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CASE REPORT

Hepatic cirrhosis

Prepared by:

S.MUGINRARAO (070100289)

C.VISALINI (070100241)

Supervisor:

PEDIATRIC HEALTH DEPARTMENT

ADAM MALIK GENERAL HOSPITAL

MEDICAL FACULTY

NORTH SUMATERA UNIVERSITY

2011

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CONTENT

Acknowledgement.................................................................................................................... I

Chapter 1 __________________________________________________________________

1. Hepatic cirrhosis.................................................................................................................. 1

1.1 Introduction....................................................................................................................... 1

1.2 Definition.......................................................................................................................... 2

1.3 Etiology............................................................................................................................. 3

1.4 Epidemiology.................................................................................................................... 3

1.5 Classification.................................................................................................................... 4

1.6 Pathophysiology............................................................................................................... 7

1.7 Symptoms and sign.......................................................................................................... 9

1.8 Stage of cirrhosis.............................................................................................................. 10

1.9 Diagnosis......................................................................................................................... 11

2.1 Differential Diagnosis..................................................................................................... 18

2.2 Treatment........................................................................................................................ 21

2.3 Prognosis......................................................................................................................... 28

Chapter 2__________________________________________________________________

Case study…………………………………………………………………………………... 29

Chapter 3__________________________________________________________________

Discussion…………………………………………………………………………………… 33

Summary…………………………………………………………………………………….. 35

Reference............................................................................................................................... 36

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PREFACE

First of all, Praises and Gratitude to God , that due to His Grace and Blessings this

assignment entitled “Hepatic Cirrhosis” was completed in time. This assignment was written

to fulfill duties of the Senior Clinical Assistances, Department of Pediatrics, Universitas

Sumatera Utara/ Haji Adam Malik General Hospital, and will discuss about Hepatic Cirrhosis,

as a part to train ourselves in treating correctly patients with Hepatic Cirrhosis.

Words of gratitude to Dr. Nelly Rosdiana, SpA for her advice and guidance

contributing to the completion of this assignment. And not to forget, then writer would like to

thank every person who has contributed to this assignment and case.

The writer is aware of the imperfection of this assignment, thus encourage critics and

constructional advice for the common good.

Medan, February 2011

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CIRRHOSIS HEPATIC

1.1 Introduction

The liver weighs about 3 pounds and is the largest solid organ in the body. The liver is

an important organ in the body. It performs many critical functions, two of which are

producing substances required by the body, for example, clotting proteins that are necessary in

order for blood to clot, and removing toxic substances that can be harmful to the body, for

example, drugs. The liver also has an important role in regulating the supply to the body

of glucose and lipids that the body uses as fuel. In order to perform these critical functions, the

liver cells must be working normally, and they must have an intimate relationship with the

blood since the substances that are added or removed by the liver are transported to and from

the liver by the blood.

Cirrhosis is a complication of many liver diseases that is characterized by abnormal

structure and function of the liver. The diseases that lead to cirrhosis do so because they injure

and kill liver cells and the inflammation and repair that is associated with the dying liver cells

causes scar tissue to form. The liver cells that do not die multiply in an attempt to replace the

cells that have died. This results in clusters of newly-formed liver cells (regenerative nodules)

within the scar tissue.

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. 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.

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A second reason for the problems caused by cirrhosis is the disturbed relationship

between the liver cells and the channels through which bile flows. The bile that is produced by

liver cells is secreted into very tiny channels that run between the liver cells that line the

sinusoids, called canaliculi. The canaliculi empty into small ducts which then join together to

form larger and larger ducts. Ultimately, all of the ducts combine into one duct that enters

the small intestine. In this way, bile gets to the intestine where it can help with the digestion of

food. In cirrhosis, the canaliculi are abnormal and the relationship between liver cells and

canaliculi is destroyed, just like the relationship between the liver cells and blood in the

sinusoids. As a result, the liver is not able to eliminate toxic substances normally, and they can

accumulate in the body. To a minor extent, digestion in the intestine also is reduced.

A wide variety of diseases and conditions can damage the liver and lead to cirrhosis,

including chronic alcohol abuse, hepatitis B, hepatitis C, cystic fibrosis, destruction of the bile

ducts (primary biliary cirrhosis), fat that accumulates in the liver (nonalcoholic fatty liver

disease), hardening and scarring of the bile ducts (primary sclerosing cholangitis), inability to

process sugars in milk (galactosemia), iron buildup in the body (hemochromatosis),

autoimmune hepatitis, schistosomiasis, poorly formed bile ducts (biliary atresia), problems

storing and releasing energy your cells need to function (glycogen storage disease), too much

copper accumulated in the liver (Wilson's disease).

1.2 Definition

Cirrhosis is a chronic liver disease of highly various etiology characterized by

inflammation, degeneration, and regeneration in differing proportions. Pathologic hallmark is

formation of microscopic or macroscopic nodules separated by bands of fibrous tissue.

Impairment of hepatocellular function and obstruction to portal circulation often lead to

jaundice, ascites, and hepatic failure.

1.3 Etiology

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Hepatitis C, fatty liver, and alcohol abuse are the most common causes of cirrhosis of

the liver in the U.S., but anything that damages the liver can cause cirrhosis, including fatty

liver associated with obesity and diabetes, chronic viral infections of the liver (hepatitis types

B, C, and D; Hepatitis D is extremely rare). On the other hand, blockage of the bile duct,

which carries bile formed in the liver to the intestines where it helps in the digestion of fats. In

babies, this can be caused by biliary atresia in which bile ducts are absent or damaged, causing

bile to back up in the liver. In adults, bile ducts may become inflamed, blocked, or scarred,

due to another liver disease called primary biliary cirrhosis.

Certain inherited diseases also can cause cirrhosis such as cystic fibrosis, glycogen

storage diseases, in which the body is unable to process glycogen, a form of sugar that is

converted to glucose and serves as a source of energy for the body, Alpha 1 antitrypsin

deficiency, an absence of a specific enzyme in the liver, diseases caused by abnormal liver

function, such as hemochromatosis, a condition in which excessive iron is absorbed and

deposited into the liver and other organs, and Wilson's disease, caused by the abnormal

storage of copper in the liver. Although less likely, other causes of cirrhosis include reactions

to prescription drugs, prolonged exposure to environmental toxins, or parasitic infections.2

1.4 Epidemiology

Liver cirrhosis is a leading cause of morbidity and mortality worldwide. It is the fifth

most common cause of death between the ages of 25 and 45. To date it is not possible to

inhibit or reverse progression of cirrhosis in most patients. Accordingly, clinicians have to

deal primarily with the various complications of cirrhosis, while liver transplantation is only

available for selected patients.

