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CONTINUING PROFESSIONAL DEVELOPMENT
Page 58
Hepatology multiple
choice questionnaire

Page 59
Read Nicola Davies practice
profile on the ageing process

Page 60
Guidelines on how to
write a practice profile

Management of patients with

advanced liver cirrhosis
NS369 Sargent S (2006) Management of patients with advanced liver cirrhosis. Nursing Standard.
21, 11, 48-56. Date of acceptance: September 27 2006.

Summary
This article provides an overview of liver cirrhosis. The
pathophysiology, common investigations and the nursing management
of patients with advanced liver cirrhosis are examined.

Be familiar with the clinical features, common

complications of liver cirrhosis and portal
hypertension.

Explain the medical and nursing management
of these conditions.

Author
Suzanne Sargent is lecturer practitioner hepatology, Kings College
Hospital, London. Email: suzanne.sargent@kingsch.nhs.uk

Keywords
Alcohol and Alcoholism; Ascites; Cirrhosis; Liver disorders
These keywords are based on the subject headings from the British
Nursing Index. This article has been subject to double-blind review.
For author and research article guidelines visit the Nursing Standard
home page at www.nursing-standard.co.uk. For related articles
visit our online archive and search using the keywords.

Aims and intended learning outcomes

The aim of this article is to update nurses and
provide an overview on managing patients with
chronic liver disease and cirrhosis, which is an
emergent health problem in the UK. Liver
cirrhosis can be caused by excessive alcohol
consumption, obesity, viral hepatitis, or genetic,
autoimmune, metabolic and idiopathic factors.
After reading this article you should be able to:

Outline the common causes of chronic liver
disease and current incidence in the UK.

List the functions of the liver and the impact
that impaired function can have on patients
with liver cirrhosis.

Describe the common investigations and
biochemical, haematological and virological
tests for patients with chronic liver disease and
the significance of any abnormalities.
48 november 22 :: vol 21 no 11 :: 2006

Background
Liver fibrosis and its end stage, cirrhosis, is an
enormous worldwide healthcare problem.
According to the Office for National Statistics
(ONS), in the past 20 years deaths linked to
cirrhosis and liver-related disease have risen by
121 per cent for women and 68 per cent for men
in England and Wales (ONS 2003). The average
mortality among patients admitted with liver
disease is 18.2 per cent (Williams 2005).
Liver disease has many causes (Box 1), which
are increasing in prevalence (Williams 2005).
Alcohol consumption has doubled in the past 40
years. It is a major healthcare problem causing
about 4 per cent of the global burden of disease
(Leon and McCambridge 2006).The British Liver
Trust (BLT) acknowledges that, despite alcoholic
liver disease taking 10-15 years to develop, patients
are now presenting earlier for transplantation (BLT
2005). However, only 25 per cent of liver disease is
alcohol-related (Moore et al 2004).
It has been estimated that about 200,000500,000 people are infected with the hepatitis C
virus (HCV) in England and Wales. However, it is
also estimated that only 47,000 people with HCV
infection have been diagnosed and just 7,000
patients have been treated (National Institute for
Health and Clinical Excellence (NICE) 2006).
Consequently, the future burden of HCV health
care related to new incidence of cirrhosis will
increase by 60 per cent by 2008, and in the next
six to ten years there will be a 500 per cent
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BOX 1
Causes of chronic liver disease

Chronic viral hepatitis B, C

Autoimmune hepatitis

Alcohol

Haemochromatosis genetic condition of iron
overload

Wilsons disease genetic condition of copper
overload

Alpha1-antitrypsin deficiency genetic deficiency
of alpha1-antitrypsin

Primary biliary cirrhosis

Primary sclerosing cholangitis type of hepatic
autoimmune disease

Prolonged cholestasis

Toxins/drugs

Storage diseases

Hepatic venous outflow obstruction

Cryptogenic (idiopathic)

