STRUCTURE OF THE LIVER AND BILIARY SYSTEM

Ê


The liver is the largest internal organ in the body (1.2-1.5 kg) and is situated in the right
hypochondrium. Functionally, it is divided into right and left lobes by the middle hepatic vein.
The right lobe is larger and contains the caudate and quadrate lobes. The liver is further
subdivided into a total of eight segments by divisions of the right, middle and left hepatic
veins. Each segment receives its own portal pedicle, permitting individual segment resection
at surgery.

The blood supply to the liver constitutes 25% of the resting cardiac output and is via two
main vessels:

3 Ê

 

^ which is a branch of the coeliac axis, supplies 25% of the total
blood flow. Autoregulation ensures a constant total liver blood flow.
3 Ê
 
 drains most of the GIT and the spleen. It supplies -5% of the blood
flow. The normal portal pressure is 5-8 mmHg; flow increases after meals.

Both vessels enter the liver via the hilum (porta hepatis). The blood from these vessels is
distributed to the segments and passes into the sinusoids via the portal tracts.

Blood leaves the sinusoids, entering branches of the hepatic vein which join into three main
branches before entering the inferior vena cava.

The


is an autonomous segment as it receives an independent blood supply
from the portal vein and hepatic artery, and its hepatic vein drains directly into the inferior
vena cava.

„
^ formed mainly in the perisinusoidal space, is collected in lymphatics which are
present in the portal tracts. Eventually drain into the hepatic ducts.

Ê

  is the functional unit of the liver. This consists of parenchyma supplied by the
smallest portal tracts containing
3 Portal vein radicles.
3 Hepatic arterioles.
3 Bile ductules. The hepatocytes near this triad (zone 1) are well supplied with
oxygenated blood and are more resistant to damage than the cells nearer the
terminal hepatic (central) veins (zone 3).

The d
d d lack a basement membrane and are loosely surrounded by specialist
fenestrated endothelial cells and Kupffer cells (phagocytic cells). Sinusoids are
separated by plates of liver cells (hepatocytes). The subendothelial space that lies between
the sinusoids and hepatocytes is the space of Disse^ which contains a matrix of basement
membrane constituents and stellate cells.





 store retinoids in their resting state and contain the intermediate filament,
desmin. When activated (to myofibroblasts) produce extracellular matrix components,
including collagen and they are contractile and probably regulate sinusoidal blood flow.
Endothelin and nitric oxide play a major role in modulating stellate cell contractility.

Ê


Ôile canaliculi form a network between the hepatocytes. These join to form thin bile
ductules near the portal tract, which in turn enter the bile ducts in the portal tracts. These
then combine to form the right and left hepatic ducts that leave each liver lobe. The hepatic
ducts join at the porta hepatis to form the common hepatic duct. The cystic duct connects
the gall bladder to the lower end of the common hepatic duct. The gall bladder lies under the
right lobe of the liver and stores and concentrates hepatic bile; it has a capacity of
approximately 50 mL. The common bile duct is formed by the combination of the cystic and
hepatic ducts and is approximately 8 mm in diameter, narrowing at its distal end to pass
into the duodenum. The common bile duct and pancreatic duct open into the second
part of the duodenum through a common channel at the ampulla of Vater . The lower
end of the common bile duct contains the muscular sphincter of Oddi , which contracts
rhythmically and prevents bile from entering the duodenum in the fast ing state.

·
 


The liver is the principal site of synthesis of all circulating proteins apart from X-globulins,
which are produced in the reticuloendothelial system. The liver receives amino acids from
the intestine and muscles and, by controlling the rate of gluconeogenesis and transamination,
regulates levels in the plasma. Plasma contains 60-80 g/L of protein, mainly in the form of
albumin, globulin and fibrinogen.

÷
 has a half-life of 16-24 days, and 10-12 g are synthesized daily. Its main
functions are
1. to maintain the intravascular oncotic (colloid osmotic) pressure.
2. to transport water-insoluble substances. Reduced synthesis over prolonged periods
produces hypoalbuminaemia and is seen in CLD and malnutrition, hyper catabolic
states (e.g. trauma with sepsis) and in diseases where there is an excessive loss
(e.g. nephrotic syndrome, protein-losing enteropathy).

