SIROSIS HEPATIS
ARRANGED BY:
PRESEPTOR :
2015
1
KATA PENGANTAR
AssalamualaikumWr. Wb.
Makalah refreshing ini disusun dalam rangka untuk dapat lebih mendalami dan
memahami mengenai Sirosis Hepatis . Tujuan khususnya adalah sebagai pemenuhan tugas
kepaniteraan Stase Ilmu Penyakit Dalam.
Semoga dengan adanya laporan kasus ini dapat menambah khasanah ilmu pengetahuan
dan berguna bagi penyusun maupun peserta didik lainnya.
Penyusun menyadari bahwa laporan kasus ini masih jauh dari kesempurnaan, oleh karena
itu penyusun sangat membutuhkan saran dan kritik untuk membangun laporan kasus yang lebih
baik di masa yang akan datang.
Terimakasih.
WassalamualaikumWr. Wb
Penulis
2
BAB I
PATIENT STATUS
A. Patients identity
Name : Mr. B
Religion : Moslem
MR number : 00932959
B. Anamnesis
a. Chief complaint :
Another complaint :
ago. Patient said that his stomach enlarged slowly, and felt bloated while before and after
eating. Patient did not complain of abdominal pain. Complaints lump in the abdomen
denied. Patients also complained of nausea and decreased appetite. Nausea felt by the
patient throughout the day. Patients admitted decreased appetite, patient usually eat
3
one plate full, now only 5 tablespoons. Patients also felt the weight loss from 110 kg to
92 kg within one month. Patient denied any vomiting. Patients also complained about
the color of his urine become darker like a tea. His color of feces also changes
become more darker than before. Complain Shortness of breath denied. Complaints of
fever denied. Patient also felt dizziness. Patient denied of vertigo. Patients had been
hospitalized in Rs Islam Cempaka Putih for this complaint about a month ago.
d. History of family
None of his family has same problem
No history of hypertension
No history of DM
No history of allergic
No history of hematologic disease
e. History of allergy
Patient has no allergy to food, drugs and weather.
f. History of treatment
Patient just consume panadol to healing his problem. Patient had been hospitalized
for this complain about a month ago within 2 weeks. After hospitalized patient just
g. Habits
Smoking habits : Patient smoke 1 cigarettes on a day
Drinking alcohol : Denied
Taking any medication or jamu : patient often consume jamu kupu-kupu,
tolak angin and panado to healing his problems. Patient also love to currycomb.
4
Eating : patient love to eat spicy food and salty
food.
C. Physical Examination
- Generalis status : Moderate ill
- Conciusness: composmentis
Vital sign
- Body weight : 92 kg
- Body height : 160 cm
Thorax
Percussion : Sonor
Heart
5
Palpation : ictus cordis palpable in ICS 5
Auscultation : Regular 1st & 2nd heart sounds, murmur (-), gallop (-)
Abdomen
Inspection: enlargement
Extremities
Laboratory examination
6
Leukocytes 13.44 /l 3.80-10.60
Hematocrit 21 % 40-52
Erythrocyte 3.66 Juta/l 4.40-5.90
Erythrocyte index
MCV 58 Fl 80-100
MCH 20 Pg 26-34
MCHC 35 g/Dl 32-36
Laboratory examination
(CHE)
7
Bilirubin total 9.4 g/dl < 1.0
MCST Result
- Sirosis hepatis
- Splenomegali
- Ascites
Laboratory examination
23th January 2016
Laboratory examination
Resume :
8
Mr. B, 52nd years old, came to hospital with complaints his stomach felt bloated and
enlarge since two months ago, Patients also complained of nausea and decreased appetite.
