Liver Cirrhosis

Dr. Soegiarto Gani, SpPD

Causes of Cirrhosis

Viral hepatitis; B, D, and C

Alcohol
Metabolic
Haemochromatosis
Wilsons disease
Alpha-1-antitrypsin deficiency
Chronic biliary obstruction
Extrahepatic biliary obstruction
Intrahepatic biliary obstruction
Venous outflow obstruction
Veno-occlusive disease
Budd-Chiari syndrome
Cardiac failure
Autoimmune chronic active hepatitis
Drug and toxins

Complications of Cirrhosis

Variceal bleeding
Ascites, refractory ascites
Hepatorenal syndrome
Hepatic encephalopathy
Spontaneous bacterial peritonitis
Hepatocelluler carcinoma

Causes of death

Variceal hemorrhage
Spontaneous bacterial peritonitis
Sepsis
Liver failure
Hepatic coma
Functional renal failure
Hepatocelluler carcinoma

Portal Hypertension Syndrome

Continuing Liver damage

Nodular regeneration

Fibrosis
Increased sinusoidal
pressure
Portal Hypertension

Splancnic vasodilatation

Increased gastroesophageal
collateral

Decreased effective blood

volume

Formation of
oesophagogastric varices

Increased sodium retention

Variceal rupture

Ascites

Variceal bleeding

Variceal Bleeding

A. Bleeding from varises is reported in about 20 60

% of case whit cirrhosis.
B. Mortality of the first bleeding episode is around 50
%
Preventime measure rationalto avoid development
of Varices and bleeding (Primary proplylaris).
C. Up to 70 % Of Patient Whoo do not receive
treatment die within 1 year of the initial bleeding
episode
The Efforts in preventing bleeding seems to be
crucial (secondary, prophylaxis)

Consensus in Portal Hypertension Baveno III

Monitoring for the Development of Varices in the
Portal Hypertensive Patient.
1. All cirrhotic patients should be screened for the
presence of varices at the time of the initial
diagnosis of cirrhosis.
2. In compensated patients without varices, endoscopy
should be repeated at 2-3 year intervals to
evaluate the development of varices.
3. In compensated patients with small varices,
endoscopyshould be repeated at 2 year intervals to
evaluate progression of varices.
4. There is no indication for subsequent evaluations
once large varices are detected.

Algorithm for cirrhosis Without Bleeding

Algorithm For
Cirrhosis Without
Bleeding
Cirrhosis
Established
Upper Endoscopy

No varices

Observe

(2 3 years Evaluation)

Small or Medium
Varices

Observe

(1 2 years Evaluation)

Large Varices

Primary Bleeding
Prophylaxis
Reguler Interval
Usually one week

Non Selectne Blockers

(and /or long actmy Nitrates)
Ligation

Algorithm For Bleeding Cirrhotis

Algorithm For
Bleeding Cirrhotis
Resuscitae

Begin Octreotide
(or Vasopressin)
Early endoscopy
Esophagel
Non-Portal
Gastric Varices
Portal
Varices
Hypertensive Cause
Hypertensive
Gastropathy
Treat appropriately

Continue octreotide 5 days

Begin beta-blocker when stable

Band ligation or injection

Sclerotheraphy
Ballon Tamponade
Rebleeding

No rebleeding
Continue treatment

Shunt (Child A)
Preventation of Rebleeding
TiPSS. or
Pharmacological Treatment
Liver transplantation (Child B or C)
Ligation /Sclerotheraphy
Reguler Interval
Usually one week
Eradication
Repeated Endoscopy
3 6 month
Rebleeding
Shunt (Child A)
TIPSS or Liver transplantation
(Child B or C)

Obat

Dosis dan cara pemberian obat-obat vasoaktif pada

perdarahan varises
Cara pemberian Dosis

Lama
pemberian

Vasopressin
(VP) +
Nitroglyserin
(NG)

VP: i.v infus

NG:
percutaneus,
bolus

VP:
0,4UU/menit

48 jam

Terlipressin

i.v, bolus

Somatostatin

i.v bolus dan

infus

2 mg/4 jam
2-5 hari
selama 24-48
jam pertama,
kemudian 1
mg/ 4 jam
250 ug diikuti 2-5 hari
250-500 ug/jam

Octreotide

i.v, bolus dan

infus

50 ug diikuti
50 ug/jam

2-5 hari

Spontaneus Bacterialis
Peritonitis

Cirrhotic patients at high risk of SBP

Hospitalized cirrhotic patients with ascites and low ascitic
fluid total protein (< 1 g/dl)
Cirrhotic patients with gastrointestinal hemorrhage
Cirrhotic patients with low ascitic fluid total protein (< 1
g/dL) and / or high serum bilirubin (>2.5 mg/dl)
Survivors of an episode of SBP.

Diagnosis Peritonitis Bakterialis Spontan

Pasien sirosis hati dengan asites

Pungsi asites

Gejala menyertai:
Syok, perdarahan, gangguan
kesadaran, gangguan
motilitas, hipotensi, dll
Asimtomatik.

Nyeri perut panas

Pungsi asites:
periksa: PMN
Kultur

Sel PMN > 250

Sel PMN < 250

Kultur + Monomikrobial

Ulangi pungsi
24 jam
Kultur + Monomikrobial

PBS

BMNN
(Bakterasites Monomikrobial
Non-Neutrosistik)

Penatalaksanaan Peritonitis Bakterialis Spontan

PBS simtomatik

Profilaksis PBS

Antibiotik pilihan :
Sefotaksim 1-2 gram/hari selama 5-7 hari
Amoksisilin+Asam klavulanat selama 5-7 hari

Ofloksasin
Siprofloksasin
Dosis standar
5-7 hari

Parasentesis ulang setelah 24 jam

antibiotik

Sel PMN

Sel PMN

Antibiotik
diteruskan

Ganti antibiotik

HEPATORENAL SYNDROME

Pathogenesis of Hepatorenal Syndrome

Cirrhosis
Sinusoidal portal
hypertension

Splanchnic vasodilatation

Arterial underfilling
Reduced renal
vasodilator factors

Baroreceptor-mediated
activation of systemic
Vasoconstriction factors
Renal vasoconstriction
Hepatorenal syndrome

Increased intrarenal
vasoconstriction
factors

HEPATOCELLULAR CARCINOMA

 Treatment of HCC depends on

1. Local resources
2. Stage of the disease
3. Presence of cirrhosis

Liver Transplantation
Hepatic resection treatment of choice for the
few patients with HCC and normal liver.
Trans Arterial Chemo Embolization
Cytostatica
Interferon

Five years survival of pts with HCC treated by

transplantation in 82 Europeans centers between 1988 and
june 1994
Indication to transplantation

HCC with Cirrhosis

HCC without cirrhosis
Cirrhosis with HCC

Patients

% Alive

361
446
176

46
34
54

p = 0.0004
from European Transplantation Register

KESIMPULAN
Sirosis hati, stadium terakhir dari penyakit hati kronis
yang manifestasi kliniknya mengenai berbagai
macam sistem dan organ tubuh.
Komplikasi yang tersering adalah: Asites, Perdarahan
varises, SBP, Ensepalopati hepatik, HCC.
Penanganannya masih merupakan masalah yang
menyulitkan
Pengelolaan yang menyeluruh adalah hal yang terbaik