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. Each year, 2000 additional deaths are attributed to fulminant hepatic failure

(FHF). FHF may be caused viral hepatitis (eg, hepatitis A and B), drugs (eg, acetaminophen),

toxins (eg, Amanita phalloides, the yellow death-cap mushroom), autoimmune hepatitis,

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Wilson disease, and a variety of less common etiologies. Cryptogenic causes are responsible

for one third of fulminant cases. Patients with the syndrome of FHF have a 50-80% mortality

rate unless they are salvaged by liver transplantation.

In Indonesia, 40-50% of cirrhosis disease is caused by hepatitis b virus while 30-40% is caused by hepatitis c virus. 10-20% is not known.

1.5 Classification

Gross Inspection

Microndular Cirrhosis: Small rather uniform 2m nodules seperated by thin�

fibroussepta usually due to a chemicalagent as alcohol which diffuseuniformly

throught the liver.

Macronodular Cirrhosis: Larger nodules separated by wider scars and irregularly

distributed throughout the liver usually due to an infectious agent such as viral

hepatitis which does not diffuse uniformly throughout the liver.

Microscopic Changes

Dissection Nodules:

Contain remnants of portal tracts and central veins.

Are separated by wide scars but contain thin fibrous septa.

Contain dilated sinusoids especially at their periphery looking like multiple central

veins obviously produced by the inflow of arterial blood coming from the surrounding

wide scars.

The portal tracts within large nodules may be hypoplastic containing portal venule and

arteriole but no bile ducts giving the impression of a disappearing bile duct disorder.

Within wide scars regenerative nodules may develop.

Hypoplastic Portal Field:

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In a dissecting nodule. Notice presence of portal vein, portal artery but no bile duct.

This case was interpreted as "vanishing duct syndrome.

Regenerative Nodules:

These occur in micro and macro nodular cirrhosis.

They arise in the midst of scars favored by the rich arterial blood of scar tissue.

They are round nodules with a fibrous pseudo capsule with bile ductules due to

obstruction of bile flow.

They have embryonal type of cell plates, two cells thick, "twinning of cell plates".

Nuclei are aligned at the sinusoidal pole of the plates.

They often show focal cholestasis.

They may undergo dysplastic and malignant changes.

They compress the vessels of the capsule contributing to the perpetuation of the

cirrhosis.

The Fibrous Septa

Fibrous septa are, with nodules, the other characteristic component of cirrhosis and

they are visible even with the naked eye. They have been termed "fibro-vascular membranes"

which provide a diversion of the blood flow through an alternative route along these fibrous

septa instead of through the acinar sinusoids, thus affecting the physiology of the hepatocytes

the fibrous septa are basically granulation tissue more or less active according to the degree of

edema, capillarization, inflammatory cell infiltration and fibrosis. They reflect the activity of

the cirrhotic process.

Fibrous septa are classified into:

Passive Septa: Slender connective tissue bands containing few chronic inflammatory

cells and sharp demarcation of the parenchymal liver tissue.

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Active Septa: Thick connective tissue bands containing edema, many chronic

inflammatory cells and irregular demarcation of the parenchymal liver tissue.

Classification according to Evolution of Cirrhosis:

The evolution can be assessed on degree of fibrosis and nodule formation. The

following stages can be identified with some approximation even on a needle biopsy

specimen:

Incomplete Septal Cirrhosis (Incomplete bridging fibrosis, no nodules) Presence of

very slender septa radiating from enlarged fields toward the center of the lobule. There

are distended efferent vessels around the septum. This type of cirrhosis produces only

portal hypertension and no liver failure. The prognosis is very good if the portal

hypertension is controlled.

Early Cirrhosis: (Thin bridging fibrosis with dissecting nodules) Thin fibrous septa

with dissecting nodules. No regenerative nodules. Presence of multiple efferent

vessels. (Reticulim stain by silver impregnation).

Moderately Advanced cirrhosis: (Thick bridging fibrosis with dissecting nodules)

Advanced cirrhosis: (Wide septa with regenerative hyperplastic nodules) Wide scars

containing clusters of regenerative hepatocytes. Large scars may contain large portal

fields recognizable with a stain for elastic fibers.

Classification according to Activity of Cirrhosis

Activity is assessed by extent of cell damage, inflammatory reaction within the scar

tissue, piecemeal necrosis along fibrous septa, edema of the septa and changes in the

parenchymal nodules such as necrosis and cholestasis. Activity indicates the progression of

the cirrhotic process and is graded as:

Inactive: No inflammation and intact limiting plates around septa whiich are fibrotic

Slight: Mild inflammation; segmental erosion of limiting plates

Moderate: Moderate inflammation and damage of limiting plates

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Severe: Marked inflammation, extensive damage of limiting plates, piecemeal

necrosis

and parenchymal damage, i.e.: necrosis, cholestasis, dysplasia, malignant

transformation.

1.6 Pathophysiology

The development of hepatic fibrosis reflects an alteration in the normally balanced

processes of extracellular matrix production and degradation. Extracellular matrix, the normal

scaffolding for hepatocytes, is composed of collagens (especially types I, III, and V),

glycoproteins, and proteoglycans.

Stellate cells, located in the perisinusoidal space, are essential for the production of

extracellular matrix. Stellate cells, which were once known as Ito cells, lipocytes, or

perisinusoidal cells, may become activated into collagen-forming cells by a variety of

paracrine factors. Such factors may be released by hepatocytes, Kupffer cells, and sinusoidal

endothelium following liver injury. As an example, increased levels of the cytokine

transforming growth factor beta1 (TGF-beta1) are observed in patients with chronic hepatitis

C and those with cirrhosis. TGF-beta1, in turn, stimulates activated stellate cells to produce

type I collagen. (TGF-β1,leads to a fibrotic response and proliferation of connective tissue

which leads to a fibrotic response and proliferation of connective tissue)

Increased collagen deposition in the space of Disse (the space between hepatocytes

and sinusoids) and the diminution of the size of endothelial fenestrae lead to the

capillarization of sinusoids. Activated stellate cells also have contractile properties. Both

capillarization and constriction of sinusoids by stellate cells contribute to the development of

portal hypertension.