Transport or carrier proteins such as transferrin and caeruloplasmin, acute-phase and other
proteins (e.g. Į1-antitrypsin and Į-fetoprotein) are also produced in the liver.

The liver also synthesizes all factors involved in coagulation (apart from one-third of factor
VIII) and the complement system. The liver stores large amounts of vitamins, particularly A,
D and B12, and lesser amounts of others (vitamin K and folate), and also minerals - iron in
ferritin and haemosiderin and copper.

Degradation (nitrogen excretion)

Amino acids are degraded by transamination and oxidative deamination to produce ammonia
ĺ urea and excreted by the kidneys. This is a major pathway for the elimination of
nitrogenous waste. Failure of this process occurs in severe liver disease.

Y 



Ê

 stores approximately 80 g of glycogen^
 

3 Glucose homeostasis
3 The maintenance of the blood sugar.
›n the immediate fasting state^ blood glucose is maintained either by :
3 Glycogenolysis (glucose released from the breakdown of glycogen)
3 or by gluconeogenesis (newly synthesized glucose). ources for gluconeogenesis
are lactate, pyruvate, amino acids from muscles (mainly alanine and glutamine) and
glycerol from lipolysis of fat stores. ›n prolonged starvation, ketone bodies and fatty
acids are used as alternative sources of fuel as the body tissues adapt to a lower
glucose requirement.

„

Are transported in the plasma as lipoproteins. The liver synthesizes VLDLs and HDLs.
HDLs are the substrate for lecithin-cholesterol acyltransferase (LCAT), which catalyses the
conversion of free cholesterol to cholesterol ester (see below). Hepatic lipase removes
triglyceride from IDLs to produce ILDLs) which are degraded by the liver.

TGs are mainly of dietary origin but are also formed in the liver from circulating (FFAs) and
glycerol and incorporated into VLDLs. Oxidation or de novo synthesis of FFA occurs in the
liver, depending on the availability of dietary fat.

Cholesterol may be of dietary origin but most is synthesized from acetyl-CoA mainly in the
liver, intestine, adrenal cortex and skin. It occurs either as free cholesterol or is esterified with
fatty acids; this reaction is catalysed by LCAT which reduced in severe liver disease,
increasing the ratio of free cholesterol to ester, which alters membrane structures. One result
of this is the red cell abnormalities (e.g. target cells) seen in chronic liver disease.
Phospholipids (e.g. lecithin) are synthesized in the liver.

V  

Bile secretion and bile acid metabolism
Ôile consists of water, electrolytes, bile acids, cholesterol, phospholipids and conjugated
bilirubin. Two processes are involved in bile secretion - a 
 


and a 

  


process - each contributing about 230 mL/ day. The remainder of the bile
(about 150 mL daily) is produced by the epithelial cells of the bile ductules.

Bile formation requires firstly the uptake of bile acids and other organic and inorganic ions
+ +
across the basolateral (sinusoidal) membranes. This process is driven by Na /K -ATPase in
the basolateral membrane. .

Bile acids are also synthesized in hepatocytes from cholesterol. The rate-limiting step in
their production is that catalysed mainly by cholesterol-7Į-hydroxylase and the P450
enzymes (CYP7A1 and CYP8B1).

3 Secretion of a bicarbonate-rich solution is stimulated mainly by secretin and is

inhibited by somatostatin.

The bile acids are excreted into the bile and then pass via the common bile duct into the
duodenum. The two primary bile acids - cholic acid and chenodeoxycholic acid are
conjugated with glycine or taurine (in a ratio of 3: 1 in humans) and this process increases
their solubility. Intestinal bacteria convert these acids into secondary bile acids, deoxycholic
and lithocholic acid.

The average total bile flow is approximately 600 mL per day. ›n the fasted state half of
the bile flows directly into the duodenum and half is diverted into the gall bladder. The
mucosa of the gall bladder absorbs 80-90% of the water and electrolytes, but is impermeable
to bile acids and cholesterol. Following a meal^ cholecystokinin is secreted by the I cells of
the duodenal mucosa and stimulates contraction of the gall bladder and relaxation of the
sphincter of Oddi, so that bile enters the duodenum. An adequate bile flow is dependent on
bile salts being returned to the liver by the enterohepatic circulation.