Non-alcoholic steatohepatitis (NASH)
(Adapted from Bacon et al 2006)

encephalopathy and ascites (Box 3). Patients also

experience decreased life expectancy and quality of
life, as well as fatigue, jaundice, pruritus, anorexia,
malnutrition and the development of
hepatocellular carcinoma (Habib et al 2001).
Cirrhosis has a high mortality rate and because
of this, many treatments are now aimed at the
prevention of cirrhosis. For those with end-stage
liver cirrhosis, liver transplantation is the only
viable treatment, with an 80-85 per cent five-year
survival rate (Friedman and Keeffe 2004).
However, the growing incidence of liver cirrhosis,
and shortages of organ donors mean that for
many patients, treatment is limited to managing
the complications as they arise.
Grading the severity of liver disease is
increasingly important because of the routine use
of liver transplantation in patient management.
An estimation of prognosis is essential if the
timing of the transplant is to be optimal. The
modified Child-Pugh grading system is frequently
used to assess the severity of liver disease (Table 1)
(OGrady et al 2000).
BOX 2
The main functions of the liver

increase in the need for liver transplantation

(NICE 2006).
It is proposed that incidence of liver cancers
will have a similar level of escalation (Moore et al
2004). Moreover, 6,000 people who are hepatitis
B positive arrive in the UK each year through legal
migration (Williams 2005). Steatohepatitis (fatty
liver and hepatic inflammation) is becoming
increasingly common due to the increased
prevalence of obesity and diabetes, and in the
United States it is being referred to as the new
epidemic of cirrhosis (Williams 2005). The
current trend for escalating liver disease is set to
continue and will have significant implications
for the healthcare system.

Bile formation

Anatomy and physiology

BOX 3

Situated in the upper right quadrant of the

abdominal cavity, the liver is the largest gland in
the body, weighing between 1.3-1.8kg. It can hold
about 13 per cent of the total blood supply at any
given moment and has more than 500 estimated
functions (BLT 2002) (Box 2).
Liver cirrhosis can occur as a consequence of any
chronic liver disease when repeated hepatocyte
damage results in the formation of fibrous tissue
and the development of nodules. Once cirrhosis has
developed it is usually considered irreversible. It
generally leads to a progressive course of liver
failure and the development of portal hypertension,
which is associated with many complications.
These include oesophageal varices, hepatic

Clinical effects of chronic liver disease

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Cholesterol and lipid metabolism

Drug metabolism

Carbohydrate metabolism

Fatty acid metabolism

Ammonia metabolism

Protein synthesis

Storage of iron, fat, glycogen and vitamins

Phagocytosis of bacteria

Hormone and steroid catabolism

Heat production (as by-product)

Synthesis of all clotting factors apart from factor
VIII

Cutaneous stigmata

Jaundice

Ascites

Encephalopathy

Bleeding tendency

Malnutrition

Portal hypertension

Splenomegaly

Endocrine abnormalities

Hepatocellular carcinoma
(Bacon et al 2006)

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Time out 1
List and describe six functions of the
liver. Explain what the consequences
of impaired liver function will have on these.

Signs and symptoms

Patients with chronic liver disease have many signs
and symptoms. Some patients may experience and
initially present with non-specific symptoms that
do not directly indicate liver disease, such as
lethargy, weakness, anorexia and nausea (Starr and
Hand 2002). Nonetheless patients with significant
liver disease and portal hypertension often present
with marked stigmata (Box 3). While these
symptoms suggest an underlying hepatic aetiology,
they may not necessarily indicate the disease
aetiology (Starr and Hand 2002). Consequently, a
patient with liver disease needs careful clinical
assessment and various investigations to establish
a definitive diagnosis and management plan
(Howdle 2006). It is important that nurses are
familiar with the significance of the patients
underlying history, presenting signs and
symptoms, common investigations and the
relevance of any abnormalities.

Time out 2
Make a list of the potential
complications associated with
percutaneous liver biopsies.

