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CASE REPORT

SIROSIS HEPATIS

ARRANGED BY:

Annisa Kartika 2011730007

PRESEPTOR :

dr Ihsanil Husna, Sp.PD

STASE ILMU PENYAKIT DALAM RSIJ CEMPAKA PUTIH

PROGRAM STUDI KEDOKTERAN

FAKULTAS KEDOKTERAN DAN KESEHATAN

UNIVERSITAS MUHAMMADIYAH JAKARTA

2015

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KATA PENGANTAR

AssalamualaikumWr. Wb.

Alhamdulillah, Puji syukur penyusun panjatkan kehadiran ALLAH SWT atas


terselesaikannya tugas Laporan Kasus Sirosis Hepatis.

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

Jakarta, Februari 2016

Penulis

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BAB I
PATIENT STATUS

A. Patients identity

Name : Mr. B

Age : 52nd years old

Education : Junior High school

Marital status : Married

Occupation : Motorcycle Taxi

Religion : Moslem

Date of admission : January 2016

MR number : 00932959

B. Anamnesis

a. Chief complaint :

Patient complained of his stomach felt bloated since 2 months ago.

Another complaint :

Nausea, Decrease of appetite, weight loss, dizziness.

b. History of present illness


Patient came with complaints his stomach felt bloated and enlarge since two months

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

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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.

c. History of past illness


Have history of same problem 20 years ago.
No history of Hypertension
No history of DM
No history of urinary or kidney disease
No history of asthma
No history of allergic
No history of hematologic disease

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

control to the doctor.

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

- blood pressure: 180/70 mmHg


- Heart rate: 85x/minute
- Respiratory rate: 20x/minute
- Temperature : 36.8 C

- Body weight : 92 kg
- Body height : 160 cm

D. General physical examination


Head : normocephal, deformity (-)
Faces : symmetric
Eyes : anemic conjungtiva (+/+), icteric sclera (+/+)
Mouth : the oral mucosa moist
Neck : not palpable mass, lymphadenopathy (-)

Thorax

Inspection : the movement of the chest symmetrical

Palpation : same vocal fremitus in dextra and sinistra

Percussion : Sonor

Auscultacion : vesicular breath sounds + / +, ronkhi - / -, wheezing - / -

Heart

Inspection : ictus cordis not seen

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Palpation : ictus cordis palpable in ICS 5

Percussion: ICS 5 parasternal sinistra

Auscultation : Regular 1st & 2nd heart sounds, murmur (-), gallop (-)

Abdomen

Inspection: enlargement

Auscultation: bowel (+) sounds, 7x/minutes

Palpation: hepatomegaly+), pressure pain (-), ascites (+)

Percussion: shifting dullness (+)

Extremities

Superior: Edema (- / -), warm akral(+ / +), RCT <2 seconds (+ / +)

Inferior: Edema (- / -), warm akral (+ / +), RCT <2 seconds (+ / +)

Laboratory examination

18th January 2016

Examination Value Units Normal


Routine Blood
Hemoglobin 7,4 g/Dl 13,2-17,3

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Leukocytes 13.44 /l 3.80-10.60

Hematocrit 21 % 40-52
Erythrocyte 3.66 Juta/l 4.40-5.90

Platelet 203 /l 150-440

Erythrocyte index
MCV 58 Fl 80-100
MCH 20 Pg 26-34
MCHC 35 g/Dl 32-36

Examination Value Units Normal


Na darah 139 mEq/L 135-147
K darah 4.0 mEq/L 3.5-5.0
Cl darah 106 mEq/L 94-111

Bilirubin total 9.4 Mg/Dl < 1.0


Bilirubin direct 5.3 Mg/Dl < 0.3

Bilirubin indirect 4.1 Mg/Dl < 0.8

Laboratory examination

19th January 2016

Examination Value Units Normal


Albumin 2.3 g/dl 4.0-5.2
Ureum darah 33 Mg/Dl 10-50
Kreatinin darah 1.1 Mg/dl < 1.4