Patients also felt the weight loss from 110 kg to 92 kg within one month. Patients also
complained about the color of his urine become darker like a tea. His color of feces also
changes become more darker than before. Patients had been hospitalized in Rs Islam
Cempaka Putih for this complaint about a month ago. History of past illness: Have
history of same problem 20 years ago. Physical Examination: Blood pressure: 180/70
Juta/l, MCV : 58 fL, MCH: 20 Pg, Bilirubin total : 9.4 Mg/Dl, Bilirubin direct: 5.3
Albumin : 2.3 g/Dl, Bilirubin total: 9.4 g/Dl, Bilirubin direct: 5.3 /ml, Bilirubin indirect:
MCST Result:
9
Bilirubin total: 6.2 g/dL, Bilirubin direct: 3.6/ml, Bilirubin indirect: 2.6%
Problem List:
Ascites
Hepatitis B
Assessment :
Chirrosis hepatis e.c Hepatitis B with complication
- Ascites
- Hipoalbuminemia
- Anemia
- Hiperbilirubinemia
Differential Diagnosis :
S : His stomach felt bloated and enlarge since 2 months ago, nausea, decreased appetite,
O: Blood pressure: 180/70 mmHg, Heart rate: 85x/minute, Respiratory rate: 20x/minute,
Temperature : 36.8 C), Physical Examination: , anemic conjungtiva (+/+), icteric sclera
10
Lab examination:
Juta/l, MCV : 58 fL, MCH: 20 Pg, Bilirubin total : 9.4 Mg/Dl, Bilirubin direct: 5.3
Albumin : 2.3 g/Dl, Bilirubin total: 9.4 g/Dl, Bilirubin direct: 5.3 /ml, Bilirubin indirect:
MCST Result:
Bilirubin total: 6.2 g/dL, Bilirubin direct: 3.6/ml, Bilirubin indirect: 2.6%
-Ascites
- Hipoalbuminemia
11
- Anemia
- Hiperbilirubinemia
P: Laboratory :
- Hematology routine
- LFTs
-Amonium
- ascites puncture
Therapy :
IVFD Albumin
Propranolol
If ascites > 5 L are removed, 8 gr of albumin should be given per liter of ascetic fluid
removed
Antiviral therapy
12
BAB II
LITERATURE REVIEW
A. Anatomy of Liver
The liver is the largest organ in the body, contributing to about 2% of total body
weight, or about 1.5 kg in adults. The liver is an organ of soft plastic and printed by the
surrounding structures. Convex superior surface and is located right below the dome of
the diaphragm and the dome partially left. The bottom of the heart-shaped concave and
the roof of the right kidney, stomach, pancreas, and intestines. The liver has two main
lobes, the right and left. The right lobe is divided into anterior and posterior segment by
segmentalis fissures that are not visible from the outside. The left lobe is divided into
medial and lateral segments by the falciform ligament that can be seen from the outside.
Falciform ligament runs from the liver to the diaphragm and the front wall of the
abdomen. Liver surface covered by visceral peritoneum, except for a small area on the
posterior surface of which is attached directly to the diaphragm. Some of the ligament
which is a fold of peritoneum helps to support the liver. Under the peritoneum are dense
connective tissue called Glisson's capsule, which covers the entire surface of the organ;
This capsule is coating the start of the hilum or porta hepatis on the inferior surface,
extending themselves into the liver mass, forming the framework for the branches of the
13
A. Physiology of liver
The liver is essential to sustain life and play a role in almost every metabolic
function of the body, and in particular is responsible for more than 500 different
activities. Fortunately, the liver has a large reserve capacity, and only 10-20% with a
functioning network, be able to sustain life. Total destruction or disposal of the liver
resulting in death within 10 hours. The liver has a high regeneration ability. In most
cases, partial removal of the liver, either because the cell is dead or ill, will be replaced
with a new heart tissue. The formation and excretion of bile is the main function of the
liver; bile duct transports bile whereas only store and retrieve the gallbladder to the small
intestine empedi as needed. The liver secretes bile yellow around 1 liter per day. The
main elements of bile is water (97%), electrolytes, bile salts, phospholipids (especially
lecithin) cholesterol and bile pigments (especially conjugated bilirubin). Bile salts
essential for the digestion and absorption of fat in the small intestine. After being
processed by the intestinal bacteria smooth, then most of bile salts will be reabsorbed in
14
the ileum, experienced recirculation to the liver, as well as re-conjugated and secreted.
unimportant, but it is an indication of liver disease and bile duct which is important,
because bilirubin tend to underlie the tissue and fluids that come into contact with it.
The liver plays an important role in the metabolism of three groceries delivered oeh
portal vein after absorption in the intestine. These foods are carbohydrates, proteins, and
fats. Monosaccharide of the small intestine is converted into glycogen and stored in the
liver (glikogenesis). From the depot this glycogen, glucose is released into the blood
constant (glycogenolysis) to meet the body's needs. Most of the glucose is metabolized
within the network to produce heat and energy, and the rest is converted into glycogen
and stored in the subcutaneous tissue. The liver is able to synthesize glucose from protein
and fat (gluconeogenesis). The role of the liver in the metabolism is essential for survival.