Ôile acids act as detergents; their main function is lipid solubilization. Bile acid molecules
have both a hydrophilic and a hydrophobic end . In aqueous solutions they aggregate to
form micelles, with their hydrophobic (lipid-soluble) ends in the centre. Micelles are expanded
by cholesterol and phospholipids (mainly lecithin), forming mixed micelles.

Bilirubin metabolism
Bilirubin is produced mainly from the breakdown of mature red cells in the Kupffer cells and
in the reticuloendothelial system; 15% of bilirubin comes from the catabolism of other
haem-containing proteins^ such as myoglobin, cytochromes and catalases.

Normally^ 250-300 mg (425-510 mmol) of bilirubin is produced daily. The iron and globin are
removed from the haem and are reused. Ôiliverdin is formed from the haem and this is
reduced to form bilirubin. The bilirubin produced is unconjugated and water-insoluble, due
to internal hydrogen bonding, and is transported to the liver attached to albumin. Bilirubin
dissociates from albumin and is taken up by the hepatic cell membrane and transported to the
endoplasmic reticulum by cytoplasmic proteins, where it is conjugated with glucuronic acid
and excreted into bile. The microsomal enzyme, 
  
  ·

 

^ catalyses the formation of bilirubin monoglucuronide and then diglucuronide.
This conjugated bilirubin is water -soluble and is actively secreted into the bile canaliculi
and excreted into the intestine within the bile. It is not absorbed from the small intestine
because of its large molecular size. ›n the terminal ileum, bacterial enzymes hydrolyse the
molecule, releasing free bilirubin which is then reduced to urobilinogen. Some of this is
excreted in the stools as stercobilinogen. The remainder is absorbed by the terminal
 ileum, passes to the liver via the enterohepatic circulation, and is re-excreted into the bile.
Urobilinogen bound to albumin enters the circulation and is excreted in the urine via the
kidneys. When hepatic excretion of conjugated bilirubin is impaired, a small amount of
conjugated bilirubin is found strongly bound to albumin. It is not excreted by the kidneys and
accounts for the continuing hyperbilirubinaemia for a short time after cholestasis has
resolved.

m
  
  
The liver catabolizes hormones such as insulin, glucagon, oestrogens, growth hormone,
glucocorticoids and parathyroid hormone. It is also the prime target organ for many hormones
(e.g. insulin). Fat-soluble drugs are converted to water-soluble substances that facilitate their
excretion in the bile or urine. Cholecalciferol is converted to 25-hydroxycholecalciferol.

› 

 
The reticuloendothelial system (RES) of the liver contains many immunologically active cells.
The liver acts as a 'sieve' for the bacterial and other antigens carried to it via the portal tract
from the GIT. These antigens are phagocytosed and degraded by Kupffer cells^ which are
macrophages attached to the endothelium. Kupffer cells have specific membrane receptors
for ligands and are activated by several factors, such as infection. They secrete interleukins,
TNF, collagenase and lysosomal hydrolases. Antigens are degraded without the production of
antibody, as there is very little lymphoid tissue. They are thus prevented from reaching other
antibody- producing sites in the body and thereby prevent generalized adverse immunological
reactions. The RES plays a role in tissue repair, T and B lymphocyte interaction, and cytotoxic
activity in disease processes. Following stimulation by, for example, endotoxin, the Kupffer
cells release IL-6, IL-8 and TNF-Į. These cytokines stimulate the sinusoidal cells, stellate
cells and natural killer cells to release proinflammatory cytokines. The stimulated hepatocytes
themselves express adhesion molecules and release IL-8, which is a potent neutrophil
chemoattractant. Homing of mucosal lymphocytes (enterohepatic circulation) has been
proposed. These exogenous leucocytes again release more cytokines- all damaging the
function of the hepatocyte, including hepatocellular bile formation which leads to cholestasis.
Cytokines also stimulate hepatic apoptosis.