Cholinesterase 4151 % 4900-11900

(CHE)

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Bilirubin total 9.4 g/dl < 1.0

Bilirubin direct 5.3 /ml < 0.3

Bilirubin indirect 4.1 % < 0.8


HbsAg (+) positif

MCST Result

19th January 2016

- Sirosis hepatis
- Splenomegali
- Ascites
Laboratory examination
23th January 2016

Examination Value Units Normal


Bilirubin total 6.2 g/Dl < 1.0
Bilirubin direct 3.6 /ml < 0.3
bilirubin indirect 2.6 % < 0.8

Laboratory examination

24th January 2016

Examination Value Units Normal


Hematologi
Hemoglobin 7.1 g/dl 13.2-17.3

Resume :

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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

mmHg, Heart rate: 85x/minute, Respiratory rate: 20x/minute, Temperature : 36.8 C,

anemic conjungtiva (+/+), icteric sclera (+/+ ), Abdomen Inspection: enlargement,

Palpation: ballotement sign (+) (Ascites) , splenomegali suffner line 3, Percussion:

shifting dullness (+). Laboratory examination:

18th January 2016

Hemoglobin : 7,4 g/Dl, Leukocytes : 13.44/l , Hematocrit : 21 %, Erythrocyte: 3.66

Juta/l, MCV : 58 fL, MCH: 20 Pg, Bilirubin total : 9.4 Mg/Dl, Bilirubin direct: 5.3

Mg/Dl, Bilirubin indirect: 4.1 Mg/Dl

19th January 2016

Albumin : 2.3 g/Dl, Bilirubin total: 9.4 g/Dl, Bilirubin direct: 5.3 /ml, Bilirubin indirect:

4.1 %, HbsAg: (+)positif

MCST Result:

Sirosis hepatis, Splenomegali, Ascites

23th January 2016

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Bilirubin total: 6.2 g/dL, Bilirubin direct: 3.6/ml, Bilirubin indirect: 2.6%

24th January 2016

Hemoglobin : 7.1 g/dL

Problem List:

Ascites
Hepatitis B

Assessment :
Chirrosis hepatis e.c Hepatitis B with complication
- Ascites
- Hipoalbuminemia
- Anemia
- Hiperbilirubinemia

Differential Diagnosis :

1. Hepatocarcinoma cellular (HCC) e.c hepatitis B

S : His stomach felt bloated and enlarge since 2 months ago, nausea, decreased appetite,

weight loss from 110 kg until 92 kg within one month.

O: Blood pressure: 180/70 mmHg, Heart rate: 85x/minute, Respiratory rate: 20x/minute,

Temperature : 36.8 C), Physical Examination: , anemic conjungtiva (+/+), icteric sclera

(+/+ ), Abdomen Inspection: enlargement, Auscultation: bowel (+) sounds, 7x/minutes,

Palpation: hepatomegaly(-), pressure pain (-), ballotement sign (+) (Ascites) ,

splenomegali suffner line 3, Percussion: shifting dullness (+).

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Lab examination:

18th January 2016

Hemoglobin : 7,4 g/Dl, Leukocytes : 13.44/l , Hematocrit : 21 %, Erythrocyte: 3.66

Juta/l, MCV : 58 fL, MCH: 20 Pg, Bilirubin total : 9.4 Mg/Dl, Bilirubin direct: 5.3

Mg/Dl, Bilirubin indirect: 4.1 Mg/Dl

19th January 2016

Albumin : 2.3 g/Dl, Bilirubin total: 9.4 g/Dl, Bilirubin direct: 5.3 /ml, Bilirubin indirect:

4.1 %, HbsAg: (+)positif

MCST Result:

Sirosis hepatis, Splenomegali, Ascites

23th January 2016

Bilirubin total: 6.2 g/dL, Bilirubin direct: 3.6/ml, Bilirubin indirect: 2.6%

24th January 2016

Hemoglobin : 7.1 g/dL

A: Chirrosis hepatis e.c Hepatitis B with complication

-Ascites

- Hipoalbuminemia

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- Anemia

- Hiperbilirubinemia

P: Laboratory :

- Hematology routine

- LFTs

-Tumor Marker (HCC)

-Amonium

- ascites puncture

Radiology : Usg Abdomen

Therapy :

IVFD Albumin

Propranolol

Furosemid 20-40 mg/day

If ascites > 5 L are removed, 8 gr of albumin should be given per liter of ascetic fluid

removed

Antiviral therapy

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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

portal vein, hepatic artery and bile duct.

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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

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the ileum, experienced recirculation to the liver, as well as re-conjugated and secreted.

Bilirubin (a bile pigment) is the end product of metabolism and is physiologically

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

steroids, as well as the detoxification of a large number of endogenous and exogenous

substances. Detoxification function is very important and is done by the enzymes in the

liver via oxidation, reduction, hydrolysis, or conjugation of substances that can be

harmful, and convert it into a substance which is physiologically inactive. Finally, the

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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

bacteria and harmful substances by means of phagocytosis.

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

components of the extracellular matrix (ie, collagens, glycoproteins, proteoglycans) in the

liver. This response to liver injury potentially is reversible. By contrast, in most patients,

cirrhosis is not a reversible process.

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

virus (non B non C).

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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

extracellular matrix formation and degradation processes. Pembentukan fibrosis showed

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

replaced by connective tissue.

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+

lymphocytes recognize various HBV-derived peptides on the surface of the hepatocytes.

Impaired immune reactions (eg, cytokine release, antibody production) or a relatively tolerant

immune status result in chronic hepatitis. In particular, a restricted T-cellmediated lymphocytic

response occurs against the HBV-infected hepatocytes.

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The final state of HBV disease is cirrhosis. With or without cirrhosis, however, patients with

HBV infection are likely to develop hepatocellular carcinoma (HCC).

Viral life cycle

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.

Stage 1: Immune tolerance

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.

Stage 2: Immune active/immune clearance

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

takes place, HCC develops, or the chronic HBeAg-negative variant emerges.

Stage 3: Inactive chronic infection

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

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that an integration of the viral genome into the host's hepatocyte genome takes place. HBsAg still

is present in the serum.

Stage 4: Chronic disease

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

course of HBV infection.

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

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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.

F. Signs and Symptoms


All chronic liver diseases that progress to cirrhosis have in common the histologic

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

and have no complications of portal hypertension. In both cases, medical management is

focused on the relief of symptoms. Liver transplantation should be considered as a

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

muscle wasting. Cutaneous manifestations of cirrhosis include jaundice, spider

angiomata, skin telangiectasias palmar erythema, white nails, disappearance of lunulae,

and finger clubbing, especially in the setting of hepatopulmonary syndrome. Patients with

cirrhosis may experience increased conversion of androgenic steroids into estrogens in

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

explain spider angiomata and palmar erythema.

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Other Manifestations

Anemia may result from folate deficiency, hemolysis, or hypersplenism.

Thrombocytopenia usually is secondary to hypersplenism and decreased levels of

thrombopoietin. Coagulopathy results from decreased hepatic production of coagulation factors.

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

diaphragmatic elevation caused by massive ascites may alter ventilation-perfusion relations.

Interstitial edema or dilated precapillary pulmonary vessels may reduce pulmonary diffusing

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capacity. Patients also may have hepatopulmonary syndrome (HPS). In this condition, pulmonary

arteriovenous anastomoses result in arteriovenous shunting. HPS is a potentially progressive and

life-threatening complication of cirrhosis. Classic HPS is marked by the symptom of platypnea

and the finding of orthodeoxia, but the syndrome must be considered in any patient with cirrhosis

who has evidence of oxygen desaturation.

