Case Report

A 57 Years Old Man Came With Abdominal Enlargement

Since 4 Months Before Admission

By:
Ariana Deviana, S.Ked
Seftiani, S.Ked
Advisor:
Prof. dr. Eddy Mart Salim, SpPD, K-AI
Obligate Opponents
Septyan Putra Y, S.Ked
Muthmainnah A, S.Ked
Yossi Febrizky, S.Ked
Anugerah Justi P, S.Ked
Sundari Hervinda, S.Ked
Rizky Amy L, S.Ked
Sriwulan R.P, S.Ked
Imanda Husna S, S.Ked
Atika Wulandari, S.Ked

Free Opponents
Ceyka Maduma, S.Ked Khairunnisa, S.Ked
Mardalena, S.Ked
Rizky A A, S.Ked
Ramadhani, S.Ked
Stefani G, S.Ked
Nadia Ayu, S.Ked
Retno S, S.Ked
Noviyanti E, S.Ked
Lastri R S, S.Ked
Gusnella I, S.Ked
Byanka F,S.Ked
Aditya C, S.Ked
Dwika P, S.Ked
Ayu Hasim, S.Ked
Ridho F, S.Ked
Novrilia K, S.Ked

Filissa T H,S.Ked
Stella, S.Ked
Alfatul, S.Ked
Tri A, S.Ked
Inta A, S.Ked
Luqman,S.Ked
Leonardus, S.Ked
Rizki D,S.Ked
Cindy, S.Ked

DEPARTMENT OF INTERNAL MEDICINE

FACULTY OF MEDICINE SRIWIJAYA UNIVERSITY
DR. MOHAMMAD HOESIN GENERAL HOSPITAL
2014

APPROVAL PAGE
Case Report
Title

A 57 Years Old Man Came With Abdominal Enlargement

Since 4 Months Before Admission

By:
Ariana Deviana, S.Ked
Seftiani, S.Ked

Has been accepted and approved as one of the qualification in senior clerkship at
Internal Medicine Department Dr. Mohammad Hoesin Hospital Palembang on
November 17th 2014 January 26th 2014.

Palembang, December 2014

Prof. dr. Eddy Mart Salim, SpPD, K-AI

ii

PREFACE
We give thanks to Prof. dr. Eddy Mart Salim, SpPD-KAI as our advisor.
We are grateful that this case report can be finished according to the schedule. We
give thanks to the contribution of every person in finishing this case report.
This case report is about cirrhosis hepatic. We hope that this case report
will be useful for our colleagues in internal medicine department so that we apply
the adequate diagnosis and treatment for the patients.

Palembang, December 2014

Author

CONTENT
Page
COVER PAGE.................................................................................................. i
APPROVAL PAGE........................................................................................... ii
PREFACE......................................................................................................... iii
CONTENTS..................................................................................................... iv
CHAPTER I INTRODUCTION....................................................................... 1

iii

CHAPTER II CASE REPORT......................................................................... 3

CHAPTER III CASE ANALYSIS.................................................................... 13
REFERENCES................................................................................................. 19

iv

CHAPTER I
INTRODUCTION
Cirrhosis hepatic is a complication of many liver diseases characterized by
abnormal structure and function of the liver. This disease is defined histologically
as a diffuse hepatic pathologic process characterized by fibrosis and the
conversion of normal liver architecture into structurally abnormal nodules.This
fibrosis process, which is defined as an excess deposition of the components of
the extracellular matrix (such as collagens, glycoproteins and proteoglycans)
within the liver. This response to liver injury potentially is not a reversible
process. Cirrhosis represents the final common histologic pathway for a wide
variety of chronic liver disease. The term cirrhosis was first introduced by
Laennec in 1826. It is derived from the Greek term scirrhus or kirrhos refers to
the orange or tawny surface of the liver seen at autopsy.1
World Health Organization (WHO) estimates prevalence of cirrhosis
hepatic in 2006 is up to 170 million cases. This report reflects that approximately
3% of human world population have cirrhosis hepatic.2Cirrhosis hepatic affects an
estimated 7 million individuals in Indonesia. The prevalence of this disease in
Indonesia is approximately 1-2,4% in 2007. Cirrhosis predominantly occurs in
man than woman, with a male-to-female ratio is 2-4:1.The prevalence of this
disease is highest in aged 40-50 years. 3 This disease is the seventh leading cause
of death in the world and is responsible of 25.000 of all deaths per year. There are
20-40% cases of cirrhosis, due to any causes, increases the risk of primary liver
cancer (hepatocellular carcinoma). Primary refers to the fact that the tumor
originates in the liver.4
In cirrhosis, the relationship between blood and liver cells is destroyed.
Even though the liver cells that survive or are newly-formed may be able to
produce and remove substances from the blood, they do not have the normal,
intimate relationship with the blood, and this interferes with the liver cells ability
to add or remove substances from the blood. In addition, the scarring within the
cirrhotic liver obstructs the flow of blood through the liver and to the liver cells.
1

As a result of the obstruction to the flow of blood through the liver, blood "backsup" in the portal vein, and the pressure in the portal vein increases, a condition
called portal hypertension.5
Because of the obstruction to flow and high pressures in the portal vein,
blood in the portal vein seeks other veins in which to return to the heart, veins
with lower pressures that bypass the liver. Unfortunately, the liver is unable to add
or remove substances from blood that bypasses it. It is a combination of reduced
numbers of liver cells, loss of the normal contact between blood passing through
the liver and the liver cells, and blood bypassing the liver that leads to many of the
manifestations of cirrhosis. This condition refers that the cirrhosis hepatic has
fallen into the decompensated phase. And it can lead to increase the morbidity and
mortality rate in patient with cirrhosis hepatic.6
With this kind of data, we can conclude that cirrhosis hepatic is a disease
that needs a special attention, because, this disease is a chronic progressive that
may increase morbidity and mortality if we dont act in a professional manner.
Appropriate theraphy can be done if the medical practitioner is familiar with the
risk factors, etiology, pathogenesis, clinical signs and symptoms of cirrhosis
hepatic. Therefore, we take this case as a case presentation with our expectations
is as a medical practitioner, we can identify this disease and able to make a
clinical diagnosis so this case can be managed appropriately. We hope it will help
to reduce the incidence of morbidity and mortality caused by cirrhosis hepatic.

CHAPTER II
CASE REPORT
I.

ANAMNESIS
(November 24th 2014, 05.00 pm)
1. Identification
a. Name
: Mr. I bin S
b. Age
: 57 years old
c. Sex
: Male
d. Religion
: Moeslim
e. Status
: Married
f. Occupation
: Rubber Farmer
g. Address
: Village II, Sukamaju District, Muara Enim
h. Medical Record : 858892
i. Date of Admission: November 20th 2014, 11.35 am.
2. Chief Complaint
Abdominal enlargement since 4 months before admission.
3. Historyof Illness
+4 months before admission, patient complained about abdominal
enlargement, full on abdominal, weak (+), loss of appatite (+), difficult
to defecation (+). Nausea (-), vomiting (-), epigastric pain (-), upper right
abdominal pain (-), fever (-), cough (-), shortness of breath (-), night
sweating (-), yellowish body (-), yellowish eye (-), swelling of entired
body (-), swelling of eye (-), no abnormality in urination. Patient went to
a shamanand he got lime water. But, the patient feels that there is no
improvement.
+2 months before admission, patientcomplained his abdomen is more
enlarge, enlargement is on all of the area of abdomen, full on abdominal.
Patient also complained about enlargement of the breasts, swelling on
both of his legs, weak (+), loss of appatite (+). Black defecation (-),
nausea (-), vomiting (-), yellowish body (-), yellowish eye (-), swelling

of entired body (-), swelling of eye (-). Patient went to a shamanagain

but there are no improvement.
+10 days before admission, patient still complained about abdominal
enlargement, swelling on both legs (+), enlargement of breasts,
constipation (+), nausea (-), vomiting (-), weak (+), loss of appatite (+),
black defecation (-), nausea (-), vomiting (-), yellowish body (-),
yellowish eye (-), swelling of entired body (-), swelling of eye (-), no
abnormality on urination.Then patient went to RSMH Palembang.
4.

History of Past Illness

History of hypertension is denied
History of diabetes mellitus is denied
History of jaundice is denied
History of alcoholic drinking is denied
History of blood transfusion is denied
History of traditional medicine consumption is denied
History of drug consumption (+) patient consumped Acetosal, 1
tablet/day, since + 10 years ago.
History of smoking (+), since he was 15 years old, 1-2 packs/day.

5.

Historyof Familial Disease

History of similar complaints with patient in the family is denied

II. PHYSICAL EXAMINTAION

(November 24th 2014, 05.00 pm)
a. General Condition

General appearance: looked moderately sick

Conciousness
: compos mentis
Blood pressure
: 110/70 mmHg
Pulserate
: 72x/minute, regular
Respiration rate
: 20x/minute, regular, dyspnea (-), orthopnea (-)
Temperature
: 36,3 C
Body weight
: 46 kg
Body height
: 160 cm
RBW
: 77% (Underweight)

Abdominal circumference : 90 cm

b. Specific Condition

Skin
Skin color is brown, abnormal pigmentation (-), efflourecention and scar
(-), icteric (-).
Lymph Glands
There are no enlargement of the lymph node on submandibular, neck,
axilary, and inguinal.
Head
Normocephaly, alopecia (-), symmetrical face shape (+), deformity (-)
Nose
Epistaxis (-), normal nasal septum, normal mucous layer, secret (-).
Eye
Exopthalmus (-/-),edematous palpebra (-/-), pale of conjunctiva
palpebrae (+/+), icteric sclera (-/-). Pupil round isokor (+), light reflex (+/

+), diameter 3mm, symmetrical eyes movement.

Ear
No abnormality on meatus auditory externus, secret (-)
Mouth
Lips : cyanotic (-), fissure (-), no gum hypertrophy (-), tongue atrophy of
the optic disc (-)
Neck
Jugular Vein Pressure/JVP (5-2) cmH2O, no enlargement of lymph

nodes, no enlargement of thyroid gland, no deviation of trachea.

Axilla
Alopecia axillaries (+)
Thoracic
Normal shape,gynecomastia (+), spider naevi (+)
Cor
o I : Ictus cordis is not seen
o P : Ictus cordis is not palpable
o P : Upper boundary of cor is ICS II
Right boundary of cor is linea sternalis dextra
Left boundary of cor is linea midclavicula sinistra ICS V.
o A : HR=72x/minute, regular, murmur (-), gallop (-)
Pulmo
o I: Static : symmetrical of right and left side are equal

Dynamic : same movementof right and left lung

Retraction of intercostal space (-)

o P: Stemfremitus right = left
Pain on palpation (-)
o P: Sonor on all area of right and left lung
Border of lung and liver on ICS V
Shifting of border on inspiration is two intercostal space
o A: Vesicular (+) normal, ronkhi (-), wheezing (-)
Abdomen
o I: distended, venectation (+), caput medusa (-)
o P: soft, tenderness (-), liver and lien are difficult to palpation
o P: shifting dullness (+), undulation (+)
o A: normal bowel sounds
Extremities :
Upper: pale (-), palmar erythema (-), white nail (+)
Lower: edematous of pretibial (+/+), white nail (+)
External Genitalia : testicular atrophy (-)
III.

ADDITIONAL EXAMINATION
a. LaboratoryExamination (November 21st, 2014)

