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Liver Cirrhosis
Dr. Soegiarto Gani, SpPD
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Causes of Cirrhosis Viral hepatitis; B, D, and C
Alcohol
Metabolic
Haemochromatosis
Wilsons disease
lpha!"!antitr#psin deficienc#
Chronic biliary obstruction
$%trahepatic &iliar# o&struction
'ntrahepatic &iliar# o&struction
Venous outflow obstruction
(eno!occlusive disease
)udd!Chiari s#ndrome
Cardiac failure Autoimmune chronic active hepatitis
Drug and toxins
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Complications of Cirrhosis
Variceal bleeding
Ascites, refractory ascites
Hepatorenal syndrome
Hepatic encephalopathy
Spontaneous bacterial peritonitis Hepatocelluler carcinoma
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Causes of death
Variceal hemorrhage
pontaneous bacterial peritonitis
epsis
!iver failure
"epatic coma #unctional renal failure
"epatocelluler carcinoma
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Continuing Liver damage
Nodular regeneration
Fibrosis
Increased sinusoidal
pressure
Portal Hypertension
Splancnic vasodilatation Increased gastroesophageal
collateral
Formation of
oesophagogastric varices
Decreased effective bloodvolume
Variceal rupture
Variceal bleeding
Increased sodium retention
scites
Portal H#pertension S#ndrome
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(ariceal )leeding
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A.A. Bleeding from varises is reported in about 20 60Bleeding from varises is reported in about 20 60
% of case whit cirrhosis.% of case whit cirrhosis.
B.B. Mortality of the first bleeding episode is around 0Mortality of the first bleeding episode is around 0%%
!.!. "p to #0 % $f atient &hoo do not receive"p to #0 % $f atient &hoo do not receive
treatment die within ' year of the initial bleedingtreatment die within ' year of the initial bleedingepisodeepisode
reventime measure rationalto avoid developmentreventime measure rationalto avoid developmentof (arices and bleeding )rimary proplylaris*.of (arices and bleeding )rimary proplylaris*.
+he ,fforts in preventing bleeding seems to be+he ,fforts in preventing bleeding seems to becrucial )secondary- prophylais*crucial )secondary- prophylais*
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!onsensus in ortal /ypertension Baveno !onsensus in ortal /ypertension Baveno
Monitoring for the 1evelopment of (arices in the
ortal /ypertensive atient.'. All cirrhotic patients should be screened for thepresence of varices at the time of the initialdiagnosis of cirrhosis.
2. n compensated patients without varices- endoscopy
should be repeated at 23 year intervals toevaluate the development of varices.
3. n compensated patients with small varices-endoscopyshould be repeated at 2 year intervals to
evaluate progression of varices.4. +here is no indication for subse5uent evaluationsonce large varices are detected.
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Algorithm for cirrhosis $ithout Bleeding
Algorithm ForCirrhosis Without
BleedingCirrhosis
!stablished
Reguler Interval
Usually one week
"pper !ndoscopy
%o varices mall or Medium
VaricesLarge Varices
#bserve#bserve
$% & ' years !valuation(Primary )leeding
Prophyla*is
%on electne Bloc&ers
'and (or long actmy %itrates) !igation
(2 3 years Evaluation)
lgorithm *or )leeding Cirrhotis
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lgorithm *or )leeding Cirrhotis
Algorithm #or
Bleeding CirrhotisResuscitaeBegin Octreotide
(or Vasopressin)
Early endoscopy
on!"ortal
#ypertensiveCause
Gastric (arices Esop$agel
Varices"ortal
#ypertensive
%astropat$y
+reat appropriatelyContinue octreotide * days)egin beta,bloc-er .hen stable
)and ligation or in+ection
Sclerotheraph#
)allon amponade
-e&leeding o re&leeding
'$unt ($ild )
*i"''+ or,iver transplantation ($ild B or )
ontinue treat-ent
"reventation o. Re&leeding Pharmacological +reatment/ Ligation /Sclerotheraphy
Reguler Interval
Usually one week
Repeated Endoscopy
3 0 -ont$
Eradication
'$unt ($ild )
*I"'' or ,iver transplantation($ild B or )
Re&leeding
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Dosis dan cara pem&erian o&at!o&at vasoatif pada
perdarahan varises+bat Cara pemberian Dosis !ama
pemberianVasopressin
'V) -
%itroglyserin
'%.)
V/ i0v infus
%./
percutaneus,
bolus
V/
1,233(menit
24 5am
6erlipressin i0v, bolus 7 mg(2 5am
selama 72824
5am pertama,
&emudian 9
mg( 2 5am
78* hari
omatostatin i0v bolus dan
infus
7*1 ug dii&uti
7*18*11 ug(5am
78* hari
+ctreotide i0v, bolus dan
infus
*1 ug dii&uti
*1 ug(5am
78* hari
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Spontaneus )acterialis
Peritonitis
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Cirrhotic patients at high ris of S)P
Hospitali/ed cirrhotic patients 0ith ascites and lo0 ascitic
fluid total protein 12 " g3dl4
Cirrhotic patients 0ith gastrointestinal hemorrhage
Cirrhotic patients 0ith lo0 ascitic fluid total protein 12 "
g3dL4 and 3 or high serum &iliru&in 156.7 mg3dl4
Survivors of an episode of S)P.
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Pasien sirosis hati dengan asites
Nyeri perut panas 0e1ala menyertai2Syo-3 perdarahan3 gangguan
-esadaran3 gangguan
motilitas3 hipotensi3 dll
simtomati-4
Pungsi asites
Pungsi asites2peri-sa2 P5N
6ultur
Sel P5N 7 '89 Sel P5N : '89
)5NN
$)a-terasites 5onomi-robial
Non,Neutrosisti-(
6ultur ; 5onomi-robial
P)S
6ultur ; 5onomi-robial
"langi pungsi
'< 1am
Diagnosis Peritonitis )aterialis Spontan
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P)S simtomati- Profila-sis P)S
#flo-sasinSiproflo-sasin
Dosis standar
8,= hari
ntibioti- pilihan 2
Sefota-sim %,' gram/hari selama 8,= hari
mo-sisilin;sam -lavulanat selama 8,= hari
Parasentesis ulang setelah '< 1am
antibioti-
Sel P5N Sel P5N
0anti antibioti-ntibioti-
diterus-an
Penatalasanaan Peritonitis )aterialis Spontan
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H$P8-$9L S:9D-8;$
P h i f H l S d
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Cirrhosis
Splanchnic vasodilatation
rterial underfilling
)aroreceptor,mediated
activation of systemic
Vasoconstriction factors
>enal vasoconstriction
Hepatorenal syndrome
>educed renal
vasodilator factors
Increased intrarenal
vasoconstriction
factors
Sinusoidal portal
hypertension
Pathogenesis of Hepatorenal S#ndrome
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H$P8C$LL
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reatment of HCC depends on
1. Local resources2. Stage of the disease
3. Presence of cirrhosis
Liver ransplantation
Hepatic resection treatment of choice for the
fe0 patients 0ith HCC and normal liver.
rans rterial Chemo $m&oli/ation
C#tostatica
'nterferon
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*ive #ears survival of pts 0ith HCC treated
transplantation in =6 $uropeans centers &et0een ">== and
+une ">>?
:ndication to transplantation atients Alive
HCC 0ith Cirrhosis @A" ?A
HCC 0ithout cirrhosis ??A @?
Cirrhosis 0ith HCC "BA 7?
p .?
from $uropean ransplantation -egister
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E$S';P
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