All plasma proteins, except gamma globulin, synthesized by the liver. These proteins
include albumin necessary to maintain the colloid osmotic pressure, and prothrombin,
fibrinogen and other clotting factors. In addition, the majority of amino acid degradation
starts in the liver through the process of deamination or disposal group ammonia (NH3).
Ammonia is released then synthesized into urea and secreted by the kidneys and
intestines. Ammonia is formed in the intestine by the action of bacteria in the protein also
converted into urea in the liver. Other liver metabolic function is in fat metabolism,
storage of vitamins, iron, and copper; conjugation and excretion of adrenal and gonadal
substances. Detoxification function is very important and is done by the enzymes in the
harmful, and convert it into a substance which is physiologically inactive. Finally, the
15
liver function is as a container or filter chamber because of its strategic location between
the intestine and the general circulation. Sinusoid Kupffer cells in portal blood filter out
B. Cirrhosis Hepatic
Cirrhosis is defined histologically as a diffuse hepatic process characterized by fibrosis
and conversion of the normal liver architecture into structurally abnormal nodules. The
progression of liver injury to cirrhosis may occur over weeks to years. Many forms of
liver injury are marked by fibrosis, which is defined as an excess deposition of the
liver. This response to liver injury potentially is reversible. By contrast, in most patients,
C. Epidemiology
Chronic liver disease and cirrhosis result in about 35,000 deaths each year in the United
States. Cirrhosis is the ninth leading cause of death in the United States and is responsible
for 1.2% of all US deaths. Many patients die from the disease in their fifth or sixth
decade of life.
D. Etiology
In western countries, the main causes of cirrhosis are alcoholics, while in Indonesia,
mainly due to virus infection with hepatitis B or C. Based on the results of research in
Indonesia, noted that hepatitis B virus cause liver cirrhosis by 40-50%, and 30-40% of
hepatitis C virus , whereas 10-20% the cause is unknown and not included group B and C
16
E. Patophysiology
The pathogenesis of liver cirrhosis, according to recent research, shows the role of stellate
cells (stellate cells). Under normal circumstances stellate cells have a role in the balance of
equilibrium process changes. When exposed to certain factors that continues over time (eg, viral
hepatitis, materials hepatotoxic), then it will stellate cells into cells that form collagen. If the
process runs continuously then fibrosis will continue in stellate cells, and normal liver tissue is
Immune response
The pathogenesis and clinical manifestations of hepatitis B infection are due to the
interaction of the virus and the host immune system. The immune system attacks HBV and
causes liver injury, the result of an immunologic reaction when activated CD4 + and CD8+
Impaired immune reactions (eg, cytokine release, antibody production) or a relatively tolerant
17
The final state of HBV disease is cirrhosis. With or without cirrhosis, however, patients with
The 5 stages that have been identified in the viral life cycle of hepatitis B infection are briefly
discussed below. Different factors have been postulated to influence the development of these
stages, including age, sex, immunosuppression, and coinfection with other viruses.
This stage, which lasts approximately 2-4 weeks in healthy adults, represents the incubation
period. For newborns, the duration of this period is often decades. Active viral replication is
known to continue despite little or no elevation in the aminotransferase levels and no symptoms
of illness.
In the immune active stage, also known as the immune clearance stage, an inflammatory reaction
with a cytopathic effect occurs. HBeAg can be identified in the sera, and a decline in the levels
of HBV DNA is seen in some patients who are clearing infection. The duration of this stage for
patients with acute infection is approximately 3-4 weeks (symptomatic period). For patients with
chronic infection, 10 years or more may elapse before cirrhosis develops, immune clearance
In the third stage, the inactive chronic infection stage, the host can target the infected hepatocytes
and HBV. Viral replication is low or no longer measurable in the serum, and anti-HBe can be
detected. Aminotransferase levels are within the reference range. It is most likely at this stage
18
that an integration of the viral genome into the host's hepatocyte genome takes place. HBsAg still
The emergence of chronic HBeAg-negative disease can occur from the inactive chronic infection
stage (stage 3) or directly from the immune active/clearance stage (stage 2).