INVESTIGATIONS
Investigative tests can be divided into:

3 Ôlood tests
î (a) Liver 'function' tests: ALB, PT and bilirubin.
î (b) Liver biochemistry: ALT, AST, ALP, GGT, total protein.
î (c) Viral markers
î (d) Additional blood investigations.
3 |rine tests - for bilirubin and urobilinogen.

Ô
 

Serum albumin
3 A marker of synthetic function.
3 A guide to the severity of CLD. Low serum albumin in CLD is a bad prognostic sign.
In acute liver disease initial albumin levels may be normal.
·rothrombin time (·

A marker of synthetic function. Because of its short half-life, it is a sensitive indicator of both
acute and CLD. Vitamin K deficiency should be excluded (give an IV bolus (10 mg)).
Vitamin K deficiency commonly occurs in biliary obstruction, as the low intestinal
concentration of bile salts results in poor absorption of vitamin K.


Ôilirubin (Normally, serum bilirubin is almost all unconjugated). Determination of whether the
bilirubin is conjugated or unconjugated is only necessary in:
3 Congenital disorders of bilirubin metabolism.
3 To exclude haemolysis.
÷minotransferases(often referred to as transaminases

These enzymes are present in hepatocytes and leak into the blood with liver cell damage.
Two enzymes are measured:

3 ÷S is primarily a mitochondrial enzyme (80%; 20% in cytoplasm) and is also

present in heart, muscle, kidney and brain. High levels are seen in hepatic necrosis,
muscle injury, MI and CHF.
3 ÷ is a cytosol enzyme^ rise (specific to) only with liver disease.

÷lkaline phosphatase (÷ ·

This is present in the canalicular and sinusoidal membranes of the liver, but is also
present in many other tissues, such as bone^ intestine and placenta. If there is also an
abnormality of the Ȗ-GT, the ALP can be presumed to come from the liver.

Serum ALP is raised.

3 In Cholestasis from any cause (cholestatic jaundice), levels may be 4-6 times the
normal limit.
3 May occur with infiltration of the liver (e.g. metastases) and in cirrhosis, frequently
in the absence of jaundice.
3 The highest serum levels due to liver disease (>1000 ›|/L) are seen with hepatic
metastases and primary biliary cirrhosis.
X¦ lutamyl transpeptidase and 5¦nucleotidase
These are microsomal enzymes. X-GT is present in many tissues as well as the liver. Its
activity can be induced by such drugs as phenytoin and by alcohol. ›f the ALP is normal, a
raised serum Ȗ-GT is a good guide to alcohol intake and can be used as a screening test.
Mild elevation of the Ȗ-GT is common even with a small alcohol consumption and does not
necessarily indicate liver disease if the other liver biochemical tests are normal. In cholestasis
the Ȗ-GT rises in parallel with the ALP as it has a similar pathway of excretion.
otal proteins
A raised globulin fraction, seen in liver disease, is usually due to increased circulating
immunoglobulins and is polyclonal.

÷   
    

Haematological
A CBC is always performed.
3 Anaemia may be present. RBCs are often macrocytic and can have abnormal
shapes - target cells and spur cells - owing to membrane abnormalities.
3 Vitamin Ô12 levels are normal or high.
3 Folate levels are often low owing to poor dietary intake.

3 Ôleeding produces a hypochromic, microcytic picture.

3 Alcohol causes macrocytosis, sometimes with leucopenia and thrombocytopenia.
3 Hypersplenism results in pancytopenia.
3 Cholestasis often produces abnormal-shaped cells & also deficiency of vitamin K.
3 Haemolysis accompanies acute liver failure and jaundice.
3 Aplastic anaemia is present in up to 2% of patients with acute viral hepatitis.
3 A raised serum ferritin with transferrin saturation (>60%) is seen in hereditary
haemochromatosis.
Biochemical
3 ÷ ÷   . Deficiencies produce cirrhosis.
3 ´V

 . This is normally produced by the fetal liver. Its reappearance in
increasing and high concentrations in the adult indicates hepatocellular carcinoma.
Increased concentrations in pregnancy in the blood and amniotic fluid suggest neural
tube defects of the fetus. Blood levels are also slightly raised with regenerative liver
tissue in hepatitis, CLDs and also in teratomas.

