Infection
< 5%
HBeAg- HBeAg+
Chronic Cirrhosis Chronic
Hepatitis B Hepatitis B
Inactive
Carrier
Courtesy of W. Ray Kim, MD.
Chen DS, et al. J Gastroenterol Hep. 1993;8:470-475.
Seeff L, et al. N Engl J Med. 1987;316:965-970.
Natural History of HBV Infection
< 5%
HBeAg- HBeAg+
Chronic HCC Chronic
Hepatitis B Hepatitis B
Inactive
Carrier
Courtesy of W. Ray Kim, MD.
Chen DS, et al. J Gastroenterol Hep. 1993;8:470-475.
Seeff L, et al. N Engl J Med. 1987;316:965-970.
Phases of Chronic HBV
Infection
Immune Immune Low Replicative Reactivation
Tolerance Clearance Phase Phase
HBeAg+ HBeAg-/anti-HBe+ (precore/core promoter variants)
< >< >
> 2000 IU/mL
HBV DNA < 2000 IU/mL
2 x 108 -
2 x 1011 IU/mL 200,000 - 2 x 109 IU/mL
ALT
Lai CL, et al. Lancet. 2003:362:2089. Lok AS, et al. Gastroenterology. 2001:120:1828.
Risk Factors for Progression of Liver
Disease (Cirrhosis, Liver Failure, HCC)
HBV genotype High geographic endemicity
RNA genome
Nucleocapsid
(core) protein
Envelope
Disease progression in hepatitis C:
person-to-person variability
(Slow)
Decompensation
(~20%)
HCC
Normal Acute Chronic Chronic Cirrhosis (14% per
liver infection infection hepatitis (20%) year)
(80%)
Death
Bacteralmia
Bacterascites
SBP Resolution
SBP
Ascites polymorh > 250 cells/mm3
and positive cultur monomicrobial
Therapy of SBP :
Cefotoxine 2 gr/12 h during 5 days.
Amixycillin or clavulamic acid i.v.
followed by oral therapy
Hepatic Encephalopathy
A reversible neuropsychiatric state that
complicates liver disease
Aetiological factors.
Diuresis
Haemorrhage
Paracentesis
Diarrhoea & voviting
Sedatives
Infections
Constipation
Alcaholic surgery
Diarrhoea & vomiting
Therapy :
Identification and treatment of the
precipitating cause
Intervention to reduce production
and absorrption of gut-derived
ammonia and other toxins
Give agents to modity
neurotransmitter balance diurectly
biomocriptine, fluororenil) or
indirectly (BCAA)
Hepato Renal syndrome
Development of Renal failure in the
absence of any identifiable renal
pathology in severe liver disease
patients
Gambar : Anatomi Sistem Portal
No Varices
HVPG normal/-10 mmHg
Variceal hemorrhage
Pressure > variceal wall tension (>10-12 mmHg)
Esophageal hemorrhage 5%-15% yearly
Gastric hemorrhage: bleeding in patients with gastric varices
Is reported in approximately 25% in 2 years (higher for fundal varices)
Recurrent hemorrhage
Persistence of portal pressure and variceal status
Variceal hemorrhage
Size of varices highes risk of first hemorrhage (15% per year)
in patients with large varices)
Decompensated cirrhosis (Child-Pugh B/C)
Endoscopic presence of Red wale marks
Figure : Faktor Risiko Terbentuknya Varices dan Perdarahan (Dite et al, 2008)