Stage5: Recovery
In the fifth stage, the virus cannot be detected in the blood by DNA or HBsAg assays, and
antibodies to various viral antigens have been produced. The image below depicts the serologic
Serologic course of hepatitis B virus (HBV) infection. The flat bars show the duration of
seropositivity in self-limited acute HBV infection. The pointed bars show that HBV DNA and
the e antigen (HBeAg) can become undetectable during chronic infection. Only immunoglobulin
G (IgG) antibodies to the HBV core antigen (anti-HBc) are predictably detectable after resolution
of acute hepatitis or during chronic infection. Antibody to hepatitis B surface antigen (Anti-HBs)
is generally detectable after resolution of acute HBV infection but may disappear with time. It is
19
only rarely found in patients with chronic infection and does not indicate that immunologic
recovery will occur or that the patient has a better prognosis. ALT = alanine transaminase.
features of hepatic fibrosis and nodular regeneration. However, the patients' signs and
symptoms may vary, depending on the underlying etiology of the disease. As an example,
patients with end-stage liver disease caused by hepatitis C may develop profound muscle
wasting, marked ascites, and severe hepatic encephalopathy, with only mild jaundice. In
contrast, patients with end-stage primary biliary cirrhosis may be deeply icteric, with no
evidence of muscle wasting. These patients may complain of extreme fatigue and pruritus
potential therapeutic option, given the inexorable course of most cases of end-stage liver
disease. Many patients with cirrhosis experience fatigue, anorexia, weight loss, and
and finger clubbing, especially in the setting of hepatopulmonary syndrome. Patients with
skin, adipose tissue, muscle, and bone. Males may develop gynecomastia and impotence.
Loss of axillary and pubic hair is noted in men and women. Hyperestrogenemia also may
20
Other Manifestations
If cholestasis is present, decreased micelle entry into the small intestine leads to decreased
vitamin K absorption, with resulting reduction in hepatic production of factors II, VII, IX, and X.
Patients with cirrhosis also may experience fibrinolysis and disseminated intravascular
coagulation.
Patients with cirrhosis may have impaired pulmonary function. Pleural effusions and the
Interstitial edema or dilated precapillary pulmonary vessels may reduce pulmonary diffusing
21
capacity. Patients also may have hepatopulmonary syndrome (HPS). In this condition, pulmonary
and the finding of orthodeoxia, but the syndrome must be considered in any patient with cirrhosis
the United States. It typically occurs in about of 3% of patients per year, when the etiology of
cholangitis. Early diagnosis of HCC is critical because it is potentially curable through either
liver resection or liver transplant. Other conditions that appear with increased incidence in
patients with cirrhosis include peptic ulcer disease, diabetes, and gallstones.
Other individuals have a multitude of the most severe symptoms of end-stage liver
disease and a limited chance for survival. Common signs and symptoms may stem from
decreased hepatic synthetic function (eg, coagulopathy), portal hypertension (eg, variceal
Portal hypertension
Hepatomegaly
Abdominal pain
22
Ascites
Abdominal distention
Bulging flanks
Shifting dullness
Hepatic encephalopathy
The symptoms of hepatic encephalopathy may range from mild to severe and may be observed in
as many as 70% of patients with cirrhosis. Symptoms are graded on the following scale:
to perform mental tasks, irritability, disorder of sleep pattern (ie, inverted sleep cycle)
Grade 2 - Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious
regard to time)
Grade 3 - Somnolent, but arousable state; inability to perform mental tasks; disorientation
with regard to time and place; marked confusion; amnesia; occasional fits of rage; speech
G. Supporting examinations
23
Liver function tests include amino transferase, alkaline phosphatase, gamma
(ALT) or serum glutamyl pyruvic transaminase (SGPT) increased but not too high. AST
more than ALT increased, but when normal transaminase not rule out cirrhosis. Alkaline
phosphatase, an increase of less than 2 to 3 times the upper limit of normal. High
concentrations can be found in patients with primary sclerosing cholangitis and primary
disease, because the alcohol in addition to induce hepatic microsomal GGT, GGT can
kompensata, but can be increased at the advanced cirrhosis. Albumin, synthesis occurs in
the liver tissue, the concentration decreases with worsening cirrhosis. Globulin
24
25
Abdominal ultrasound, already routinely used for the examination of non-invasive and