Immunological tests
Serum immunoglobulins
Increased Ȗ-globulins are due to reduced phagocytosis by sinusoidal and Kupffer cells of the
antigens absorbed from the gut. These antigens stimulate antibody production in the spleen,
lymph nodes and lymphoid and plasma cell infiltrate in the portal tracts. ›n PÔC^ the
predominant serum immunoglobulin is IgM, while in autoimmune hepatitis it is IgG.
Serum autoantibodies
3 AMA is found in the serum in over 95% of patients with PBC.
3 ÷÷c

^c


 
 „
in high titre in
autoimmune hepatitis. Also in other autoimmune conditions and other liver diseases.
3 ANCA in PC.

uarkers of liver fibrosis

3 Fibrotest/fibrosure tests measure Į2-macroglobulin, Į2-haptoglobulin, Ȗ-globulin,

apoprotein A1, Ȗ-GT and total bilirubin. These results are formulated to determine a
fibrosis index. The index is sensitive and specific (>90%) for the absence of fibrosis,
and has 80% sensitivity and specificity for severe fibrosis.

3 Markers of matrix deposition include procollagen I and III peptide and Type IV
collagen. 
 
  ^ e.g. matrix metalloproteinase (MMP) 2, 3,
9, and tissue inhibitors of metalloproteinases (TIMPS), e.g. TIMP1 and 2 all are being
used as markers of fibrosis.

3 Genetic analysis is performed routinely for haemochromatosis (m
gene), Į1-

antitrypsin deficiency and Wilson¶s disease.

|rine tests
Bilirubinuria is due to the presence of conjugated (soluble) bilirubin. It is found in the
jaundiced patient with hepatobiliary disease; its absence implies that the jaundice is due to
increased unconjugated bilirubin. |robilinogen in the urine is^ in pra ctice^ of little value
but suggests haemolysis or hepatic dysfunction of any cause.

›maging techniques
1. |ltrasound examination
The normal liver appears as a homogeneous structure. The gall bladder, CBD, pancreas,
portal vein and other structures in the abdomen can be visualized. Abdominal ultrasound is
useful in:

3 A jaundiced patient.
3 Hepatomegaly/splenomegaly^ Masses^ lymph node enlargement^ focal liver
disease - lesions >1 cm, general parenchymal liver disease^ the detection of
gallstones. Assessing portal and hepatic vein patency. Biopsies obtained under
 guidance.

Colour Doppler ultrasound will demonstrate the vascularity of a lesion and the direction of
blood flow in the portal and hepatic veins. Ultrasound contrast agents enhance the vascularity
within a lesion.

m
 
 
 (elastography). Stiffness (measured in kPa) increases with increasing
liver fibrosis (sensitivity and specificity 80-95% compared to liver biopsy). It cannot be used in
the presence of ascites and morbid obesity.
. pndoscopic ultrasound (p|S
(ultrasound probe in the duodenum)
ë Accurate staging of small pancreatic tumours (small neuroendocrine tumours).
ë Offers a less invasive method for bile duct imaging.
ë EUS-guided fine-needle aspiration provides cytological/histological tissue.
ë To drain pancreatic and peripancreatic fluid collections.

å. Yomputed tomography (Y
examination

This technique is complementary to ultrasound, which is usually performed first (Ultrasound is
usually more valuable for lesions in the bile duct and gall bladder. CT has advantages in
obese subjects).
Excellent visualization of the internal organs but involves a high radiation dose.
More sensitive in detecting calcification than plain X-rays.

piral CT enables rapid, more precise characterization of a lesion and its vascular supply
with no increase in the radiation dose. Multi-planar and three-dimensional reconstruction in
the arterial phase can create a CT angiogram, often making formal invasive angiography
unnecessary. CT also provides guidance for biopsy. ›n general^ lesions over 2 cm can
usually be biopsied under ultrasound guidance^ which is quicker and more cost -
effective.