Investigations
Healthcare professionals involved in the care of
patients with liver disease need to be aware and

understand the implications and relevance of

these tests and investigations to nursing practice.
They may be required to explain the results of
these investigations to patients and/or family
members and carers.
Liver function tests (LFTs) These are biochemical
tests that are used to assess the livers synthetic
function (bilirubin and albumin) or liver
enzymes, which include aspartate
aminotransferase (AST), alanine
aminotransferase (ALT), alkaline phosphatase
(ALP), albumin, and gamma-glutamyl
transpeptidase (GGTP) (Giuliani 2003).
However, it can also include a prothrombin time
(PT) or international normalised ratio (INR) to
assess hepatic function. Table 2 demonstrates the
normal values, and explains the significance of
abnormalities in patients with liver disease.
It is common in patients with liver cirrhosis to
undertake the following additional laboratory
investigations: full blood count, urea and
electrolytes, and a liver disease screen which may
include viral hepatitis and viral screen,
autoimmune antibody screen, ferritin and
transferrin saturation (haemochromatosis)
alpha-fetoprotein (hepatocellular carcinoma).
Liver biopsy Liver biopsy is considered by many
physicians as the gold standard for diagnosing and
staging a variety of liver disorders, and assessment
for treatment. However, it is not always necessary
for patients with genotypes 2 or 3 in HCV, or if
biopsy poses an increased risk of complications to
the patient (NICE 2006).
Important contraindications of the procedure
include severe coagulopathy or
thrombocytopenia, ascites, pleural effusion,
confusion, hepatic encephalopathy or noncooperation, bacterial cholangitis, extrahepatic
biliary obstruction, cystic lesions or conditions
such as amyloidosis in which abnormal protein
deposition in tissues increases the risk of bleeding
(Grant and Neuberger 1999).

TABLE 1
Childs grading disease severity in chronic liver disease with Pughs 1973 modifications
Criteria assessed
Encephalopathy (grade)
Ascites

Points scored for increasing abnormality

1

None

1-2

3-4

Absent

Slight

Moderate

Serum bilirubin

<35mol/l

35-50mol/l

>50mol/l

Serum albumin

>35g/l

35-28g/l

<28g/l

Prothrombin time (prolongation (seconds))

1-4

4-10

>10

Total score

10-15

5-6

7-9

Childs grade equivalent

Overall mortality in Pughs series (%)

29

38

88

(OGrady et al 2000)

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TABLE 2
Normal values of common liver function tests and causes of derangement in liver disease
Test
Total bilirubin

Normal range
5-7mol/L (0.3-1.0mg/dl)

Value
Diagnosis of jaundice and assessment of severity

Conjugated bilirubin

<5mol/l

Gilberts syndrome, haemolysis

Alkaline phosphatase (ALP)

35-130iu/l

Diagnosis of cholestasis, hepatic infiltration

Aspartate aminotransferase (AST)

Alanine aminotransferase (ALT)

5-40iu/l

Early diagnosis of hepatocellular disease; follow progress

5-35iu/l

ALT lower than AST in alcoholism

Gamma-glutamyl transpeptidase (GGTP)

10-48iu/l

Diagnosis of alcohol abuse, marker biliary cholestasis

Albumin

35-50g/l

Assesses severity of hepatic synthetic function

Gamma globulin
Prothrombin time (PT) after vitamin K

5-15g/l
12-16 seconds

Diagnosis of chronic hepatitis and cirrhosis

Assesses severity of hepatic function

(Adapted from Sherlock and Dooley 2002)