The pathological hallmark of cirrhosis is the development of scar tissue that replaces

normal parenchyma, blocking the portal flow of blood through the organ and disturbing

normal function. Recent research shows the pivotal role of the stellate cell, that normally

stores vitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma leads to

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activation of the stellate cell, which becomes contractile (called myofibroblast) and obstructs

blood flow in the circulation. Furthermore, it disturbs the balance between matrix

metalloproteinases and the naturally occurring inhibitors (TIMP 1 and 2), leading to matrix

breakdown and replacement by connective tissue-secreted matrix.

The fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace

the entire liver architecture, leading to decreased blood flow throughout. The spleen becomes

congested, which leads to hypersplenism and increased sequestration of platelets. Portal

hypertension is responsible for most severe complications of cirrhosis.

Portal hypertension results from a combination of increased portal venous inflow and

increased resistance to portal blood flow. The normal liver has the ability to accommodate

large changes in portal blood flow without appreciable alterations in portal pressure. 

Cirrhotic ascites forms as the result of a particular sequence of events. Development of

portal hypertension is the first abnormality to occur. As portal hypertension develops,

vasodilators are locally released. These vasodilators affect the splanchnic arteries and thereby

decrease the effective arterial blood flow and arterial pressures. The precise agent(s)

responsible for vasodilation is a subject of wide debate; however, most the recent literature

has focused on the likely role of nitric oxide.

Progressive vasodilation leads to the activation of vasoconstrictor and antinatriuretic

mechanisms, both in an attempt to restore normal perfusion pressures. Mechanisms involved

include the renin-angiotensin system, sympathetic nervous system, and antidiuretic hormone

(vasopressin). The ultimate effect is sodium and water retention. In the late stages of cirrhosis,

free water accumulation is more pronounced than the sodium retention and leads to a

dilutional hyponatremia. This explains why cirrhotic patients with ascites demonstrate urinary

sodium retention, increased total body sodium, and dilutional hyponatremia.

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1.7 Symptoms and Signs

Cirrhosis may be asymptomatic for years. One third of patients never develop

symptoms. Often, the first symptoms are nonspecific eg, generalized fatigue (due to cytokine

release), anorexia, malaise, and weight loss (see Table 1). The liver is typically palpable and

firm, with a blunt edge, but is sometimes small and difficult to palpate. Nodules usually are

not palpable.

Clinical signs that suggest a chronic liver disorder or chronic alcohol use but are not

specific for cirrhosis include muscle wasting, palmar erythema, parotid gland enlargement,

white nails, clubbing, Dupuytren's contracture, spider angiomas (< 10 may be normal),

gynecomastia, axillary hair loss, testicular atrophy, and peripheral neuropathy.

Common Symptoms and Signs Due to Complications of CirrhosisSymptom or Sign Possible Cause

Abdominal distention Ascites

Abdominal discomfort with fever or hepatic encephalopathy (infrequently with peritoneal signs)

Spontaneous bacterial peritonitis

Clubbing Hepatopulmonary syndrome

Confusion, lethargy Hepatic encephalopathy

Dyspnea, hypoxia Hepatopulmonary syndrome

Fatigue, pallor Anemia due to bleeding, hypersplenism, undernutrition with deficiency of folate (or iron or vitamin B12), chronic disease, or effects of alcohol (eg, bone marrow suppression)

Fluid overload, oliguria, dark coloured urine, symptoms of renal failure

Hepatorenal syndrome

Fragility fracture (due to a fall from standing height or less)

Osteoporosis

Jaundice Cholestasis

Petechiae, purpura, bleeding Thrombocytopenia from: splenomegaly due to portal hypertension direct effects of alcohol on the bone marrow

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Coagulopathy due to impaired liver synthetic function, vitamin K deficiency, or both

Pruritus, xanthelasmas Cholestasis

Rectal bleeding Rectal varices

Splenomegaly Portal hypertension

Steatorrhea Fat malabsorption

Upper GI bleeding Esophageal varices

Portal hypertensive gastropathy

Table 1: Common Symptoms and Signs Due to Complications of Cirrhosis

1.8 Stage of cirrhosis

According to Child-Pugh Score - Also known as the Child-Turcotte-Pugh score, assesses the

prognosis (outlook) of chronic liver disease, mainly cirrhosis. Originally, it was used to

predict mortality during surgery, but is now used to determine prognosis, as well as the

required treatment strength, and whether or not the patient needs a liver transplant. It is a

combination of numbered points and the letters A, B, C.

ScoreBilirubin

(mg/dl) Albumin (gm/dl)

PT (Sec) Hepaticencephal

Ascites (grade)

1 < 2 > 3.5 1 - 4 None None2 2 - 3 2.8 - 3.5 4 - 6 1 - 2 Mild 3 > 3 < 2.8 > 6 3 – 4 Severe

Table 2: Grading system for cirrhosis: the Child-Pugh score

Child class:

A: 5 - 6,

B: 7 - 9,

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C: > 9.

Class Points One year survival Two year survival

A 5-6 100% 85%

B 7-9 81% 57%

C 10-15 45% 35%

Table 3: Survival rate based on scoring:

1.9 Diagnosis

History

Cirrhosis often is a silent disease, with most patients remaining asymptomatic until

decompensation occurs. Physicians should inquire about risk factors that predispose patients

to cirrhosis. Quantity and duration of alcohol consumption is an important factor in the early

diagnosis of cirrhosis. Other risk factors include those for hepatitis B and C transmission (e.g.,

birthplace in endemic areas, sexual history exposure risk, intranasal or intravenous drug use,

body piercing or tattooing, accidental contamination with blood or body fluids), as well as

transfusion history and personal or family history of autoimmune or hepatic diseases.

Early and well-compensated cirrhosis can manifest as anorexia and weight loss,

weakness, fatigue, and even osteoporosis as a result of vitamin D malabsorption and

subsequent calcium deficiency. Decompensated disease can result in complications such as

ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, and variceal bleeding from

portal hypertension (discussed further in part II). Clinical symptoms at presentation may

include jaundice of the eyes or skin, pruritus, gastrointestinal bleeding, coagulopathy,

increasing abdominal girth, and mental status changes. Each of these clinical findings is the

result of impaired hepatocellular function with or without physical obstruction secondary to

cirrhosis. Because hepatic enzyme synthesis is required for drug metabolism, heightened

sensitivity and medication toxicity may occur in patients with impaired hepatic enzyme

synthesis.

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Physical examination

Physical examination of patients with cirrhosis may reveal a variety of findings that

should lead to a targeted hepatic- or gastrointestinal-based work-up (Table 2). Many patients

will already have had serologic or radiographic tests or an unrelated surgical procedure that

incidentally uncovered signs of cirrhosis.

Abdominal wall vascular collaterals (caput medusa)

Ascites

Asterixis-a hand-flapping tremor, often accompanying metabolic disorders. The tremor is

usually induced by extending the arm and dorsiflexing the wrist. Asterixis is seen frequently

in hepatic encephalopathy. Also called flapping tremor, liver flap.

Clubbing and hypertrophic osteoarthropathy

Constitutional symptoms, including anorexia, fatigue, weakness, and weight loss

Cruveilhier-Baumgarten murmur—a venous hum in patients with portal hypertension

Dupuytren’s contracture- Dupuytren contracture is a localized formation of scar tissue beneath

the skin of the palm of the hand. The scarring accumulates in a tissue (fascia) that normally

covers the tendons that pull the fingers to grip.

Fetor hepaticus—a sweet, pungent breath odor

Gynecomastia

Hepatomegaly

Jaundice

Kayser-Fleischer ring—brown-green ring of copper deposit around the cornea,

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pathognomonic for Wilson’s disease

Nail changes:

Muehrcke’s nails—paired horizontal white bands separated by normal color

Terry’s nails—proximal two thirds of nail plate appears white, whereas the distal one third is

red

Palmar erythema

Scleral icterus

Vascular spiders (spider telangiectasias, spider angiomata)

Splenomegaly

Testicular atrophy

Table 4: Common Physical Examination Findings in Patients with Cirrhosis

Most patients with cirrhosis severe enough to lead to ascites have additional stigmata

of cirrhosis on physical examination. Accurately diagnosing ascites depends upon the amount

of f luid present in the abdomen, the technique used to examine the patient, and the patient’s

habitus. The most useful physical finding in confirming the presence of ascites is f lank

dullness to percussion. When this is detected, it is helpful to determine whether it shifts with

rotation of the patient (shifting dullness) or whether it can be percussed anteriorly. One study

found absence of f lank dullness to be the most accurate predictor against the presence of

ascites; the probability of ascites without f lank dullness was less than 10 percent.11

Approximately 1,500 mL of fluid must be present before dullness is detected on physical

examination, whereas routine ultrasonography can detect as little as 50 mL of f luid in the

abdomen.

Vascular spiders (spider angiomata, spider telangiectasias) are vascular lesions usually

found on the trunk, face, and upper extremities. Although their pathogenesis is incompletely

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understood, it is believed that their presence in men is associated with an increase in the

estradiol to free testosterone ratio.12 Vascular spiders are not specific for cirrhosis: they also

occur during pregnancy, in patients with severe malnutrition, and in healthy persons. The

number and size of vascular spiders have been shown to correlate with the severity of chronic

liver disease. Patients with numerous large vascular spiders are at increased risk for variceal

hemorrhage.

Laboratory Evaluation

No serologic test can diagnose cirrhosis accurately. The term liver function test is a

misnomer because the assays in most standard liver panels do not reflect the function of the

liver correctly. Although liver function tests may not correlate exactly with hepatic function,

interpreting abnormal biochemical patterns in conjunction with the clinical picture may

suggest certain liver diseases.

When a liver abnormality is suspected or identified, a liver panel, a complete blood

count (CBC) with platelets, and a prothrombin time test should be performed. Common tests

in standard liver panels include the serum enzymes aspartate transaminase (AST), alanine

transaminase (ALT), alkaline phosphatase, and γ-glutamyltransferase; total, direct, and

indirect serum bilirubin; and serum albumin. The ALT is thought to be the most cost-effective

screening test for identifying metabolic or drug-induced hepatic injury, but like other liver

function tests, it is of limited use in predicting degree of inflammation and of no use in

estimating severity of fibrosis. One study found that a platelet count of less than 160 K per

mm has a sensitivity of 80 percent for detecting cirrhosis in patients.

A prospective study showed a strong correlation between liver function test results

elevated to greater than twice the upper limit of normal for at least six months and underlying

liver disease proved by liver biopsy. Additional serologic studies should be pursued in such

circumstances to evaluate for various etiologies of cirrhosis (Table 3). If clinical suspicion for

liver disease is high, then further serologic work-up is warranted within six months. If a

patient has a persistently increased ALT level, viral hepatitis serologies should be assayed. If

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these are negative, the remaining serologic work-up should include an antinuclear antibodies

test or anti–smooth muscle antibody test, or both, to evaluate for autoimmune hepatitis; and a

fasting transferrin saturation level or unsaturated iron-binding capacity and ferritin level18 to

evaluate for hereditary hemochromatosis.

In patients younger than 40 years in whom Wilson’s disease is suspected, serum

ceruloplasmin and copper levels should be measured, but screening all patients with chronic

hepatic injury for Wilson’s disease is not indicated. Primary biliary cirrhosis or primary

sclerosing cholangitis should be suspected in patients with chronic cholestasis. Testing for α1-

antitrypsin (A1AT) deficiency may be of benefit in patients with chronic hepatic injury and no

other apparent cause. Although the role of A1AT deficiency in liver disease in adults is not

clearly defined, testing is especially important in neonates with evidence of hepatic injury.

Ultrasonography or biopsy is necessary to establish the diagnosis of NAFLD.

Etiology Laboratory tests and results

Alcoholic liver disease AST:ALT ratio > 2*

Elevated GGT

α1-Antitrypsin deficiency Decreased serum α1-antitrypsin

Genetic screening recommended in equivocal cases

Autoimmune hepatitis

(type 1)

Positive ANA and/or ASMA in high titer

Chronic hepatitis B Positive HBsAg and HBeAg qualitative assays

Once HBeAg is negative and HBeAb is positive, HBsAg should

be monitored periodically to determine viral clearance.

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Hepatitis B virus DNA quantification used to document viral

clearance

Elevated AST and/or ALT*

Chronic hepatitis C Positive hepatitis C virus antibody qualitative assay

HCV RNA quantification used to document viral clearance

HCV viral genotype to determine potential response to

antiretroviral therapy

Elevated AST and/or ALT*

Hepatocellular carcinoma Elevated alpha fetoprotein, AST, and/or ALT*

Elevated ALP with obstruction or cholestasis

Hereditary

hemochromatosis

Elevated fasting transferrin saturation, unsaturated iron-binding

capacity, or ferritin. A transferrin saturation ≥45 percent or an

unsaturated iron-binding capacity 155 mcg per dL (27.7 μmol per

L) should be followed by analysis for HFE (hemochromatosis)

gene mutations.

Nonalcoholic fatty liver

disease

Elevated AST and/or ALT*

Ultrasonography or biopsy necessary to establish diagnosis.

Primary biliary cirrhosis

and primary sclerosing

cholangitis

Diagnosis made via contrast cholangiography, can be supported

clinically by positive antimitochondrial antibody (primary biliary

cirrhosis) or antineutrophil cytoplasmic antibody (primary

sclerosing cholangitis) in high titers.

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Elevated AST, ALT, and ALP common

Wilson’s disease Serum ceruloplasmin < 20 mg per dL (200 mg per L) (normal: 20

to 60 mg per dL [200 to 600 mg per L]), or low serum copper

level (normal: 80 to 160 mcg per dL [12.6 to 25.1 μmol per L])

Basal 24-hour urinary copper excretion > 100 mcg (1.57 μmol)

(normal: 10 to 80 mcg [0.16 to 1.26 μmol])

Genetic screening recommended in equivocal cases, but must be

able to detect multiple mutations in Wilson’s disease gene.

Table 5: Clinical Laboratory Studies Used in Diagnosing Chronic Liver Disease

[AST = aspartate transaminase; ALT = alanine transaminase; GGT = γ-glutamyltransferase;

ANA = antinuclear antibody; ASMA = anti–smooth muscle antibody; HBsAg = hepatitis B

surface antigen; HBeAg = hepatitis B e antigen; HBeAb = hepatitis B e antibody; HCV =

hepatitis C virus; ALP = alkaline phosphatase.]

*—AST and ALT levels may be normal in advanced disease.

Radiographic Studies

Although various radiographic studies may suggest the presence of cirrhosis, no test is

considered a diagnostic standard. The major use of radiographic studies is to detect ascites,

hepatosplenomegaly, hepatic or portal vein thromboses, and hepatocellular carcinoma, all of

which strongly suggest cirrhosis.

Ultrasonography

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Abdominal ultrasonography with Doppler is a noninvasive, widely available modality

that provides valuable information regarding the gross appearance of the liver and blood flow

in the portal and hepatic veins in patients suspected to have cirrhosis. Ultrasonography should

be the first radiographic study performed in the evaluation of cirrhosis because it is the least

expensive and does not pose a radiation exposure risk or involve intravenous contrast with the

potential for nephrotoxicity as does computed tomography (CT). Nodularity, irregularity,

increased echogenicity, and atrophy are ultrasonographic hallmarks of cirrhosis. In advanced

disease, the gross liver appears small and multinodular, ascites may be detected, and Doppler

flow can be significantly decreased in the portal circulation.

The discovery of hepatic nodules via ultrasonography warrants further evaluation

because benign and malignant nodules can have similar ultrasonographic appearances. A

study using high-resolution ultrasonography in patients with cirrhosis confirmed with biopsy

or laparoscopy found a sensitivity and specificity for cirrhosis of 91.1 and 93.5 percent,

respectively, and positive and negative predictive values of 93.2 and 91.5 percent,

respectively.

CT And MRI

CT and magnetic resonance imaging (MRI) generally are poor at detecting

morphologic changes associated with early cirrhosis, but they can accurately demonstrate

nodularity and lobar atrophic and hypertrophic changes, as well as ascites and varices in

advanced disease. Although MRI sometimes differentiates among regenerating or dysplastic

nodules and hepatocellular carcinoma, it is best used as a follow-up study to determine

whether lesions have changed in appearance and size. CT portal phase imaging can be used to

assess portal vein patency, although flow volume and direction cannot be determined

accurately.

Although used rarely, magnetic resonance angiography (MRA) can assess portal

hypertensive changes including flow volume and direction, as well as portal vein thrombosis.

One study reported that MRI can accurately diagnose cirrhosis and provide correlation with its

severity. Despite the potential of MRI and MRA in the diagnosis and evaluation of patients

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with cirrhosis, their widespread use is limited by their expense and by the ability of routine

ultrasonography with Doppler to obtain adequate information for the diagnosis of cirrhosis

and presence of complications.

Liver Biopsy

Referral for liver biopsy should be considered after a thorough, non-invasive serologic

and radiographic evaluation has failed to confirm a diagnosis of cirrhosis; the benefit of

biopsy outweighs the risk; and it is postulated that biopsy will have a favourable impact on the

treatment of chronic liver disease. A liver biopsy is also considered to be the gold standard for

diagnosing the liver fibrosis stage and predicting the outcome of the diseases. The sensitivity

and specificity for an accurate diagnosis of cirrhosis and its etiology range from 80 to 100

percent, depending on the number and size of the histologic samples and on the sampling

method.

Liver biopsy is performed via percutaneous, transjugular, laparoscopic, open operative,

or ultrasonography- or CT-guided fine-needle approaches. Before the procedure, a CBC with

platelets and prothrombin time measurement should be obtained. Patients should be advised to

refrain from consumption of aspirin and nonsteroidal anti-inflammatory drugs for seven to 10

days before the biopsy to minimize the risk of bleeding.

2.1 Differential Diagnosis

1. Viral hepatitis (especially B and C)

2. Schistosomiasis 

3. Other infections (uncommon; e.g., congenital syphilis, brucellosis) 

4. Primary biliary cirrhosis  

5. Primary sclerosing cholangitis 

6. Secondary biliary cirrhosis (chronic extrahepatic obstruction) 

7. Autoimmune cholangiopathy 

23

8. Autoimmune chronic active hepatitis 

9. “Cryptogenic” cirrhosis 

10. Posthepatitic (non-B, non-C) 

11. Postnecrotic 

12. Chemical 

13. Toxins 

14. Alcohol:  Carbon tetrachloride  Dimethylnitrosamine      Vinyl chloride               

15. Drugs: Halothane         Isoniazid       Methotrexate         Methyldopa     

16. Congestive  Severe chronic right heart failure  Tricuspid insufficiency  Constrictive pericarditis  Cor pulmonale  Mitral stenosis Hepatic vein obstruction (Budd-Chiari syndrome)

17. Hereditary or familial disorders  Wilson's disease  Cystic fibrosis    

18. Alpha1-antitrypsin deficiency 

Hemochromatosis  Galactosemia  Glycogen storage diseases  Tyrosinosis  Hypervitaminosis A  Osler-Rendu-Weber syndrome  Abetalipoproteinemia

24

2.2 Treatment

Treatment of cirrhosis includes:

1) Preventing further damage to the liver

25

2) Treating the complications of cirrhosis

3) Preventing liver cancer or detecting it early

4) Liver transplantation.