. uagnetic resonance imaging (u ›

MRI produces cross-sectional images in any plane within the body and does not involve
radiation. Diffuse liver disease alters the T1 and T2 characteristics, and MRI is probably the
most sensitive investigation of focal liver disease. Other fat-suppression modes such as
STIR allow good differentiation between haemangiomas and other lesions. Contrast agents
such as intravenous gadolinium allow further characterization of lesions, are suitable for those
with iodine allergy, and provide angiography and venography of the splanchnic circulation.
This has superseded direct arteriography.

5. uagnetic resonance cholangiopancreatography (u Y·

Enhances visualization of the 'water-filled' bile ducts and pancreatic ducts to produce high-
quality images of ductal anatomy. This non-invasive technique is replacing diagnostic (but not
therapeutic) ERCP.

6. ·lain X¦rays of the abdomen are rarely requested but may show:
3 gallstones - 10% contain enough calcium to be seen
3 air in the biliary tree owing to its recent instrumentation, surgery or to a fistula
between the intestine and the gall bladder
3 Pancreatic and rarely gall bladder (porcelain gall bladder) calcification.

-. adionuclide imaging ¦ scintiscanning

99m
In a technetium-99m ( Tc) colloid scan, the colloid is injected IV to be taken up by the
reticuloendothelial cells of the liver and spleen. In CLD there is poor uptake in the liver and
most of the colloid is taken up in the spleen and bone marrow. Ultrasound has largely
replaced this technique.
 99m
In a Tc-IODIDA scan, technetium-labelled iododiethyl IDA is taken up by the hepatocytes
and excreted rapidly into the biliary system. Its main uses are in the diagnosis of:

3 Acute cholecystitis.
3 Jaundice due to either biliary atresia or hepatitis in the neonatal period .

D. pndoscopy

ù. pndoscopic retrograde cholangiopancreatography (p Y·

Contrast medium with a low iodine content of 1.5 mg/mL is used for the CBD so that
gallstones are not obscured; a higher iodine content of 2.8 mg/mL is used for the pancreatic
duct.

3 CBD stones can be removed after sphincterotomy which has a serious morbidity
rate of 3-5%: acute pancreatitis is the commonest, severe haemorrhage is rare.
Overall mortality is 0.4%.
3 The biliary system can be stented through an obstruction, or placement of a
nasobiliary drain.
3 Brachytherapy can be administered after placement at ERCP for therapy of
cholangiocarcinoma.

The complication rate in diagnostic ERCP is 2-3%.

A raised serum amylase is often seen. Cholangitis with or without septicaemia is also seen,
and broad-spectrum antibiotics (e.g. 500 mg ciprofloxacin ×2) should be given
prophylactically to all patients with suspected biliary obstruction, or a history of cholangitis.

10. ·ercutaneous transhepatic cholangiography (· Y

To outline the biliary tree. ›n patients with dilated ducts , the success rate is near 100%.
ERCP is the preferred first investigation because therapy can be undertaken at the same
time. In difficult cases the two techniques are sometimes combined.

Contraindications are as for liver biopsy. The main complications are:

Ôleeding and Cholangitis with septicaemia.
Prophylactic antibiotics should be given as for ERCP.

11. ÷ngiography
This is performed by selective catheterization of the coeliac axis and hepatic artery. It detects
the abnormal vasculature of hepatic tumours, but spiral CT and MRA have replaced this in
many cases. Hepatic venous cannulation allows abnormal hepatic veins to be diagnosed in
patients with Budd-Chiari syndrome and also serves as an indirect measurement of portal
pressure. The height of portal pressure has prognostic value for survival and a reduced portal
pressure 20% from baseline values has been associated with protection from rebleeding.
Retrograde CO2portography is used when there is doubt about portal vein patency and can
be combined with transjugular biopsy and hepatic venous pressure measurement.

