REFERAT

MANAJEMNENT ASCITES
IN LIVER CIRRHOSIS
Dea Resita Azharini
102011101081

Consultant:
dr.Hudoyo, Sp. PD

Department Of Internal Medicine

Faculty Of Medicine, Jember
University
 Introduction
The term hepatic cirrhosis given by Laennec in
1819, Khirros orange yellow because the color
changes in the nodules formed
In developed countries, cirrhosis is one of the
biggest causes of death in the age of 45-46 years
old (after cardiovascular diseases and cancer).
Ascites is one of the most frequent complications
to cirrhosis occurring in approximately 60% of
patients within 10 years of diagnosis.
The development of ascites in the setting of
cirrhosis predicting a poor prognosis with 50%
mortality within 3 years
Epidemiology
The incidence of cirrhosis in the United States an
estimated 360 per 100,000 population
In dr. Sardjito Hospital, number of patients with liver
cirrhosis ranges from 4.1% of patients in 2004.
Male > female with an average age of majority
among the age group 30-59 years with a peak around
40-49 years
Ascites is one of the most frequent complications
to cirrhosis occurring in approximately 60% of
patients within 10 years of diagnosis.
The development of ascites in the setting of cirrhosis
predicting a poor prognosis with 50% mortality
within 3 years
 Etiology
Hepatitis virus (B,C,dan D)
Alcoholic cirrhosis
metabolic disorders, eg hemochromatosis, Wilson
disease, nonalkoholik steatohepatic, and others
Kholestasis prolonged (both intra and extrahepatic)
hepatic venous obstruction, eg syndrome Budd-
Chairi
Autoimmune disorders, such as autoimmune
hepatitis
Toxins and drugs, for example: methotrexate,
amiodarone, arsenic, and others
cryptogenic
 Liver Function
The formation and secretion of bile
Nutrient and vitamin metabolism
Inactivation of several substances
Immunity
 Classification
Based on morphology, Sherlock dividing
liver cirrhosis on 3 types, namely:
1. Micronodular
The nodules are formed measuring <3 mm.
2. Macronodular
The nodules are formed measuring> 3 mm.
3. Mixed
Which is a combination of micronodular and
makronodular. Nodules formed size <3 mm and
size> 3 mm.
 Diagnostic
Anamnesis
Loss of appetite and weight
Nausea
Feeling flatulence
Feeling easily tired and weak
Jaundice with tea-colored urine
And generally, the patient will be
hospitalized for their complications such
as upper gastrointestinal bleeding due
to rupture of esophageal varices, ascites
great, and jaundice in.
 Physical Examination
The liver function failure
- Jaundice
- Spider nevi
- Gynecomastia
- Hypoalbuminemia and protein calorie malnutrition
- Fur armpit loss
- ascites
- Palmar erythema
- "White nail
Portal hypertension
- Varicose veins esophagus / cardia
- Splenomegali
- Widening of venous collaterals
Laboratory examination
complete blood count
Liver function test
Electrolit
Serology test
Endoscopy
Radiology
Biopsy hepar
 Complication
Hematemesis melena
Ascites
Peritonitis spontaneus
Encephalopathy hepatic
Hepatorenal Syndrome
Ascites
 DEFINITION
Ascites is defined as accumulation of
more than 25 ml of fluid in the
peritoneal cavity.
 Grading
Grade 1 (mild)
Ascites is only detectable by ultrasound
examination.
Grade 2 (moderate)
Ascites causing moderate symmetrical
distension of the abdomen.
Grade 3 (large)
Ascites causing marked abdominal
distension.
 Pathophysiology
Ikteru Perubaha -Palmar
KERUSAKAN
s Metabolis n eritema
HEPAR
me Metabolis -Angioma
Bilirubin me -Ginecomast
Steroid ia

Varises
Hiperten Esofagu Sintesis Volume Darah
si Portal s Albumin Inaktifasi aldosteron
& ADH
Splenomeg
ali Tekanan Aldosteron & ADH
Onkotik

Tekanan
Hidrosta
tik
Na & Retensi
Cairan
Ascites
Edema
 Diagnostik
Anamnesis
USG Abdomen
Parasintesis Abdomen
Investigasi cairan asites
Jumlah neutrophil dan kultur
Protein cairan asites Serum
Albumin Ascites Gradient (SAAG)
 Investigasi Cairan Asites
Jumlah Neutrofil
PMN > 250 cells/mm3 (0.25 109/l)
SBP ec. perforated viscus or
inflammation of intrabdominal organs

Bloody Ascites
N<1000 cells/mm3
Bloody ascitic fluid (>50,000
cells/mm3) idiopatik, malignancy
 SAAG
Trandusate or exudate??
Serum albumin cons. serum ascetic cons.
 Therapy
Bedrest
Treatment
 Restriksi sodium
Low sodium intake diet negative
sodium balance increased
mobilization of the fluid retention.
4-6 g/hr

Restriksi Water
<1 l/hr
 Diuretik
Assessed bodyweight (edema (+)
500 g/hr; edema (-) 1 kg/hr)
and creatinine and electrolytes
avoid electrolyte disturbances &
diuretic-induced renal failure.
For grade 2 ascites
Spironolacton antagonis
aldosterone, hiperkalemia
Furosemide hipokalemia
 Parasintesis (LVP)
 For grade 3 ascites/ascites refrakter
Coagulopathy is not a
contraindication
Followed by administration of
albumin reduce the risk of
postparacentesis circulatory
dysfunction (PPCD)
 Transjugulas Intrahepatic
Portosistemik Shunt (TIPS)
 I : Large vol paracintesis (LVP) > 3
bln
Functions : sideto-side portocaval
anastomosis between the high
pressure portal vein side and low
pressure hepatic vein side
decompresses the portal
system
 Complication
Spontaneous Bacterial Peritonitis
(SBP)
Symptoms : abdominal pain, fever, vomiting
Suspected in : worsening of liver function,
hepatic encephalopathy, renal failure,
gastrointestinal bleeding
Culture : Escherichia coli and Streptococcus
Tx : 3rd cephalosporins cefotaxim 2 gr IV
twice a day in 5 days
 Hepato Renal Syndrome (HRS)
Et causa : splanchnic arterial vasodilation,
central hypovolemia and deceasing renal
blood flow.
Tx :
Vasoconstrictor drugs terlipressin,
vasopressin
Albumin 1 g/kgBB
HD to control azotemia and electrolyte
balance
 Prognosis

Mortalitas 50% dlm 2 tahun setelah

diagnosis
Asites refrakter 50% mortalitas dlm 6
bln
Terima Kasih