No Laboratory
1 Hemoglobin
2
3
4
5

e
Erythrocite
Hematocrite
Leukocyte
Platelet

Result
9,1

Normal Value
13-17 g/dL

Interpretation
Anemia

2,83
28
6400
78

4,20-4,87 103/mm3
43-49 vol%
5000-10000/mm3
150-400 103/L

Thrombocytopeni
a

7
8
9
10
11

Diff count
Basophil

0-1 %

Eosinophil

1-6 %

Segment

2-6 %

Band

66

50-70 %

Lymphocyte

20

25-40 %

Monocyte
BSS
Uric Acid
Ureum
Creatinine
Total

7
118
11,5
70
2,54
0,2

2-8%
<200 mg/dl
<8 mg/dl
10-50 mg/dl
0,7-1,2 mg/dl
0,1-1,0 mg/dl

Hiperuricemia
Increase
Increase

12

Bilirubine
Bilirubin

0,09

0,2 mg/dl

13

Direct
Bilirubin

0,11

<0,8 mg/dl

14
15
16
17
18
19

Indirect
Total protein
Albumine
Globuline
SGOT
SGPT
Prothrombin

7,1
2,7
4,4
19
15
15,1

6,4-8,3 mg/dl
3,5-5,0 mg/dl
2,6-3,6 mg/dl
0-38 U/L
0-41 U/L
12-18

1,16
47,2
303
144
5
7,7
Negatif
Negatif

27-42
200-400
135-155 mEq/L
3,5-5,5 mEq/L
6,4-9,7 mg/dl
Non-Reactive
Negatif

Brown
soft
negative
0-1/lp
3-4/lp
+++
negative
negative

Negative
Negative
Negative
Negative
Negative
Negative

- protein

Negative

Negative

- fat

Negative

- carbohydrat
Blood

negative
negative

Time
20
21
22
23
24
25
26
27

INR
APTT
Fibrinogen
Sodium
Kalium
Calcium
HBsAg
Anti HCV
Feses
Colour
Consistency
Amoeba
Erythrocyte
Leukocyte
Bacteria
Fungi
Worm egg
Food residue

Negative

Hipoalbuminemia
Increase

b. USG Abdomen Examination

Result :
Hepar : size is smaller, irregular surfaces, sharp edges, rough inhomogen
parenchyma, portal vein and hepatic vein is not dilated.
Gall bladder : normal size, not thickened walls
Lien : normal size, normal parenchyma
Pancreas : normal size, normal parenchyma
Right kidney : normal size, clear boundary of cortex and medulla, calix is not
widen.
Left kidney : normal size, clear boundary of cortex and medulla, calix is not
widen.
Aorta : KGB paraaorta (-)
Conclusion : cirrhosis hepatic with ascites
c. Additional Examination Planning
o Serum iron, TIBC, transferrin saturation, ferritin serum
o Benzidine Test

o Endoscopy
o Liver biopsy
IV.

RESUME
A man, 57 years old, came with chief complaint is abdominal
enlargement since 4 months before admission. Patient complained
about abdominal enlargement, full on abdominal, weak (+), loss of
appatite (+), constipation (+). Patient went to a shamanand he got lime
water. But, the patient feels that there is no improvement. +2 months
before admission, patientcomplained his abdomen is more enlarge,
enlargement is on all of the area of abdomen, full on abdominal.
Patient also complained about enlargement of breasts, swelling of both
his legs, weak (+), loss of appatite (+), black defecation (-). Patient
went to a shamanagain but there is no improvement. +10 days before
admission, patient still complained about abdominal enlargement,
swelling on both legs (+), enlargement of breasts, constipation (+),
black defecation (-), there are no abnormality in urination, nausea (-),
vomiting (-). weak (+), loss of appatite(+). Then patient went to RSMH
Palembang.
From physical examination, this patient has pale of
conjungtivaepalpebrae, alopecia axillary, gynecomastia, spider nevi
(+),venectation (+), distended abdominal,shifting dullness (+),
undulation (+), edematous of pretibial (+/+). From the laboratory
findings, Hb 9,1 mg/dl, erythocyte 2,83x106 mg/dl, hematocrite 28%
L, thrombocyte 78.000/uL, albumin serum 2,7 mg/dl, globuline
serum 4,4 mg/dl, uric acid 11,5 mg/dl, ureum 70 mg/dl, creatinine 2,54
mg/dl. The diagnosis of this patient is cirrhosis hepatic decompensate
with hepatorenal syndrome and anemia chronic disease.

V.

WORKING DIAGNOSIS
Cirrhosis hepatic decompensate with hepatorenal syndrome and
anemia chronic disease.

VI.

DIFFERENTIAL DIAGNOSIS
Cirrohis hepatic decompensate with chronic renal failure and anemia
chronic disease.

VII.