The most common types of liver biopsy

performed are percutaneous guided either by
abdominal percussion, computed tomography
(CT) or ultrasonography. In high risk patients,
this is often done radiologically using the
transjugular or femoral approach. It is, however
vital that nurses are aware of patients platelet
count and coagulation; ideally this should be
checked 24 hours before the biopsy. In addition,
all patients undergoing percutaneous biopsies
should be blood grouped and serum saved, and
their baseline observations should be recorded.
Informed consent should be obtained in writing
before the procedure in accordance with the
policies of individual hospitals (British Society of
Gastroenterology (BSG) 2004).
Nursing staff should ensure the patient lies on his
or her right side or flat for two hours post procedure
to prevent haemorrhage. Vital signs on standard
percutaneous biopsies should be recorded for a
minimum of six hours starting at 15-minute
intervals for the first two hours, then every 30
minutes for two hours, and then hourly (BSG
2004). The underlying rationale for the frequency
and length of monitoring vital signs is because 61
per cent of complications occur in the first two
hours, which include haemorrhage, pain,
hypotension and vasovagal episodes,
pneumothorax, puncture of other nearby organs,
emphysema, sepsis, and a reaction to the
anaesthesia (Grant and Neuberger 1999).
Therefore, it is imperative that nurses are familiar
with such complications and their signs, to sanction
prompt and appropriate investigations or
treatment.
Liver imaging Plain abdominal X-rays add little
to the evaluation of liver disease (Friedman and
Keeffe 2004). Liver ultrasonography is the initial
radiological study of choice for many liver
disorders because it is relatively cheap and
non-invasive, and can demonstrate a wide range
of clinical abnormalities, such as dilated bile
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ducts, hepatic tumours, cirrhosis and ascites. It

also allows visualisation to drain hepatic
abscesses, ascites or to guide biopsies. CT and
magnetic resonance imaging (MRI) scanning are
considered more accurate in defining hepatic
anatomy. However, they are more expensive and
are not portable, but may be used in conjunction
with other liver investigations.
Endoscopic retrograde
cholangiopancreatography (ERCP) is primarily
used for the evaluation or treatment of patients
with suspected biliary or pancreatic disease.
However, as ERCP is an invasive procedure with
a complication risk of 2-3 per cent and mortality
rate of 0.1-0.2 per cent, it is usually only used
after an ultrasound or CT imaging (Sherlock and
Dooley 2002). Other diagnostic investigations
used are endoscopy, endoscopic ultrasound and
hepatic angiography.
Box 3 lists the clinical effects of chronic liver
disease, which are associated with increased
mortality, a reduced quality of life and altered
body image. It is essential that nurses are familiar
with the underlying pathophysiology and current
medical and nursing management of the
associated complications.

Hepatic encephalopathy
Hepatic encephalopathy is a reversible
neurological state that complicates liver disease,
and is a syndrome of unknown pathogenesis. It is
believed that the causes of hepatic
encephalopathy are multifactorial, and are
attributed to endogenous neurotoxins such as
ammonia, mercaptans (derivatives of
methionine), phenols and short and medium
chain fatty acids (Friedman and Keeffe 2004), an
increase in permeability of the blood brain barrier
or changes in neurotransmitter and receptors
(Gerber and Schomerus 2000). However,
ammonia toxicity is the simplest and most
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supported theory in chronic liver disease
(Friedman and Keeffe 2004).
There are several reversible factors that can
contribute to altered mental status in patients
with liver cirrhosis. The first line of treatment is
to identify and correct these abnormalities which
include: alterations in acid base balance or
electrolyte disturbances; dehydration;
constipation; infections; gastrointestinal tract
bleeding; use of sedative medication; and
non-concordance with treatments such as
lactulose therapy (Habib et al 2001).
The clinical manifestations of hepatic
encephalopathy vary from a slightly altered
mental state to deep coma (Box 4). As the level of
hepatic encephalopathy can reflect the underlying
degree of liver function, this may be a useful sign
of acute deterioration, and consequently should
be reported to the appropriate medical team.
The mainstay of treatment in hepatic
encephalopathy remains the pharmacological use
of non-absorbable disaccharides such as
lactulose. Lactulose is metabolised in the colon
and broken down by bacteria to lactic acid. As a
consequence the pH of the intestine is lowered
affecting both the production and absorption of
ammonia (Sherlock and Dooley 2002). Dosages
of lactulose usually range from 10-30ml two to
four times per day with the aim of producing two
to three soft stools daily. Mild side effects are
increased flatulence, bloating and cramps.
However, more severe side effects, such as
diarrhoea, dehydration and acidosis, may
necessitate either dose reduction or temporary
cessation of therapy (Blei 2006). Improvements in
severe encephalopathy can take up to 48-72
hours, and, therefore, lactulose is sometimes used
in conjunction with enemas.
The priorities in nursing patients with liver
cirrhosis who have hepatic encephalopathy
should include: close monitoring and
documentation of the patients neurological status
and level of hepatic encephalopathy, maintaining
a safe environment, frequently assessing the

patients respiratory status including respiratory

rate and oxygen saturations protecting the
patients airway in grade 3-4 hepatic
encephalopathy and recording and monitoring
bowel actions closely aiming for two to three soft
stools per day (Sargent 2005).

