LIVER CIRRHOSIS

leonardo dairi

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,PURP
URA,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

13

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.

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

Variceal Bleeding

A. Bleeding from varises is reported in about 20 60

% of case with cirrhosis.
B. Mortality of the first bleeding episode is around 50
%
Prevention
of Varices

measures rational to avoid development

bleeding (Primary prophylaxis).

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)

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

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

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

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
Hypokalemia
Alkalosis
Hypoxia
Hyponatremia
Drugs
Narcotics, transquilizers, sedatives, Diuretics.
Miscellaneous
Infection, Surgery, Superimposed liver disease

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

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)

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

Patients

% Alive

HCC with Cirrhosis

HCC without cirrhosis
Cirrhosis with HCC

361
446
176

46
34
54

p = 0.0004
from European Transplantation Register