Hepatocellular carcinoma (HCC) ultimately arises in 10-25% of patients with cirrhosis in

the United States. It typically occurs in about of 3% of patients per year, when the etiology of

cirrhosis is hepatitis B, hepatitis C, or alcohol. It develops more commonly in patients with

underlying hereditary hemochromatosis or alpha-1 antitrypsin deficiency. HCC is observed less

commonly in primary biliary cirrhosis and is a rare complication of Wilson disease.

Cholangiocarcinoma occurs in approximately 10% of patients with primary sclerosing

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

bleeding), or decreased detoxification capabilities of the liver (eg, hepatic encephalopathy).

Portal hypertension

Portal hypertension can have prehepatic, intrahepatic, or posthepatic causes. Budd-Chiari

syndrome, a posthepatic cause, is characterized by the following symptoms:

Hepatomegaly

Abdominal pain

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Ascites

Ascites is suggested by the following findings on physical examination:

Abdominal distention

Bulging flanks

Shifting dullness

Elicitation of a "puddle sign" in patients in the knee-elbow position

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:

Grade 0 - Subclinical; normal mental status but minimal changes in memory,

concentration, intellectual function, coordination

Grade 1 - Mild confusion, euphoria or depression, decreased attention, slowing of ability

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

personality changes, inappropriate behavior, intermittent disorientation (usually with

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

is present but incomprehensible

Grade 4 - Coma, with or without response to painful stimuli

G. Supporting examinations

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Liver function tests include amino transferase, alkaline phosphatase, gamma

glutamyl peptidase, bilirubin, albumin and prothrombin time. Aspartate aminotransferase

(AST) or serum glumatil oxaloacetic transaminase (AST) and alanine aminotransferase

(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

billier cirrhosis. Gamma-glutamyl transpeptidase (GGT), alkaline phosphatase

concentration as well as in liver disease. High concentration in chronic alcoholic liver

disease, because the alcohol in addition to induce hepatic microsomal GGT, GGT can

also cause leaking of hepatocytes. Bilirubin, concentration can be normal in cirrhosis

kompensata, but can be increased at the advanced cirrhosis. Albumin, synthesis occurs in

the liver tissue, the concentration decreases with worsening cirrhosis. Globulin

concentration increased in cirrhosis. Secondary to shortcuts, bacterial antigens from

portal system to lymphoid tissue, further induces the production of immunoglobulin.


Prothrombin time reflects the degree / level synthesis of liver dysfunction,

resulting in cirrhosis compounds. Decreased serum sodium, especially in cirrhosis with

ascites, associated with an inability free water excretion.


Hematologic abnormalities anemia, the cause can vary, anemia normokrom, normositer,

mikrositer or hypochromic hypochromic makrositer. Anemia with thrombocytopenia,

leukopenia and neutropenia due to congestive splenomegaly associated with portal

hypertension causing hypersplenism.

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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

liver carcinoma screening in cirrhotic patients.

H. Treatment
a. Pharmacology
Specific medical therapies may be applied to many liver diseases in an effort to

diminish symptoms and to prevent or forestall the development of cirrhosis.

Examples include prednisone and azathioprine for autoimmune hepatitis,

interferon and other antiviral agents for hepatitis B and C, phlebotomy for

hemochromatosis, ursodeoxycholic acid for primary biliary cirrhosis, and trientine

and zinc for Wilson disease. These therapies become progressively less effective

26
if chronic liver disease evolves into cirrhosis. Once cirrhosis develops, treatment

is aimed at the management of complications as they arise. Certainly variceal

bleeding, ascites, and hepatic encephalopathy are among the most serious

complications experienced by patients with cirrhosis. However, attention also

must be paid to patients' chronic constitutional complaints. According to an

analysis of data from the TURQUOISE-II study, presented in October 2014 at the

Annual Scientific Meeting of the American College of Gastroenterology (ACG),

treatment with the combination of the protease inhibitor ABT-450 boosted with

ritonavir, the NS5A inhibitor ombitasvir, and the non-nucleoside polymerase

inhibitor dasabuvir plus ribavirin (3D + RBV) improved measures of liver

function at 12 weeks in hepatitis C patients with cirrhosis. Highly significant

improvements from baseline were seen at 12 weeks for the liver enzymes alanine

aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase.