Oesophageal varices
Patients with liver cirrhosis develop oesophageal
varices as a consequence of portal hypertension
(Figure 1). This rise in portal pressure is
associated with the development of a collateral
circulation which allows the portal blood to be
diverted back into the systemic circulation (Jalan
and Hayes 2000). These collateral vessels are
inelastic and become more fragile as they enlarge
and the lumens become thinner and, therefore,
are at risk of rupturing (McArdle 1999). These
collateral vessels are classified by their location
and are most commonly found in the intrinsic and
extrinsic gastro-oesophageal veins (oesophageal
and gastric varices), the haemorrhoid veins, and
umbilical circulation (Jalan and Hayes 2000).
The incidence of variceal bleeding is
estimated between 25 and 35 per cent, with an
associated mortality of 30 to 50 per cent for each
bleeding episode, and is considered one of the
most feared complications of portal
hypertension (Jalan and Hayes 2000). Wide
bore peripheral and central venous access, fluid
resuscitation to correct and prevent
hypovolaemia, haemodynamic monitoring,
oxygen therapy and airway protection to
prevent hypoxia and aspiration are the main
priorities on initial bleeding. Patients may need
to be intubated with an endotracheal tube in
cases of impaired consciousness for example,
hepatic encephalopathy uncontrollable
FIGURE 1
Oesophageal varices: abnormally dilated
veins in the oesophagus caused by portal
hypertension

BOX 4
Different levels of conscious alteration in patients with
hepatic encephalopathy

SCIENCE PHOTO LIBRARY

Alterations in consciousness in hepatic encephalopathy

Stage I Mild disturbance, personality change, sleep disturbance

Stage II Drowsiness, intermittent disorientation, short attention span

Stage III Somnolent but arousable, gross disorientation

Stage IVa Coma, arousable by painful stimuli

Stage IVb Coma, unresponsive
(Adapted from Friedman and Keeffe 2004)

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bleeding, inability to maintain saturations

greater than 90 per cent, or in cases of aspiration
pneumonia (Jalan and Hayes 2000).
Once the patient is haemodynamically stable,
bleeding cessation is then normally achieved
endoscopically with either variceal band ligation
or in the case of no banding facilities or
uncontrolled bleeding, sclerotherapy (Jalan and
Hayes 2000). Unless contraindicated terlipressin
a synthetic analogue of vasopressin is given
intravenously (IV). It works by constricting the
splanchnic arterioles and thus decreasing the
portal inflow and pressure.
It is important, however, to be aware of the
vasoconstrictive effects that this may have on other
organs. Ideally, patients should have daily
electrocardiograms and regular monitoring of their
limbs and neurological status to assess for potential
ischaemic side effects (Sargent and Martin 2006).
Patients with upper gastrointestinal bleeding have a
high incidence of bacterial infections. As this is
associated with an increased mortality and
morbidity, prophylactic IV antibiotics are usually
administered (Jalan and Hayes 2000).
Balloon tamponade tubes may provide
haemostasis by compression of varices through
inflation of the tubes gastric balloon. However,
balloon tamponade tubes are associated with a
high complication risk and incidence of
rebleeding post-removal. Consequently, these
should only be used in cases of bleeding when
pharmacological and endoscopic therapies have
failed, or are unavailable and should not be used
for longer than 24 hours (Jalan and Hayes 2000).
Secondary prophylaxis of variceal
haemorrhage is aimed at reducing portal
hypertension and preventing rebleeding. It
includes the use of further endoscopic therapies,
pharmacological agents, such as beta blockers,
surgery, and the use of radiological procedures,
such as transjugular intrahepatic portosystemic
shunt (TIPS) in which a self-expandable metal
stent is inserted between the hepatic vein and
intrahepatic portion of the portal vein.
It is important to remember that a variceal
bleed is not only life-threatening but is also
frightening and distressing for patients.