easy to do. Ultrasound examination included a corner liver, liver surface, size,
homogeneity, and their masses. In advanced cirrhosis, liver shrink and nodular, irregular
surface, and there is increasing ekogenitas liver parenchyma. In addition Ultrasound can
also assess ascites, splenomegaly, portal vein thrombosis, dilation of the portal vein and
H. Treatment
a. Pharmacology
Specific medical therapies may be applied to many liver diseases in an effort to
interferon and other antiviral agents for hepatitis B and C, phlebotomy for
and zinc for Wilson disease. These therapies become progressively less effective
26
if chronic liver disease evolves into cirrhosis. Once cirrhosis develops, treatment
bleeding, ascites, and hepatic encephalopathy are among the most serious
analysis of data from the TURQUOISE-II study, presented in October 2014 at the
treatment with the combination of the protease inhibitor ABT-450 boosted with
improvements from baseline were seen at 12 weeks for the liver enzymes alanine
interferon. Now it has developed therapeutic strategy change parts patients with
27
b) induction therapy IFN
c) dose of IFN therapy every day
IFN and ribavirin combination therapy consisting of IFN 3 million units 3 x RIB
week and 1000-2000 mg per day depending on body weight (1000mg to weigh
less than 75kg given for 24-48 weeks. Interferon Induction therapy is interferon
administered at a dose that higher than million units daily for 2-4 weeks followed
by 3 million units 3 times a week for 48 weeks with or without combination with
the RIB. Doses of interferon therapy every day. Basic administration of IFN a
dose of 3 million or 5 million units per day until HCV-RNA negative in serum and
liver tissue.
3. The specific treatment of Cirrhosis will be given if there has been a
patients receive adequate calories and protein in their diets. Patients frequently
benefit from the addition of commonly available liquid and powdered nutritional
supplements to the diet. Only rarely are patients not able to tolerate proteins in the
low-protein diet out of concern that hepatic encephalopathy may develop places
the patient at risk for profound muscle wasting. The 2010 practice guidelines for
alcoholic liver disease published by the American Association for the Study of
28
cirrhosis. Multiple feedings per day, including breakfast and a snack at night, are
encouraged in patients with cirrhosis, to prevent these patients from slipping into
I. Complication
Ascites
Spontaneous bacterial peritonitis
Hepatorenal syndrome
Ensefalophaty hepatic
J. Patients Monitoring
Patient with cirrhosis should undergo routine follow-up monitoring of their complete
blood count, renal and liver chemistries, and prothrombin time. The author's policy is to
The author performs routine diagnostic endoscopy to determine whether the patient has
are not present. If varices are present, treatment is initiated with a nonselective beta
blocker (eg, propranolol, nadolol), aiming for a 25% reduction in heart rate. Such therapy
offers effective primary prophylaxis against new onset of variceal bleeding. Patients with
29
The incidence of hepatocellular carcinoma (HCC) has risen in the United States. The
practice guidelines of the American Association for the Study of Liver Diseases
recommend that patients with cirrhosis undergo surveillance for HCC with
ultrasonography every 6 months. The discovery of a liver nodule should prompt the
performance of a 4-phase CT scan or an MRI scan (ie, unenhanced, arterial, venous, and
delayed phases). Lesions that enhance in the arterial phase and exhibit "washout" in the
Many authors contend that the combination of arterial enhancement and washout on CT
scanning or MRI offers greater diagnostic power for HCC than does guided liver biopsy.
Indeed, guided liver biopsies have a 20-30% false negative rate in making the diagnosis
of HCC. Current guidelines support the use of CT scanning and MRI in confirming the
presence of HCC. Biopsy is not required in order to define a lesion as HCC. However, CT
by chest and abdominal CT scans and by bone scan, should be offered curative therapy.
Commonly, this therapy entails liver resection surgery for patients with Child Class A
cirrhosis and an accelerated course to liver transplantation for patients with Child Class B
or C cirrhosis. Patients who are awaiting liver transplantation are often offered minimally
invasive therapies in an effort to keep tumors from spreading. These therapies include
30
ablation, chemoembolization, intensity-modulated radiation therapy, and
radioembolization.
REFERENCES
2015
o http:// www.iasusa.org/sites/default/files/tam/23-3-111.pdf. HBV/HIV Coinfection
Ilmu Penyakit Dalam Jilid II Edisi VI. Pusat penerbitan departemen penyakit
dalam FKUI.2014
31
32