1. iver biopsy

The mortality rate is less than 0.02% when performed by experienced operators. Do:

3 The coagulation (prothrombin time, platelets).

3 The blood group and serum for crossmatching.
3 After the procedure the patient should be observed, with pulse and blood pressure
measurements taken regularly for at least 6 h.
 3 The liver margins are delineated using percussion. Alternatively
ultrasound examination can be used to confirm liver margins and
position of the gall bladder.
3 Local anaesthetic is injected at the point of maximum dullness in
the mid-axillary line through the intercostal space during
expiration. Anaesthetic (1% lidocaine, approximately 5 mL) should
be injected down to the liver capsule.
3 A tiny cut is made in the skin with a scalpel blade.
3 A special needle (Menghini, Trucut or Surecut) is used to obtain
the liver biopsy whilst the patient holds his breath in expiration.
3 The biopsy is laid on filter paper and placed in 10% formalin. If a
culture of the biopsy is required it should be placed in a sterile pot.

›ndications for liver biopsy

1. Liver disease
2. |nexplained hepatomegaly
3. ome cases of jaundice
4. Persistently abnormal liver biochemistry
5. Occasionally in acute hepatitis
6. Chronic hepatitis^ Cirrhosis
-. ›nfiltrations
8. Tumours: primary or secondary
9. ›nfections (e.g. tuberculosis)
10. torage disease (e.g. glycogen storage)
11. Pyrexia of unknown origin .
|sual contraindications to percutaneous needle biopsy
Ú |ncooperative patient
Ú Prolonged prothrombin time (by more than 3 s)
Ú Platelets < 80 × 109/L
Ú Ascites
Ú Extrahepatic cholestasis
Yomplications of liver biopsy Most occur within 24 hours (usually in the first 2 hours). They
are often minor and include
Ú Abdominal or shoulder pain which settles with analgesics.
Ú Minor intraperitoneal bleeding can occur, but this settles spontaneously.
Rare complications include
Ú Major intraperitoneal bleeding.
Ú Haemothorax and pleurisy.
Ú Biliary peritonitis.
Ú Haemobilia: produces biliary colic, jaundice and melaena within 3 days of the biopsy.
Ú Transient septicaemia.

SYMPTOMS OF LIVER DISEASE

a ÷
 

 
This may be asymptomatic and anicteric. Symptomatic disease, which is often viral, produces
generalized symptoms of malaise, anorexia and fever. Jaundice may appear as the illness
progresses.



  

 
Patients may be asymptomatic or complain of non-specific symptoms, particularly fatigue.
Specific symptoms include:
symptom
1. Right hypochondrial pain.
2. Abdominal distension^ ankle
swelling.
3. Haematemesis and melaena.
4. Pruritus.
5. Gynaecomastia^ loss of libido
and amenorrhea.
6. Confusion and drowsiness.
cause
Liver distension.
Ascites, fluid retention
Gastrointestinal haemorrhage.
Cholestasis - this is often an early symptom
of PBC.
Endocrine dysfunction.
Neuropsychiatric complications
(portosystemic encephalopathy).

SIGNS OF LIVER DISEASE

Acute liver disease
There may be few signs apart from jaundice and an enlarged liver. Jaundice is best seen in
the conjunctivae and sclerae. In the cholestatic phase of the illness, pale stools and dark
urine are present. Spider naevi and liver palms usually indicate CLD but they can occur in
severe acute disease.

Chronic liver disease

It is possible for the physical examination to be normal in patients with advanced chronic liver
disease.

Ú 
r na
. These are telangiectases that consist of a central arteriole with
radiating small vessels. They are found in the distribution of the superior vena cava
(i.e. above the nipple line) in the chest and upper body. They are also found in
pregnancy.
Ú Slate¦grey appearance in haemochromatosis.
Ú ·almar rythma which is a non-specific change in the hands indicative of a
hyperdynamic circulation; it is also seen in pregnancy^ thyrotoxicosis or R.A.
Ú Ylubbing occasionally occurs.
Ú upuytren's contracture is often seen in alcoholic cirrhosis.
Ú wanthomas (cholesterol deposits
are seen in the palmar creases or above the
eyes in PBC.
Ú Initial hepatomegaly will be followed by a small liver in well -established cirrhosis.
Ú Splenomegaly is seen with portal hypertension.
Ú
acomast
a (occasionally unilateral) and tst
cular atroph
may be found in
males. The cause of gynaecomastia is complex, but it is probably related to altered
oestrogen metabolism or to treatment with spironolactone.
Ú In decompensated cirrhosis, additional signs that can be seen: