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1
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
2
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
3
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
4
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.
5
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
6
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,
7
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:
8
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.
9
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
10
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
11
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.
12
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
13
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,
14
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.
15
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,
16
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
17
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
18
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.
19
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.
20
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
21
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
22
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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