A 57-year-old Man Came With Abdominal Enlargement Since 2 Weeks Before

Admission
Fitri Nurrahmi*, Dimas Swarahanura*, Eddy M. Salim**
ABSTRACT

INTRODUCTION

It was reported that there was a case of abdominal

enlargement with anemia presented with an
asymptomatic reactive HBsAg. A man, 57 years old,
was admitted to the hospital with abdominal
enlargement. 2 weeks prior to admission, patient
complained about abdominal enlargement getting
bigger each day, shortnees of breath (+) particularly on
activities.2 days prior to admission, patient complained
abdominal is getting bigger, swelling on both legs, void
frequencies and volume lesser than usual. Patient went
to RSMH. From physical examination, this patient has
pale of conjungtivae palpebrae, spider nevi (+),
distended abdominal, shifting dullness (+), edematous
of pretibial (+/+). From the laboratory findings, Hb
10,4 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, and reactive HBsAg.
Patient was diagnosed with decompensated hepatic
cirrhosis with hepatorenal syndrome and anemia
chronic disease and was given furosemide tablet 40 mg,
spironolactone tablet 100 mg, and propranolol tablet 10
mg.

Hepatic cirrhosis is a complication of many liver

diseases characterized by abnormal structure and
function of the liver. Histologically, this disease is
defined as a diffuse hepatic pathologic process
characterized by fibrosis and the conversion of normal
liver architecture into structurally abnormal nodules.
Fibrosis is an excess deposition of the components of
the extracellular matrix (such as collagens,
glycoproteins and proteoglycans) within the liver.
Cirrhosis represents the final common histologic
pathway for a wide variety of chronic liver disease.1
World Health Organization (WHO) estimated
prevalence of hepatic cirrhosis in 2006 is up to 170
million cases. This report reflects that approximately
3% of human world population have hepatic cirrhosis. 2
Hepatic cirrhosis 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 maleto-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. As a result
of the obstruction to the flow of blood through the liver,
blood "backs-up" 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 by passes it. It is a
combination of reduced numbers of liver cells, loss of
the normal contact between blood passing through the

Keywords: hepatic cirrhosis, abdominal enlargement,

hepatorenal syndrome

* Medical Student of Sriwijaya University, Clerkship

Program Moh. Hoesin General Hospital
** Staff of Allergy-Immunology Division of Internal
Medicine Department of Dr. Moh. Hoesin General
Hospital
1

liver and the liver cells, and blood bypassing the liver
that leads to many of the manifestations of cirrhosis.
This condition refers that the hepatic cirrhosis has fallen
into the decompensated phase. And it can lead to
increase the morbidity and mortality rate in patient with
hepatic cirrhosis.6
With this kind of data, we can conclude that hepatic
cirrhosis 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 hepatic cirrhosis. 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
hepatic cirrhosis.