Preventing further damage to the liver:

Consume a balanced diet and one multivitamin daily. Patients with PBC with impaired

absorption of fat soluble vitamins may need additional vitamins D and K.

Avoid drugs (including alcohol) that cause liver damage. All patients with cirrhosis

should avoid alcohol. Most patients with alcohol induced cirrhosis experience an

improvement in liver function with abstinence from alcohol. Even patients with chronic

hepatitis B and C can substantially reduce liver damage and slow the progression towards

cirrhosis with abstinence from alcohol.

Avoid nonsteroidal antiinflammatory drugs (NSAIDs, e.g., ibuprofen). Patients with

cirrhosis can experience worsening of liver and kidney function with NSAIDs.

Eradicate hepatitis B and hepatitis C virus by using anti-viral medications. Not all

patients with cirrhosis due to chronic viral hepatitis are candidates for drug treatment. Some

patients may experience serious deterioration in liver function and/or intolerable side

effects during treatment. Thus, decisions to treat viral hepatitis have to be individualized, after

consulting with doctors experienced in treating liver diseases (hepatologists).

Remove blood from patients with hemochromatosis to reduce the levels of iron and

prevent further damage to the liver. In Wilson's disease, medications can be used to increase

the excretion of copper in the urine to reduce the levels of copper in the body and prevent

further damage to the liver.

Suppress the immune system with drugs such as prednisone andazathioprine (Imuran)

to decrease inflammation of the liver in autoimmune hepatitis.

Treat patients with PBC with a bile acid preparation, ursodeoxycholic acid (UDCA),

also called ursodiol (Actigall). Results of an analysis that combined the results from several

clinical trials showed that UDCA increased survival among PBC patients during 4 years of

26

therapy. The development of portal hypertension also was reduced by the UDCA. It is

important to note that despite producing clear benefits, UDCA treatment primarily retards

progression and does not cure PBC. Other medications such

as colchicineand methotrexate also may have benefit in subsets of patients with PBC.

Immunize patients with cirrhosis against infection with hepatitis A and B to prevent a

serious deterioration in liver function. There are currently no vaccines available for

immunizing against hepatitis C.

Treating the complications of cirrhosis

Retention of salt and water can lead to swelling of the ankles and legs (edema) or

abdomen (ascites) in patients with cirrhosis. Doctors often advise patients with cirrhosis to

restrict dietary salt (sodium) and fluid to decrease edema and ascites. The amount of salt in the

diet usually is restricted to 2 grams per day and fluid to 1.2 liters per day. In most patients

with cirrhosis, however, salt and fluid restriction is not enough, and diuretics have to be

added.

Diuretics are medications that work in the kidneys to promote the elimination of salt

and water into the urine. A combination of the diuretics spironolactone (Aldactone)

and furosemide can reduce or eliminate the edema and ascites in most patients. During

treatment with diuretics, it is important to monitor the function of the kidneys by measuring

blood levels of blood urea nitrogen (BUN) and creatinine to determine if too much diuretic is

being used. Too much diuretic can lead to kidney dysfunction that is reflected in elevations of

the BUN and creatinine levels in the blood.

Sometimes, when the diuretics do not work (in which case the ascites is said to be

refractory), a long needle or catheter is used to draw out the ascitic fluid directly from the

abdomen, a procedure called abdominal paracentesis. It is common to withdraw large amounts

(liters) of fluid from the abdomen when the ascites is causing painful abdominal distension

and/or difficulty breathing because it limits the movements of the diaphragms.

Another treatment for refractory ascites is a procedure called transjugular intravenous

portosystemic shunting which is explained below.

27

Bleeding from varices. If large varices develop in the esophagus or upper stomach,

patients with cirrhosis are at risk for serious bleeding due to rupture of these varices. Once

varices have bled, they tend to rebleed and the probability that a patient will die from each

bleeding episode is high (30%-35%). Therefore, treatment is necessary to prevent the first

(initial) bleeding episode as well as rebleeding. Treatments include medications and

procedures to decrease the pressure in the portal vein and procedures to destroy the varices.

Propranolol (Inderal), a beta blocker, is effective in lowering pressure in the portal

vein and is used to prevent initial bleeding and rebleeding from varices in patients with

cirrhosis. Another class of oral medications that lowers portal pressure is the nitrates, for

example, isosorbide dinitrate (Isordil). Nitrates often are added to propranolol if propranolol

alone does not adequately lower portal pressure or prevent bleeding.

Octreotide (Sandostatin) also decreases portal vein pressure and has been used to treat

variceal bleeding.

During upper endoscopy (EGD), either sclerotherapy or band ligation can be

performed to obliterate varices and stop active bleeding and prevent rebleeding. Sclerotherapy

involves infusing small doses of sclerosing solutions into the varices. The sclerosing solutions

cause inflammation and then scarring of the varices, obliterating them in the process. Band

ligation involves applying rubber bands around the varices to obliterate them. (Band ligation

of the varices is analogous to rubber banding of hemorrhoids.) Complications of sclerotherapy

include esophageal ulcers, bleeding from the esophageal ulcers, esophageal perforation,

esophageal stricture (narrowing due to scarring that can cause dysphagia), mediastinitis

(inflammation in the chest that can causechest pain), pericarditis (inflammation around the

heart that can cause chest pain), and peritonitis (infection in the abdominal cavity). Studies

have shown that band ligation may be slightly more effective with fewer complications than

sclerotherapy.

Transjugular intrahepatic portosystemic shunt (TIPS) is a non-surgical procedure to

decrease the pressure in the portal vein. TIPS is performed by aradiologist who inserts a stent

(tube) through a neck vein, down the inferior vena cava and into the hepatic vein within the

liver. The stent then is placed so that one end is in the high pressure portal vein and the other

end is in the low pressure hepatic vein. This tube shunts blood around the liver and by so

28

doing lowers the pressure in the portal vein and varices and prevents bleeding from the

varices. TIPS is particularly useful in patients who fail to respond to beta blockers, variceal

sclerotherapy, or banding. (TIPS also is useful in treating patients with ascites that do not

respond to salt and fluid restriction and diuretics.) TIPS can be used in patients with cirrhosis

to prevent variceal bleeding while the patients are waiting for liver transplantation. The most

common side effect of TIPS is hepatic encephalopathy. Another major problem with TIPS is

the development of narrowing and occlusion of the stent, causing recurrence of portal

hypertension and variceal bleeding and ascites. The estimated frequency of stent occlusion

ranges from 30%-50% in 12 months. Fortunately, there are methods to open occluded stents.