THERAPY
Non Pharmacology:
Education
Fluid Balance
Hepatic diet category III
Pharmacology
o
o
o
o
o
o

IVFD RL gtt X/m

Spironolaktontab 3x100 mg
Furosemide tab 1x40 mg
Propranolol tab 2x10 mg
Infusion of human albumin 25% 1 x 1 flash
Lactulosa syrup 2x 1 C

VIII. PROGNOSIS
Quo ad vitam

: dubia ad bonam

Quo ad functionam

: dubia ad malaM

Follow up (since 24th 29th of November 2014)

10

The patients had improvement from receiving treatment, patients response

to diuretic treatment with decrease of abdominal circumference day per day.
In general examination we found sensorium is compos mentis, blood
pressure is 110/70 mmHg, pulse rate 73x/minute, respiration rate 20x/minute, and
temperature 36,3o C.
In physical examination we obtained pale of conjungtivae palpebrae,
alopecia axillary, gynecomastia (+), abdomen : distended, venectation (+), shifting
dullness (+), undulation (+), liver and spleen are hard to palpable, ballotement (-).
Treatment of this patient is still divided into non pharmacology and
pharmacology therapy. Non pharmacology patient bed rest, hepatic diet II and
fluid balance, education. Pharmacology is furosemide tab, spironolactone tab,
propranolol tab, infusion of human albumin, and lactulac syrup.

11

CHAPTER III
CASE ANALYSIS
A man, 57 years old, came with chief complaint is abdominal enlargement
since 4 months before admission. + 4 months before admission, patient
complained about abdominal enlargement, full on abdominal, weak (+), loss of
appatite (+), constipation (+). Patient went to a shaman and he got lime water. But,
the patient feels that there is no improvement. + 2 months before admission,
patient complained his abdomen is more enlarge, enlargement is on all of the area
of abdomen, full on abdominal. Patient also complained about enlargement of
breasts, swelling of both his legs, weak (+), loss of appatite (+). Patient went to a
shaman again but there is no improvement. + 10 days before admission, patient
still complained about abdominal enlargement, swelling on both legs (+),
enlargement of breasts, constipation (+), black defecation (+), frequency 1-2
times/day, there are no abnormality in urination, nausea (-), vomiting (-).weak (+),
loss of appatite(+). Then patient went to RSMH Palembang. From physical
examination on abdomen area, from inspection we found distented abdomen,
venectation (+), soft, tenderness (-), hepar and lien are difficult to palpable,
shifting dullness (+), undulation (+) and normal bowel sound. It means that
abdominal enlargement of this patients is accumulation of fluid or ascites.
Ascites is the accumulation of fluid in the abdominal cavity. Fluids occur
due to various underlying chronic diseases. The most common chronic disease are
chronic liver function deterioration. Other diseases which can cause ascites are
congestive heart failure, nephrotic syndrome, peritonitis tuberculosis and
metastases of cancer to the abdominal cavity. But, in this case, nephrotic
syndrome can be removed through: 1. Patient never complain about swelling of
entired body and swelling of the palpebrae, 2. There is no anasarca edema, just a
history of leg edema. And in this case, there are no signs of congestive heart
failure according to the criteria Frangmingham both major criteria and minor
criteria. So the possibility of enlargement of the abdomen caused by congestive
heart failure can be ruled out.

From the history, physical examination and

12

laboratory examination, this case referes to cirrhosis hepatis decompensate.