Among patients with elevated transaminase levels at baseline, levels normalized

after 12 weeks in 70-90% of cases. Highly significant improvements were also

observed in conjugated bilirubin and albumin levels and in prothrombin time at 12

weeks. Treatment of liver cirrhosis in principle be:


1. symptomatic
2. Supportive, namely:
a. Enough rest
b. The setting is sufficient and balanced food; for example: enough calories, 1 g

protein / kg / day and vitamin


c. Treatment based on etiology
For example in liver cirrhosis due to hepatitis C virus infection can be tested with

interferon. Now it has developed therapeutic strategy change parts patients with

chronic hepatitis C who have not received IFN treatment such as


a) a combination of IFN with ribavirin

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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

complications such as:


Ascites
Spontaneous bacterial peritonitis
Hepatorenal syndrome
Ensefalophaty hepatic
b. Nutrition
Many patients complain of anorexia, which may be compounded by the direct

compression of ascites on the GI tract. Care should be taken to ensure that

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

form of chicken, fish, vegetables, and nutritional supplements. Institution of a

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

Liver Diseases and the American College of Gastroenterology recommend

aggressive treatment of protein calorie malnutrition in patients with alcoholic

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cirrhosis. Multiple feedings per day, including breakfast and a snack at night, are

specified. Regular exercise, including walking and even swimming, should be

encouraged in patients with cirrhosis, to prevent these patients from slipping into

a vicious cycle of inactivity and muscle wasting. Debilitated patients frequently

benefit from a formal exercise program supervised by a physical therapist.

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

monitor stable patients 3-4 times per year.

Surveillance of esophageal varices

The author performs routine diagnostic endoscopy to determine whether the patient has

asymptomatic esophageal varices. Follow-up endoscopy is performed in 2 years if varices

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

large esophageal varices should undergo prophylactic endoscopic variceal ligation.

Surveillance for hepatocellular carcinoma

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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

delayed phases are highly suggestive of HCC.

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

scanning or ultrasonographically guided liver biopsy may be useful when a nodules

enhancement characteristics are not typical for HCC.

Patients with a diagnosis of HCC and no evidence of extrahepatic disease, as determined

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

percutaneous injection therapy with ethanol, radiofrequency and microwave thermal

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ablation, chemoembolization, intensity-modulated radiation therapy, and

radioembolization.

REFERENCES

o http://emedicine.medscape.com/article/177632-update 11 jan 2015


o Clinical Journal of the American Association for the Study of Liver

Disease://Present and Future Therapies of Hepatitis B: from Discovery to Cure.

2015
o http:// www.iasusa.org/sites/default/files/tam/23-3-111.pdf. HBV/HIV Coinfection

Volume 23 Issue 3 August/September 2015


o http:// www.jabfm.org/content/28/6/822.full.pdf+html. Management of Chronic

Hepatitis B: An Overview of Practice Guidelines for Primary Care Providers.

Steven-Huy Han,MD,and Tram T.Tran,MD. NovemberDecember 2015 Vol. 28.


o American Society for Clinical Pathology. Beyond Cirrhosis A Proposal From

the International Liver Pathology Study Group. Am J Clin Pathol 2012;137:5-9


o Andri Sanityo. Hepatitis Virus Akut. Aru W. Sudoyo, Idrus Alwi editor. Buku Ajar

Ilmu Penyakit Dalam Jilid II Edisi VI. Pusat penerbitan departemen penyakit

dalam FKUI.2014

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