Other complications of TIPS include bleeding due to inadvertent puncture of the liver capsule

or a bile duct, infection, heart failure, and liver failure.

A surgical operation to create a shunt (passage) from the high-pressure portal vein to

veins with lower pressure can lower blood flow and pressure in the portal vein and prevent

varices from bleeding. One such surgical procedure is called distal splenorenal shunt (DSRS).

It is appropriate to consider such a surgical shunt for patients with portal hypertension who

have early cirrhosis. (The risks of major shunt surgery in these patients is less than in patients

with advanced cirrhosis.) During DSRS, the surgeon detaches the splenic vein from the portal

vein, and attaches it to the renal vein. Blood then is shunted from the spleen around the liver,

lowering the pressure in the portal vein and varices and preventing bleeding from the varices.

Patients with an abnormal sleep cycle, impaired thinking, odd behavior, or other signs

of hepatic encephalopathy usually should be treated with a low protein diet and oral lactulose.

Dietary protein is restricted because it is a source of the toxic compounds that cause hepatic

encephalopathy. Lactulose, which is a liquid, traps the toxic compounds in the colon.

Consequently, they cannot be absorbed into the blood stream and cause encephalopathy. To be

sure that adequate lactulose is present in the colon at all times, the patient should adjust the

dose to produce 2-3 semiformed bowel movements a day. (Lactulose is a laxative, and the

adequacy of treatment can be judged by loosening or increasing frequency of stools.) If

symptoms of encephalopathy persist, oral antibiotics such as neomycin

or metronidazole (Flagyl), can be added to the treatment regimen. Antibiotics work by

blocking the production of the toxic compounds by the bacteria in the colon.

29

The filtration of blood by an enlarged spleen (Hypersplenism) usually results in only

mild reductions of red blood cells (anemia), white blood cells (leukopenia) and platelets

(thrombocytopenia) that do not require treatment. Severe anemia, however, may require blood

transfusions or treatment with erythropoietin or epoetin alfa (Epogen, Procrit), hormones that

stimulate the production of red blood cells. If the numbers of white blood cells are severely

reduced, another hormone called granulocyte-colony stimulating factor is available to increase

the numbers of white blood cells. An example of one such factor is filgrastim (Neupogen).

No approved medication is available yet to increase the number of platelets. As a

necessary precaution, patients with low platelets should not use aspirin or othernonsteroidal

antiinflammatory drugs (NSAIDS) since these drugs can hinder the function of platelets. If a

low number of platelets is associated with significant bleeding, transfusions of platelets

usually should be given. Surgical removal of the spleen (called splenectomy) should be

avoided, if possible, because of the risk of excessive bleeding during the operation and the risk

of anesthesia in advanced liver disease.

Patients suspected of having spontaneous bacterial peritonitis usually will undergo

paracentesis. Fluid that is removed is examined for white blood cells and cultured for bacteria.

Culturing involves inoculating a sample of the ascites into a bottle of nutrient-rich fluid that

encourages the growth of bacteria, thus facilitating the identification of even small numbers of

bacteria. Blood and urine samples often are obtained as well for culturing because many

patients with spontaneous bacterial peritonitis also will have infection in their blood and urine.

In fact, many doctors believe that infection may have begun in the blood and the urine

and spread to the ascitic fluid to cause spontaneous bacterial peritonitis. Most patients with

spontaneous bacterial peritonitis are hospitalized and treated with intravenous antibiotics such

asampicillin, gentamycin, and one of the newer generation cephalosporin. Patients usually

treated with antibiotics include:

Patients with blood, urine, and/or ascites fluid cultures that contain bacteria.

Patients without bacteria in their blood, urine, and ascitic fluid but who have elevated

numbers of white blood cells (neutrophils) in the asciticfluid(>250 neutrophils/cc).

30

Elevated neutrophil numbers in ascitic fluid often means that there is bacterial

infection. Doctors believe that the lack of bacteria with culturing in some patients with

increased neutrophils is due either to a very small number of bacteria or ineffective culturing

techniques.

Spontaneous bacterial peritonitis is a serious infection. It often occurs in patients with

advanced cirrhosis whose immune systems are weak, but with modern antibiotics and early

detection and treatment, the prognosis of recovering from an episode of spontaneous bacterial

peritonitis is good.

In some patients oral antibiotics (such as Cipro or Septra) can be prescribed to prevent

spontaneous bacterial peritonitis. Not all patients with cirrhosis and ascites should be treated

with antibiotics to prevent spontaneous bacterial peritonitis, but some patients are at high risk

for developing spontaneous bacterial peritonitis and warrant preventive treatment:

Patients with cirrhosis who are hospitalized for bleeding varices have a high risk of

developing spontaneous bacterial peritonitis and should be started on antibiotics early

during the hospitalization to prevent spontaneous bacterial peritonitis

Patients with recurring episodes of spontaneous bacterial peritonitis

Patients with low protein levels in the ascitic fluid (Ascitic fluid with low levels of

protein is more likely to become infected.)

Palliative care

If cirrhosis gets worse, one may want to think about palliative care. Palliative care is a

kind of care for people who have illnesses that do not go away and often get worse over time.

It is different than care to cure patients’ illness, called curative treatment. Palliative care

focuses on improving patient’s quality of life-not just in body, but also in mind and spirit.

Palliative care can be combined with curative care.

Palliative care may help the patient manage symptoms or side effects from treatment.

It could also help to cope with one’s feelings about living with a long-term illness, make

31

future plans concerning their medical care, or help their family better understand their illness

and how to support them.

If one has not already made decisions about the issues that may arise at the end of life,

consider doing so now. Many people find it helpful and comforting to state their health care

choices in writing (with an advance directive such as a living will) while they are still able to

make and communicate these decisions. Patient may also think about who they would choose

as their health care agent to make and carry out decisions about their care if they were unable

to speak for themselves.

A time may come when doctors goals change from treating or curing an illness to

maintaining comfort and dignity. Primary doctor will be able to address questions or concerns

about maintaining comfort when cure is no longer an option. Hospice care health

professionals can provide palliative care and comforting surroundings for someone who is

preparing to die.