Addition of Soebandiri criteria for the diagnosis of liver cirrhosis is spider nevi,
collateral vein, ascites, splenomegaly, albumin-globulin ratio is reversed, palmar
erythema, hematemesis melena. In these patients it is obtained collateral vein,
ascites, albumin globulin ratio is reversed, and spider nevi. According to Baveno
IV consensus, this patient suffered from decompensated liver cirrhosis stage III
which ascites with or without varicose veins.3,4
Cirrhosis is caused by scar tissue that forms in your liver in response to
damage occurring over many years. Each time your liver is injured, it tries to
repair itself. In the process, scar tissue forms. As the scar tissue builds up, liver
function worsens. In advanced cirrhosis, the liver no longer works very well.It's
important to determine the cause of cirrhosis because treating that underlying
cause can help prevent further liver damage. A wide range of diseases and
conditions can damage the liver and lead to cirrhosis.Some of the causes of
cirrhosis are inherited or thought to be inherited, such as iron buildup in the body
(hemochromatosis), cystic fibrosis and copper accumulated in the liver (Wilson's
disease). Others occur later in life: chronic alcohol abuse, hepatitis C, hepatitis B,
fat accumulating in the liver (nonalcoholic fatty liver disease), destruction of the
bile ducts (primary biliary cirrhosis and infection by a parasite common in
developing countries (schistosomiasis). Some people may have more than one
cause for cirrhosis, such as alcohol abuse and viral hepatitis.
In these patient, we did not get the risk factors that may be suspected as a
cause of liver cirrhosis. He did not consume alcohol and never had a history of
jaundice which we suspect to be hepatitis. And the results of HBsAg which is
obtained negative HBsAg levels. These patients also do not have a particular
genetic disease. Then the most frequent causes of liver cirrhosis such as the use of
alcohol and hepatitis virus infection can be removed. These patients consume
aspirin 1 tablet per day during +10 years. Aspirin is hepatotoxic drugs. But there is
no clear data or evidence that may link the use of aspirin with the onset of liver
cirrhosis. Thus, we conclude that the risk factors of liver cirrhosis in these patients
is his job. The patient worked as a rubber farmer. After farming, patients will be

13

tapping the rubber latex. Chemical content in the sap of the rubber is one of the
substances that are hepatocarcinogenic. And these substances can lead to changes
in the architecture of the liver that can have an impact on the incidence of liver
cirrhosis.
The pathological hallmark of cirrhosis is the development of scar tissue that
replaces normal parenchyma. This scar tissue blocks the portal flow of blood
through the organ therefore disturbing normal function. Recent research shows the
pivotal role of the stellate cell, a cell type that normally stores vitamin A, in the
development of cirrhosis. Damage to the hepatic parenchyma (due to
inflammation) leads to activation of the stellate cell, which increases fibrosis
(called myofibroblast) and obstructs blood flow in the circulation. In addition, it
secretes TGF-1, which leads to a fibrotic response and proliferation of connective
tissue. Furthermore, it secretes TIMP 1 and 2, naturally occurring inhibitors
of matrix metalloproteinases, which prevents them from breaking down fibrotic
material in the extracellular matrix. The fibrous tissue bands (septa) separate
hepatocyte nodules, which eventually replace the entire liver architecture, leading
to decreased blood flow throughout.4
The clinical manifestasion of cirrhosis such as ascites is about portal
hypertension. Arising at the junction of the superior mesenteric vein with the
splenic pain, the hepatic portal vein carries the major venous drainage from the
gastroinstenial tract, pancreas and spleen to the liver. It delivers two thirds of
hepatic blood flow but account for less than half of the total oxygen supply. Portal
hypertension is defined by eiher an absolute increase in portal venous pressure
gradient between the portal vein and the hepatic vein of 5 mmHg or more. Portal
hypertension in cirrohis hepatic occurs as intrahepatic portal hypertension. Even
before fibrosis distorts sinusoidal architecture, active contraction of vascular
smooth muscle and stellate cells intiates the resistance to the flow of blood into
the liver from the portal vein. As fibrosis develops, sinusoids become increasingly
disordered. Regenerative nodules in the cirrhotic liver impinge on the hepatic
veins, thereby obstructing blood flow distal to the lobules. The small portal veins
and venules are trapped, narrowed and often obliterated by scarring of the portal