transition from compensated to decompensated

liver disease. Ascites develop in up to 50 per cent of
patients with liver disease after a 10-year period
(Friedman and Keeffe 2004). The development of
ascites in patients with cirrhosis indicates a poor
prognosis. The probability of death in cirrhotic
patients when hospitalised for ascites is 40 per cent
at two years (Gines et al 2004). Consequently, all
patients with ascites should be evaluated for liver
transplantation, especially those with recognised
complications such as refractory ascites,
spontaneous bacterial peritonitis, or hepatorenal
failure which are associated with a poor outcome
(Gines et al 2004).
The underlying pathophysiology of ascites is
complex. However, the most accepted theory is
arterial vasodilation (Figure 2). Portal
hypertension secondary to liver cirrhosis, results in
the production of vasodilators (primarily nitric
oxide), which leads to splanchnic arterial
vasodilation.
As the liver disease progresses, the amount
of splanchnic arterial vasodilation increases,
resulting in arterial underfilling which activates
the antinatriuretic renin-angiotensin-aldosterone
system and the sympathetic nervous system.
These compensatory mechanisms cause an
increase in water and sodium absorption and
vasoconstriction. The combination of portal
hypertension and splanchnic arterial vasodilation
alters intestinal capillary permeability, allowing
FIGURE 2
The pathogenesis of ascites in cirrhosis

Liver

Cirrhosis
Portal hypertension

Splanchnic vasodilation

Increase in splanchnic
capillary pressure

Arterial
underfilling

Arterial and
cardiopulmonary
receptors

Time out 3
Summarise in your own words how
patients develop oesophageal varices
and make a list of the complications
associated with these.

Ascites formation

Activation of vasoconstrictor
and antinatriuretic factors:
renin-angiotensin-aldosterone
system and sympathetic
nervous system

Ascites
Sodium retention

Ascites is the excessive accumulation of extra

cellular fluid in the peritoneal cavity. It is a common
complication of advanced cirrhosis marking the
NURSING STANDARD

Kidney

(Adapted from Cardenas et al 2006)

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the migration of fluid into the peritoneal cavity,
resulting in ascites (Gines et al 2004).
Diagnostic paracentesis (needle aspiration of
ascitic fluid) should be performed on the onset of
ascites. Any deterioration should prompt a
repeat paracentesis to investigate any clinical
evidence of spontaneous bacterial peritonitis,
which is usually suggestive of the presence of at
least 250 polymorphonuclear cells per cubic
metre (Gines et al 2004).
The treatment of patients with cirrhotic ascites
is aimed at mobilising ascitic fluid with either
dietary sodium restriction, oral diuretic therapy,
or a combination of both as 90 per cent of
patients will respond to these therapies (Friedman
and Keeffe 2004). The amount of fluid retained in
the body depends on the balance between sodium
ingested in the diet and sodium excreted in the
urine. Therefore, if the level of sodium excreted is
more than the sodium intake this causes a
decrease in both ascites and oedema as fluid
passively follows sodium. A reduced sodium
intake of 2g/day (88mmol/l) is considered a
realistic goal (Runyon 1998).
The main diuretic therapy is a morning dose of
either spironolactone (100-400mg daily), or a
combination of spironolactone and furosemide
(40-160mg daily). In non-oedematous patients
the goal of diuretic therapy in ascites is to achieve
diuresis with a gradual weight loss of
0.3-0.5kg/day. If the weight loss exceeds this it
then signifies fluid mobilisation at the expense of
the intravascular compartment which can lead to
renal failure (Habeeb and Herrera 1997). Other
complications related to diuretic therapy are
dilutional hyponatraemia (serum sodium
<130mmol/l), hepatic encephalopathy,
hyperkalaemia (serum potassium >5.5mmol/l),
gynaecomastia (breast enlargement), and muscle
cramps (OGrady et al 2000).
The most effective way to monitor the amount
of fluid loss is by weighing the patient daily. To
ensure precision this is normally done before
breakfast, with the patient wearing the same
amount of clothing (Sargent 2006).
If ascitic fluid mobilisation becomes either
resistant to the maximum diuretic therapy, or if
patients develop serious side effects which
preclude drug administration, this is termed
refractory ascites. Refractory ascites affects
5 to 10 per cent of all patients with ascites and
is associated with a survival of 20 to 50 per cent
at one year (Moore et al 2003). Refractory
ascites normally requires second-line therapy,
such as large volume paracentesis (Yeung and
Wong 2002).
54 november 22 :: vol 21 no 11 :: 2006

