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
Gastropathy
Osteopenia, osteoporosis
Etc
 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 Formation of

volume 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 Small or Medium Large Varices

Varices

Observe Observe Primary Bleeding

(2 3 years Evaluation) (1 2 years Evaluation)
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

Non-Portal Gastric Varices Esophagel

Hypertensive Cause Portal Varices
Hypertensive
Gastropathy
Continue octreotide 5 days
Treat appropriately Begin beta-blocker when stable

Band ligation or injection

Sclerotheraphy
Ballon Tamponade

Rebleeding No rebleeding

Continue treatment
Shunt (Child A)
TiPSS. or Preventation of Rebleeding
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)
 Dosis dan cara pemberian obat-obat vasoaktif pada
perdarahan varises
Obat Cara pemberian Dosis Lama
pemberian
Vasopressin VP: i.v infus VP: 48 jam
(VP) + NG: 0,4UU/menit
Nitroglyserin percutaneus,
(NG) bolus

Terlipressin i.v, bolus 2 mg/4 jam 2-5 hari

selama 24-48
jam pertama,
kemudian 1
mg/ 4 jam
Somatostatin i.v bolus dan 250 ug diikuti 2-5 hari
infus 250-500 ug/jam
Octreotide i.v, bolus dan 50 ug diikuti 2-5 hari
infus 50 ug/jam
ASCITES
 Pathophysiology of Ascites

Portal Hypertension

Splanchnic arteriolar vasodilatation

"Forward" increase of Arterial vascular underfilling

splancnic capillary pressure and activation of sodium
and permeability retaining mechanism

Lymph formation > lymph

Sodium and water retention
return

Ascites
Management of cirrhotic patients with moderate
uncomplicated ascites

Start with a low sodium diet (80 mmol /day) and anti
aldosteronic drug (100-200 mg/day) monitoring body
weight
Low doses of furosemide (20-40 mg/day, in case of poor
response to the anti aldosteronic drug.
The goal of treatment : weight loss of 500 g /day in
patients without peripheral edema, and 1 kg/day in
patients with peripheral edema.
Maximum dose of anti aldosteronic drug 400 mg/day, and
160 mg of furosemide.
Sodium restriction.
Management of cirrhotic patients with tense or large
uncomplicated ascites

Total paracentesis is the most effective and safest

procedures to mobilize large ascites
Blood volume with intravenous albumin (8 g/L of ascite
removed) is required if the volume of ascites is more than
5 liter.
Start with a low sodium diet and diuretics soon after
paracentesis
Management of refractory ascites
Paracentesis
Peritovenous shunt
Transjugular intrahepatic porto-systemic
stent-shunt (TIPSS)
Liver Transplantation
Hepatic Encephalophathy
 Common Precipitant of Hepatic encephalopathy
Increased Nitrogen Load
Gastrointestinal bleeding
Excess dietary protein
Azotemia
Constipation
Electrolyte and Metabolic Imbalance
Hypakalemia
Alkalosis
Hypoxia
Hyponatremia
Drugs
Narcotics, transquilizers, sedatives, Diuretics.
Miscellaneous
Infection, Surgery, Superimposed liver disease
 Clinical Stages of Hepatic Encephalopathy
Stage Mental status Asterixis EEG

I Euphoria or depression, +/- Normal

mild confusion, slured
speech, disordered speech
II Lethargy, moderate + Abnormal
confusion
III Marked confusion, + Abnormal
incoherent speech, sleeping
but arousable
IV Coma, initially responsive - Abnormal
to noxious stimuli, later
unresponsive
Approach to the patient with hepatic encephalopahty
Initial Evaluation
* Exclude other causes of disordered mentation
* Identify precipitant and correct
* Determinant electrolytes, BUN, creatinine, NH3,
Glucose

Protein restriction

Laxative, e.g., Lactulose 30-120 ml, 1 to 4 times

daily until 4 stools/day

Inadequate response?

Broad-spectrum antibiotics (e.g., neomycin 500

mg qid, or metronidazole 250 mg tid)

Inadequate response?

Consider liver transplatation

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

Nyeri perut panas Gejala menyertai:

Syok, perdarahan, gangguan
kesadaran, gangguan
motilitas, hipotensi, dll
Asimtomatik.

Pungsi asites:
periksa: PMN
Kultur

Sel PMN > 250 Sel PMN < 250

Ulangi pungsi
24 jam
Kultur + Monomikrobial
Kultur + Monomikrobial

PBS
BMNN
(Bakterasites Monomikrobial
Non-Neutrosistik)
 Penatalaksanaan Peritonitis Bakterialis Spontan

PBS simtomatik Profilaksis PBS

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

Parasentesis ulang setelah 24 jam

antibiotik

Sel PMN Sel PMN

Antibiotik
Ganti antibiotik
diteruskan
HEPATORENAL SYNDROME
 Pathogenesis of Hepatorenal Syndrome

Cirrhosis

Sinusoidal portal
hypertension

Splanchnic vasodilatation

Arterial underfilling

Reduced renal Baroreceptor-mediated Increased intrarenal

vasodilator factors activation of systemic vasoconstriction
Vasoconstriction factors factors

Renal vasoconstriction

Hepatorenal syndrome
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 Patients % Alive

HCC with Cirrhosis 361 46

HCC without cirrhosis 446 34
Cirrhosis with HCC 176 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