Deterrence/Prevention

Eliminating alcohol abuse could prevent 75-80% of all cases of cirrhosis. Other

preventive measures include obtaining counseling or other treatment for alcoholism, taking

precautions (practicing safe sex, avoiding dirty needles) to prevent hepatitis, getting

immunizations against hepatitis if a person is in a high-risk group, receiving appropriate

medical treatment quickly when diagnosed with hepatitis B or hepatitis C, having blood drawn

at regular intervals to rid the body of excess iron from hemochromatosis, using medicines

(chelating agents) to rid the body of excess copper from Wilson's disease and wearing

protective clothing and following product directions when using toxic chemicals at work, at

home, or in the garden.

2.3 Prognosis

32

Cirrhosis-related liver damage cannot be reversed, but further damage can be

prevented by patients who eat properly, get enough rest, do not consume alcohol, and remain

free of infection.

If the underlying cause of cirrhosis cannot be corrected or removed, scarring will

continue. The liver will fail, and the patient will probably die within five years. Patients who

stop drinking after being diagnosed with cirrhosis can increase their likelihood of living more

than a few years from 40% to 60-70%.

Case

33

A 9 years old male was admitted on 25th Jan 2011 at 14.20 complaining of stomach

enlargement for the pass 7 days. Patients weight 24kg, height 127cm. patient also have history

of yellow eyes these 7days. Patient also been having fever from 10 days ago. We were told

that fever is high and comes and goes. No shivers, no seizures. For now patient is not having

fever. From the pass 6days patient’s genital part has enlarged. There is no history of genital

enlargement before this. Patient also has history of vomiting for 10days, 3times a day. We

have been clarified that patient vomits out only the food and drinks that he consumes. No

history of travelling to malaria endemic places. Patient has history of taking medication from

midwives but patient’s parents don’t know the content of the medication. History of

immunization is complete. There is history of tea coloured urine (dark brown) for 6 days. Now

urine is normal. Defecation is normal.

Patient have been sent for consultation from Rumah Sakit Sufina Azu with a diagnose of

hepatosplenomegaly and hydrocele.

Physical Examination:

Sensorium : Compos mentis, BW= 24 Kg, BL= 127 cm, BW/BL= %, Temp. = 37 0C

Anemic (-), edema (-), cyanosis (-), icteric (+), dyspnoe (-)

Head : Eye: Light reflexes (+/+), isochoric pupil, pale inferior conj. palpebra(-/-).

Sclera icteric (+/+). Ear/ Nose/ Mouth: within normal limit

Neck : Lymph node enlargement (-), neck stiffness (-)

Thorax : Symmetrical fusiform, no retraction,

HR= 96 bpm, regular, murmur (-),

RR= 24 rpm, regular, ronchi (-).

Abdominal : Distention (+), peristaltic (+) normal, shifting dullness (+). undulation (+)

Liver and spleen difficult to assess

Sitting abdomen circumference = 63 cm

Sleeping abdomen circumference = 67cm

Anogenital : Male, penis and testis swollen, translumination (+)

Extremities : Pulse = 96 tpm, regular, adequate pressure/volume, BP=110/75 mmHg.

Acral warm.

34

Working Diagnose: hepatic cirrhosis, hepatitis, ascites, hydrocele.

Differential Diagnose: hepatic cirrhosis, hepatitis, ascites, hydrocele.

Management:

IVFD D 5% NaCl 0.45% 40 gtt/min (micro)

Investigation Planning:

Routine blood, electrolytes, blood glucose, albumin.

CT scan abdomen

Dl

Liver Function Test

Renal Function Test

Chest X-ray

USG Liver

Consult

Results of the test:

Lab: Hb/Ht/L/T:- 9.4/ 28.2%/ 6400/ 181000

Bil total/direct/ALP/ SGOT/ SGPT:- 3.2/ 3/ 785/ 321/

Albumin:- 2,5

Blood glucose:- 88,9

Ur/ Cr:- 14,70/ 0,34

Na/ K/ Cl:- 132/ 3.4/ 106

USG Report:- Liver parenchym rough

Kidney within normal limit

Urinary vesicle within normal limit

Scrotum fills with fluid

35

Discussion

Ascites (fluid retention in the abdominal cavity) is the most common complication of

cirrhosis and causes a physical appearance of stomach distention. In this patient, from physical

examination, we can find abdominal distension. Ascites is being confirmed by shifting

dullness and undulation positive.

Jaundice occurs when the diseased liver does not remove enough bilirubin from the

blood, causing yellowing of the skin and whites of the eyes and darkening of the urine.

Bilirubin is the pigment that gives bile its reddish-yellow colour. In this case, the patient has

icteric sclera, which is jaundice.

Hepatitis B causes liver inflammation and injury that can lead to cirrhosis as it is one

of the etiology of cirrhosis. Based on imunoserology test which was done on 27 of January

2011, the patients report shows anti HBs positive. This proves he is a hepatitis B positive

patient.

Advanced cirrhosis leads to a reduced level of albumin in the blood and reduced blood

clotting factors due to the loss of the liver's ability to produce these proteins. Thus, reduced

levels of albumin in the blood or abnormal bleeding suggest cirrhosis. In this case, on the 25th

of January 2011 until 28th of January 2011, liver function test shows decrease in albumin level.

And from 25th until 28th of January 2011, based on haematology test, he thrombocytes count is

less (thrombocytopenia).

Abnormal elevation of liver enzymes in the blood (such as ALT and AST) that are

obtained routinely as part of yearly health examinations suggests inflammation or injury to the

liver from many causes as well as cirrhosis. In this case, based on liver function report, AST,

ALT and bilirubin level was high from 25th of January until 9th of February 2011, but was

decreasing due to medication.

36

In this case report follow up, the diagnosis of this case was changed from hepatic

cirrhosis to hepatitis viral from 6th of February 2011 onwards because all the complication of

hepatic cirrhosis was cured and liver USG shows a normal liver appearance.

In theory, one of the classification of hepatic cirrhosis is incomplete Septal Cirrhosis

(liver is enlarged but no nodules yet). In this case, based on physical examination (palpation),

liver has enlarged with smooth surface.

One of the medication for hepatic cirrhosis is bile acid preparation, named

ursodeoxycholic acid (UDCA), also called ursodiol. It is used to suppress abnormal elevated

liver function to normal level. In this case, urdafalk( international name ursodiol) is used as

treatment of hepatic cirrhosis.

37

Summary

It has been reported that a 9 year old boy with his chief complaint of abdomen

distention. He has been diagnosed with hepatic cirrhosis based on the history taking, physical

examinations and laboratory results.

38

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