LIVER CIRRHOSIS

leonardo dairi
Departemen Penyakit Dalam

DEFINITION ANATOMICALLY AS A DIFFUSE

PROCESS WITH FIBROSIS AND NODULE
FORMATION

CLASSIFICATION:
MICRONODULAR CIRRHOSIS
MACRONODULAER CIRRHOSIS
MIXED

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

DIAGNOSIS.
1.SPIDER NAEVI
2.ERITHEMA PALMARIS
3.COLLATERAL VEIN
4.ASITES
5.SPLENOMEGALI
6.INVERTED ALBUMIN GLOBULIN
7.HEMATEMESIS/MELENA

CLINICAL CIRRHOSIS
IN CLINICAL TERM,COMPENSATED AND
DECOMPENSATED
CLINICAL APPERANCE RESULT,

HEPATOCELLULER FAILURE

PORTAL HYPERTENSION
CHRONIC ACTIVE HEPATITIS and
EARLY CIRRHOSIS
NON SPECIFIC,
DECOMPENSATED CIRRHOSIS

INVESTIGATION:
1. HAEMATOLOGY
- HAEMOGLOBIN,LEUCOCYTE,
PLATELET COUNT and PROTHROMBIN
TIME.
2. BIOCHEMICAL
BILLIRUBIN,TRANSAMINASE
(ALT/AST),ALKALINI
PHOSPATASE,ALBUMIN
GLOBULIN,IMMUNOGLOBULINT,
GAMMA GT,

- ASCITES PRESENT,
SERUM SODIUM,POTASSIUM,
BICARBONATE,CHLORIDE,UREA AND
CREATININE LEVEL,WEIHLY DAILY AND 24
HOUR URINE VOLUME

3.USG,HEPATIC CT SCAN
4.LEVER BIOPSY GOLD STANDART
5.ENDOSCOPY
6.EEG IF

EXMINATION:
NURITION,FEVER,FETOR
HEPATICUS,JAUNDICE,PIGMENTATION,PURPURA,
FINGER CLUBBING,WHITE NAILS,SPIDER
NAEVI,PALMAR
ERYTHEMA,GYNECOMASTIA,TESTICULAR
ATROPHY,DISTRIBUTION OF BODY HAIR,PAROTID
ENLARGMENT,DUPUYTREN
CONTRACTURE,BLOOD PRESSURE
ABDOMEN
ASCITES, COLLATERAL VEIN, LIVER,
SPLEEN
PERIPHERAL OEDEMA
NEUROLOGICAL CHANGES
MENTAL FUNCTIONS,
STUPOR, TREMOR.

MODIFIED CHILD-PUGH CLASSIFICATION

OF THE SEVERITY LIVER DISEASE
CHILD

BILIRUBIN

< 2 gr %

2,0 - 3,0 gr %

> 3,5 gr %.

KADAR ALBUMIN

> 3,5 gr %

2,8 - 3,5 gr %

< 2,8 gr %.

ASCITES

SLIGHT

MODERATE

ENSEFALOPATI

GRADE 1/2

GRADE 3/4

4-6

>6

PROTHROMBINE

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TOTAL SCORE ,! 6 (grade A), 7 9(grade B), 10 15(grade C)

PORTAL HYPERTENSI
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

MANAGEMENT

TERGANTUNG STADIUMNYA.

1. STD. KOMPENSASI
- KONTROL TERATUR, ISTIRAHAT CUKUP,
DIET TINGGI KALORI / PROTEIN, LEMAK
SECUKUPNYA, DIIT HATI III/IV
- HINDARI FAKTOR PENYEBAB ( ALKOHOL,
OBAT ).
- LIVER PROTEKTIF.

2. STAD. DEKOMPENSATA:
- ISTIRAHAT TOTAL.
- BATASI MASUKKAN CAIRAN < 1000 cc / HARI.
- DIURETIK HEMAT KALIUM /
SPIRONOLAKTON.
BILA GAGAL  + FUROSEMID.
- DIET RENDAH GARAM : 0,5 gr / HR.
- BILA TERJADI ENSEFALOPATI  PROTEIN .
- BERI LIVER PROTEKTIF.
- HINDARKAN PENYEBAB PENCETUS
ENSEFALOPATI.