14

tracts. In this way, portal hypertension due to obstruction of blood flow distal to
the sinusoid is augmented by increased arterial blood flow.2,4
From the laboratory examination, there are anemia, thrombocytopenia,
hypoalbunemia, inverted ratio of albumin-globuline that were the manifestation
from liver cirrhosis. Hyperuricemia, increase of ureum and creatinine are caused
low renal blood flow because of portal hypertension, this is called hepatorenal
syndrome which liver cirrhosis can effect and cause renal disorders. From
additional examination planning, endoscopy is aimed to check about the
possibility of esophageal varicous that can cause hemorrhage.
Therapy in patients with cirrhosis of the liver consists of nonpharmacological and pharmacological therapy. Nonpharmacologic therapy is
education which means that medical staff should explain the cirrhosis hepatic
disease to the patients, especially regarding its treatment process and prognosis. In
addition, other non-pharmacological therapy is fluid balance and liver diet II.
Liver diet consists of three categories: liver diet I, liver diet II and liver diet III.
Liver diet is useful to achieve optimal nutritional status and maintanance without
overloading the liver function. This liver diet I administered to the patient in an
acute state, severe liver cirrhosis patients, and patients with hepatitis. Liver diet II
given to patients of displacement diet I, which means that the condition of patients
is stable and sufficient appetite. While the liver diet III administered to patients of
liver diet displacement II, this diet was given to patients with acute hepatitis
(Hepatitis A and Hepatitis B) and liver cirrhosis who have no symptoms of active
liver cirrhosis. These patients including liver diet category II. This liver diet II is
composed of : the number of calories about 40-45 kcal/kgBBB with carbohydrates
(40-50%), fat (20-25%), protein 1 g/kg. Liver diet II is accompanied with a lowsalt diet (200-400 mg Na).7
Pharmacological therapy in patients with liver cirrhosis is that by
administering diuretics. Diuretics in this case is used to reduce ascites that occurs
in these patients. Diuretic is spironolactone. Spironolactone which is a potassiumsparing diuretic working competitively inhibits aldosterone-induced sodium ion
reabsorption and secretion of potassium ions in the distal renal tubular so it will

15

reduce Na + reabsorption. These drugs also bind to aldosterone receptors and may
also reduce the formation of the active metabolite of aldosterone in the cell. These
drugs can cause fluid in the interstitial cavity is absorbed back into the
intravascular. It must be combined with furosemide to help remove fluid in the
intravascular, so it can reduce ascites and leg edema. Propranolol was given in this
case with the aim to reduce portal hypertension in liver cirrhosis. Human albumin
infusion is also given to treat the condition hypoalbuminemia in patients with
cirrhosis.8
The prognosis of patients with liver cirrhosis depends on two things: the
severity and the complications of cirrhosis. Prognostic score on cirrhosis is useful
to estimate the likelihood of death in the specified time period, illustrates the
quantitative estimation of residual liver function and able to survive with surgery
or other aggressive interventional therapy. Cirrhosis prognosis varies, influenced
by a number of factors including the etiology, severity of liver damage,
complications and other accompanying diseases. Scores prognosis in patients with
cirrhosis hepatic using Child Pugh classification. There are 5 important variables
in Child Pugh criteria. They are serum levels of bilirubin, albumin serum, ascites,
prothrombin time, and presence or absence of encephalopathy. Furthermore, these
criteria are divided into three groups: A, B and C.9
Parameter
Serum Bilirubin
Serum Albumin
Ascites
Prothrombin Time

1
<2
>3,5
Absent

2
2-3
2,8-3,5
Mild-moderate

3
>3
<2,8
Severe

Prolonged

1-3

4-6

>6

INR
1,7
1,8-2,3
>2,3
Ensefalopati
Absent
Grade I-II
Grade III-IV
Child A :skor 5-6. Child B :skor 7-9. Child C : skor 10-15
In this case, it was found that serum levels of bilirubin of 0.2 mg/dl so the
score is 1. Levels of serum albumin is 2.7 mg/dl so the score id 3. There is ascites
so the score is 3. Levels of INR is 1.16 so the score is 1. There is no
encephalopathy in these patients so the score is 1. Then the total score of the Child

16

Pugh score in these patients was 9 so this patient is in category B which shows the
life expectancy of two years is 60%. So, the prognosis quo ad vitam in these
patients is dubia ad bonam. While the prognosis quo ad functionam is dubia ad
malam due to liver cirrhosis is progressive, diffuse and irreversible disease. It can
cause severe liver dysfunction. So the prognosis of fucntionam is dubia ad
malam.9

17

REFERENCES
1. Wolf, David. 2014. Cirrhosis. eMedicineMedscape Reference.
2. Schuppan, D., Afdhal, N.H. 2008. Liver Cirrhosis. US National Library of
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