shifting dullness and normal bowel sound on

auscultation. On the upper extremities of the patient
showed palmar erythema and lower extremities showed
pretibial edema.
Laboratory findings demonstrated that his
haemoglobin was 10,3 g/dL, RBC 2,85 106/mm3, Ht
29%, thrombocyte 113.103/l, the WBC differential
count 0/17/41/22/20, AST 154 U/L, ALT 112 U/L,
Ureum 110 mg/dL, creatinine 2,42 mg/dL, calcium 8
mg/dL and sodium 135 mg/dL. Prothrombin time 18,6 s,
INR 1,58, APTT 46,1 s. Total protein was 5,9 g/dL with
albumin of 1,8 g/dL and globulin 4,1 g/dL. HBsAg was
reactive and Anti HCV was negative. Urinalysis
demonstrated no abnormalitites and Benzidine test on
the patients faeces showed no abnormalities.
Second laboratory examination was done and the
result showed Hb was 6.8 g/dL, RBC 1,87.106/mm3,
WBC 4000mm3 Ht was 19% with thrombocytes were
61000l. The differential count was 0/14/42/28/16.
Abdominal USG showed a smaller liver size,
inhomogen parenchyma with irregular surfaces and
blunt edges. No abnormalities were showed for gall
bladder, lien, kidney and pancreas.
Differential diagnoses of this patient were
decopempensated hepatic cirrhosis with chronic kidney
diseases with chronic disease anemia and
decopempensated hepatic cirrhosis with hepatorenal
syndrome and chronic disease anemia. Based on all the
data above the working diagnosis of this patient was
decopempensated hepatic cirrhosis with hepatorenal
syndrome and chronic disease anemia.
The patient and his family were educated and
informed about his illness and therapy. The patient was
given hepatic diet category III and fluid balances are
maintained. Pharmacological therapy for this patient
were spironolactone 100 mg tablet 3 times a day,
furosemide 40 mg tablet once a day, and propranolol 10
mg tablet twice a day. For the anemia, we plan to treat
the patient with vitamin B1, B6, and B12 twice a day,
and folic acid three times each day. The
hipoalbuminemia was corrected by intravenous
albumin. The patient showed a bad functional prognosis
but a good vital prognosis.
Further examinations, such as endoscopy and liver
biopsy, are needed to accurately predict the prognosis
and outcome of the therapy.

CASE ILLUSTRATION
A man, 57 years of age, who lived in Alang-alang
Lebar (Palembang, Sumatera Selatan), was admitted to
Moh. Hoesin General Hospital on May 29th, 2015 with a
chief complaint of abdominal enlargement. The patient
suffered from abdominal enlargement and shortness of
breath two weeks prior to admission. Shortness of
breath was particularly felt on activities. There was no
complaint of cough, fever, and abnormality in urination.
Patient did not take any medications. There was no
chest pain and difficulty in sleeping. Two days prior to
admission patient realized that his abdomen is getting
even bigger and there were swelling on both legs, void
frequencies and volume lesser than usual. Patient went
to Moh. Hoesin General Hospital.
The patients was fully conscious, his general
condition was good, body weight 48 kg, and 165 cm
body height, blood pressure 110/70 mmHg, with a
72x/minute regular pulse rate, 20x/minute regular
respiration rate and 36,3OC body temperature.
Physical examination of the skin, head, nose and
ear showed no abnormalities and physical examination
of the eya showed pale of conjunctiva palpebrae and
icteric sclerae. Jugular venous pressure was (5-2)
cmH2O and lymph nodes was not enlarge and
unpalpapble. The chest was symmetric with normal
shape presenting spider naevi, ictus cordis was neither
seen nor palpable, heart boundary was normal with the
upper boundary on second ICS parasternal line, right
boundary was on right sternalis line, and left boundary
was on fifth ICS midclavicular line. On auscultation,
neither murmur nor gallop were heard. Pulmonary
physical examination was generally normal. Inspection
of abdominal region shows a distended and enlarged
abdomen. Liver and lien are not palpable with a positive

DISCUSSION
Ascites is the accumulation of fluid in the
abdominal cavity. Fluids occur due to various
underlying chronic diseases. The most common chronic
diseases causing ascites are congestive heart failure,
nephrotic syndrome, peritonitis tuberculosis and
metastases of cancer to the abdominal cavity. In this
case,there is no history of swelling of entire body and
swelling of the palpebrae. No anasarca edema was
2