PROGNOSA :
PROGNOSA JELEK,
1. ASITES REFRAKTER.
2. BILIRUBIN MENETAP > 1,5 - 2 gr %.
3. KADAR ALBUMIN < 2,5 gr %.
4. HATI MENGECIL.
5. MASA PROTROMBIN RENDAH.
6. KADAR NATRIUM DARAH RENDAH.
7. TERJADI PSCA.
8. GANGGUAN KESADARAN.

MORTALITAS PENDERITA S.H. BERDASARKAN

KRITERIA CHILD PADA OPERASI:

A : 10 15 %.
B : 30 %.
C : DIATAS 60 %.

PENYEBAB KEMATIAN :
- 43 %  DARI LUAR HATI.
- 57 %  DARI HATI.

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Causes of death

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

Complications of Cirrhosis

Variceal bleeding
Ascites, refractory ascites
Hepatorenal syndrome(HRS),HPS
Hepatic encephalopathy
Spontaneous bacterial peritonitis
Hepatocelluler carcinoma

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Variceal Bleeding

A. Bleeding from varises is reported in about 20 60

% of case with cirrhosis.
cirrhosis.
B. Mortality of the first bleeding episode is around 50
%
Prevention measure
Prevention
measuress rational to avoid development
of Varices bleeding (Primary proph
prophyla
ylax
xis).
C. Up to 70 % Of Patient who do not receive treatment
die within 1 year of the initial bleeding episode

The Efforts in preventing bleeding seems to be

crucial (secondary, prophylaxis)

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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,
endoscopy should 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


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Algorithm For Bleeding Cirrhotis

Algorithm For
Bleeding Cirrhotis
 Resuscitae

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

Dosis dan cara pemberian obat-obat vasoaktif pada

perdarahan varises
Obat

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

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ASCITES

Pathophysiology of Ascites
Portal Hypertension

Splanchnic arteriolar vasodilatation

"Forward" increase of
splancnic capillary pressure
and permeability

Arterial vascular underfilling

and activation of sodium
retaining mechanism

Lymph formation > lymph

return

Sodium and water retention

Ascites

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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

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Management of refractory ascites

Paracentesis
Peritovenous shunt
Transjugular intrahepatic porto-systemic
stent-shunt (TIPSS)
Liver Transplantation

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Hepatic Encephalophathy

Common Precipitant of Hepatic encephalopathy

Increased Nitrogen Load

Gastrointestinal bleeding
Excess dietary protein
Azotemia
Constipation
Electrolyte and Metabolic Imbalance
Hypokalemia
Alkalosis
Hypoxia
Hyponatremia
Drugs
Narcotics, transquilizers, sedatives, Diuretics.
Miscellaneous
Infection, Surgery, Superimposed liver disease

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Clinical Stages of Hepatic Encephalopathy

Stage

Mental status

Asterixis

EEG

Euphoria or depression,
mild confusion, slured
speech, disordered speech
Lethargy, moderate
confusion

+/-

Normal

Abnormal

Marked confusion,
+
incoherent speech, sleeping
but arousable
Coma, initially responsive to noxious stimuli, later
unresponsive

Abnormal

II
III

IV

Abnormal

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

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Spontaneus Bacterialis
Peritonitis

Cirrhotic patients at high risk of SBP

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.
Hospitalized cirrhotic patients with ascites and low ascitic
fluid total protein (< 1 g/dl)

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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

Ulangi pungsi
24 jam

Kultur + Monomikrobial
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

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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

Increased intrarenal
vasoconstriction
factors

Renal vasoconstriction

Hepatorenal syndrome

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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

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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

HCC without cirrhosis
Cirrhosis with HCC

361
446
176

46
34
54

p = 0.0004
from European Transplantation Register

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