dr. LAURA E.D.

DAIRI

DEFINITION - EPIDEMIOLOGY
CIRRHOSIS is a slowly progressing disease
in which healthy liver tissue is replaced with
scar tissue, eventually preventing the liver
from functioning properly. The scar tissue
blocks the flow of blood through the liver
and slows the processing of nutrients,
hormones, drugs, and naturally produced
toxins
EPIDEMIOLOGY
In the United States, alcoholic cirrhosis affected
360-100.000 peoples
In the United States, alcoholic cirrhosis accounts
for approximately 40% of deaths due to
cirrhosis.

CAUSES OF CIRRHOSIS

ALCOHOLIC CIRRHOSIS
Alcohol is the most commonly used drug in the
United States, & more than two-thirds of adults
drink alcohol each year
Excessive chronic alcohol use can cause
several different types of chronic liver disease
(alcoholic fatty liver, alcoholic hepatitis,
&alcoholic cirrhosis.

PATOGENESIS
Pengguna alkohol terus menerus
menimbulkan kerusakan hepatosit, fibroblast
termasuk aktivasi sel stelate hepatik yang
telah mengalami transformasi kedalam
myofibroblast dan kemampuan kontraktil
merupakan lokasi kerusakan dari kolagen.
Terbentuk septa dari jaringan ikat yang
menghubungkan periportal dan perisentral
zone ( trigonum porta dan vena sentral membungkus sel hati yang telah mengalami
regenerasi nodule.
Kerusakan hepatosit yang berlanjut disertai
pembentukan collagen hati mengecil
berbentuk noduler, mengeras dan
terbentuklah sirosis hati.

GAMBARAN KLINIK
Klinik asimtomatik 10-40% insidensi
(laparatomy/autopsi) onset pelan2 10 thn,
minum banyak alkohol, anoreksia + malnutrisi
BB, skletal muscle, weakness & fatique.
Hepatoseluler disfungsi + hipertensi portal
jaundice, varises bleeding, asites, HE perburukan
salah satu faktor berobat!
PD hati normal, besar, mengecil, jaundice,
eritema, spider, parotid/ lakrimal gland, clubbing
finger, splenomegali, muscle wasting, asites, laki2
(ginekomasti) / testicular atrofi/ direk efek
berkurang hormonal destruksi (Estrogen)
- menstrual irregularities

- Cause of death variceal bleeding, infeksi

renal.

LABORATORIUM
Anemia bleeding, hipersplenism, supresi
BM oleh alkohol
SGOT < 5x ULN
AST/ALT > 2 x AST sintetik dihalangi oleh
etanol, amonia clearence +
shunting HE
Coagulopati - albumin,globulin
(reticulo endothel sistem)
Glukosa intolerance-endogen insulin
resisten - bukan DM klinis

 Diagnosis, berdasarkan gabungan dari :

Anamnese : Riwayat alkoholik,Infeksi
virus
PD tanda kronik liver stigmata
Laboratorium
Biopsi menyingkirkan penyebab lain
USG
Prognosis : baik bila stop alkohol

TREATMENT OF ALCOHOLIC CIRRHOSIS

ALCOHOL ABSTINENCE!!
Good nutrition
Long term medical supervision
Screening for complications
In the absence of infection :
Glucorticoids can be used, but
restricted to patients with DF Value
>32
Oral pntoxifyline ( production of
TNF-)
Prevent the use of acetaminophe

COMPLICATION OF CIRRHOSIS PORTAL

HYPERTENSION PORTAL HYPERTENSION is
Elevation of the hepatic venous pressure gradient
(HVPG) >5 mmHg

Developed by
intrahepatic resistance of the passage of
blood flow through the liver due to cirrhosis and
regenerative nodules
splachnic blood flow secondary to
vasodilation within the splanchinc vascular bed

Responsible for :
Variceal Hemorraghe
Ascites
Hypersplenism

ESOPHAGEAL VARICES
Approximately 1/3 patients with cirrhosis will develop
Esophageal varices, confirmed by Routine Endoscopy
Another 1/3 patients with esophageal varices will develop
BLEEDING.
VARICEAL HEMORRHAGE
Life threating problem with 20-30% mortality rate associated
with each episode of bleeding

Risk Factors:
Severity of Cirrhosis (through Child Pughs Classification)
The height of wedged-hepatic vein pressure
The size of the varix
Location of the varix
Certain endoscopic stigmata (Red Wale signs,
Hematocystuc spots, diffuse erythema, bluish color,
cherry red spots, with nipple spots)
Tense Ascites

PATHOPHYSIOLOGY OF VARICEAL
HEMORRHAGE
Tekanan Portal
(HVPG > 10 mmHg)
Pembukaan pembuluh
penghubung yang
telah ada
Tekanan portal dan aliran
kolateral portal karena
amakan, alkohol,
aktifitas jasmani,
tekanan

Pembentukan kolateral
portal-sistemik dan
varises esofagus
Dilatasi varises dan penipisan
dinding pembuluh
Desakan dinding *

Catatan :
HVPG :
Hepatic Venous Pressure
Gradient
VEGF :
Venous Endothelial Growth
Factor

Varises pecah

(tekanan intravariseal tekanan lumen esofagus)

* Desakan dinding = -----------------------------------------------------------------X diameter

Tebal dinding varises

Angiogenesis
(VEGF dll)

TREATMENT OF VARICEAL
HEMORRHAGE
PRIMARY PROPHYLAXIS
Screening by endoscopy for all cirrhosis patients
Prophylaxis achieved by giving NONSELECTIVE
BETA BLOCKER or VARICEAL BAND LIGATION
If Variceal Bleed (+) TREAT THE ACUTE
BLEED!!:
Vasoconstricting Agents (Somatostatin / Octreotide)
Balon Tamponade (Sengstaken-Blakemore tube /
Minessota Tube)
Variceal Band Ligation
Transjugular Intrahepatic Portosystemic Shunt (TIPS)

PREVENTION OF REBLEEDING

This algorithm describes

an approach to
management of patients
who have recurrent
bleeding from esophageal
varices.

Thank You
Laura Dairi