found in the physical examination. Therefore we can

rule out nephrotic as the underlying diseases of ascites.
This patient meet neither major nor minor criteria of
Frangmingham, so we ruled out congestive heart failure
as the underlying disease. Results from the patients
history, physical examination and laboratory findings is
showing decompensated hepatic cirrhosis. 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. 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 this 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. The result of HBsAg
obtained is reactive, but never complain of fever and
yellow body. This patient does not have a particular
genetic disease. Thus, we conclude that the risk factors
of liver cirrhosis is Hepatitis B as the result of HBsAg
in the laboratory examination was reactive.
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 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
The laboratory findings show slight hyperchromic
macrocytic anemia possibly due to chronic disease or
low intake. Bleeding in this patient could be a reason for
the anemia and the most common cause of bleeding in
patients with cirrhosis is rupture of esophageal varicess.
Therefore endoscopy is needed to confirm eosophageal
varicess bleeding. Thrombocytopenia, hypoalbunemia,
inverted ratio of albumin-globuline showed a
malfunctioning liver as thrombocytes and albumin are
produced in liver, and globulin are destroyed in liver.
Hyperuricemia and increase of ureum and creatinine
level are caused by low renal blood flow due to portal
hypertension, this condition of liver diseases affecting
the kidney is called hepatorenal syndrome.
Another abnormal finding from the laboratory
examination is eosinophilia. First laboratory differential
count result upon admission was 0/17/41/22/20, another
blood examination was done a week later and the result
was 0/14/42/28/16 showing eosinohilia in 2
examination. Eosinophilia is a condition when the
peripheral blood eosinophil count is greater than 350 per
mm3. There are some possibilities that may cause this
condition. For patients with cirrhosis, drug-induced
eosinophilia might occur. Spironolactone is one of the
drugs that is associated with eosinophilia. However, in
this case the laboratory finding has shown an increase in
eosinophil since admission, meaning that spironolactone
has not been administered. Primary Biliary Cirrhosis
(PBC) should be considered in the differential diagnosis
3

of eosinophilia with an otherwise unknown origin. At

the present time, the exact cause of PBC is unknown.
PBC results from an abnormal reaction of the body's
immune system possibly initiated by an infection. The
immune system of PBC patients attacks the liver
causing slow, progressive damage to the bile
ducts. When the bile ducts are damaged, bile and other
substances can not be eliminated and accumulate in the
liver. The retained toxic substances and inflammation
cause further damage. This eventually results in scarring
of the liver (cirrhosis). Diagnosis is made with special
blood tests including liver bichemistry. One such test
detects the presence of Antimitochondrial Antibodies
(AMA) in blood. Also, a liver biopsy may be performed.
This is a procedure in which a small needle is inserted
into the liver to take a sample of the tissue for analysis.
Therapy in patients with cirrhosis of the liver
consists of non-pharmacological and pharmacological
therapy. Nonpharmacological therapy is education
which means that medical staff should explain the
hepatic cirrhosis disease to the patients, especially
regarding its treatment process and prognosis. In
addition, other non-pharmacological therapy is fluid
balance and liver diet III.
Liver damages from cirrhosis are irreversible and
pharmacological therapy in patients with liver cirrhosis
aims to prevent further damage of the liver. Diuretics in
this case are used to reduce ascites that occurs in this
patient. Spironolactone which is a potassium-sparring
diuretic competitively inhibits aldosterone-induced
sodium ion reabsorption and secretion of potassium ions
in the distal renal tubular so it will 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 to be absorbed
back into the intravascular. It can be combined with
furosemide to further reduce ascites and leg edema.
Propranolol was given in this case to reduce portal
hypertension in liver cirrhosis. Human albumin infusion
is also given to treat the 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.
Scoring prognosis in patients with hepatic cirrhosis
using Child Pugh classification. There are five
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.9,10
Parameter
1
2
3
Serum
<2
2-3
>3
Bilirubin
Serum
>3,5
2,8-3,5
<2,8
Albumin
MildAscites
Absent
Severe
moderate
Prothrombin
1-3
4-6
>6
Time
Prolonged
1,7
1,8-2,3
>2,3
INR
Grade
Ensefalopati
Absent
Grade I-II
III-IV
Tabel 1. Child Score Parameter
Points

Class

1-Year2-YearSurvivalSurvivalRate
Rate
5-6
A
100%
85%
7-9
B
81%
57%
10-15
C
45%
35%
Tabel 2. Child Score Interpretation

This patients Child Score is 8. Thus, the probability of

this patient to survive for 1 year is 81%.

CONCLUSION
We have discussed a case of decompensated hepatic
cirrhosis with anemia in a 57 year old male patient who
also had asymptomatic Hepatitis B presented with
ascites, anemia, and hipoalbuminemia.

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