Large volume paracentesis (>5 litres of fluid

removal) is the standard therapy for refractory
ascites and can provide rapid relief of the
symptoms associated with tense ascites (OGrady
et al 2000). However, if more than five litres of
fluid is removed without replacement volume
expanders, patients can develop post-paracentesis
hypovolaemia leading to hyponatraemia and
renal impairment (Moore et al 2003).
While the choice of fluid remains
controversial, the most accepted volume
expander is human albumin solution 6-8g
is usually administered for every litre of fluid
drained, for example, 100ml of 20% human
albumin solution for each three litres drained. A
baseline set of the patients vital signs should be
recorded, with frequent monitoring throughout
the procedure as well as accurate fluid balance
measurements. Any significant changes in blood
pressure, urine output and an increased level of
hepatic encephalopathy or signs of infection need
to be reported immediately to an appropriate
medical team (Sargent 2006).

Time out 4
Reflect on the effects of altered body
image on a patient with liver cirrhosis?
You may wish to discuss your ideas with a
colleague.

Jaundice
Jaundice (icterus) is the most common
presentation in patients with liver and biliary
disease, and occurs when serum bilirubin levels
rise above 40mol/l and become visible within the
sclera, skin and mucous membranes (Beckingham
and Ryder 2001). Bilirubin is formed after the
breakdown of haemoglobin molecules, and any
failure of the bilirubin excretory pathway will
result in an accumulation of bile pigments in the
blood (Campbell 1999).
Jaundice can be defined as prehepatic,
intrahepatic or post-hepatic. Therefore, it is
usually necessary for additional laboratory tests
or investigations to differentiate the underlying
cause. Testing the bilirubin for conjugated and
unconjugated levels may be useful for
determining a prehepatic or post-hepatic origin.
In addition, jaundice with dark urine, pale stools,
raised alkaline phosphates and gamma-glutamyl
transferase suggests an obstructive cause which
can be confirmed by the presence of dilated bile
ducts on ultrasonography (Beckingham and
Ryder 2001).
Patients with liver cirrhosis usually present with
intrahepatic jaundice as either the damaged
hepatocytes or obstructed intrahepatic bile
canaliculi (small bile ducts) result in the liver being
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unable to conjugate and excrete bilirubin (Starr and

Hand 2002). The main treatment of jaundice is to
treat the underlying cause and to alleviate any
symptoms, such as pruritus, and to help patients
cope with an altered body image.

Time out 5
Make a list of the possible
consequences of protein calorie
malnutrition and weight loss in patients with
end-stage liver disease. Discuss your answers
with a dietician or nutrition nurse specialist.

Nutrition
The incidence of protein-energy malnutrition
(PEM) and prevalence of severe muscle wasting
are estimated to be as high at 80 per cent in
patients with liver cirrhosis (Harrison et al 1997),
and are related to the underlying degree of liver
injury. Consequently, nurses should presume that
all patients with liver cirrhosis will have protein
calorie malnutrition and an inadequate dietary
intake (McCullough 2000).
There are a number of causes of PEM. It has
been attributed to anorexia (decreased dietary
intake) caused by nausea, feeling full (due to
ascites), alterations in taste and smell, medical
investigations and treatments, unpalatable diets
(for example, low sodium), and diarrhoea or
constipation. Other causes of PEM and weight
loss are linked to malabsorption (poor absorption
of nutrients from the gastrointestinal tract),
which occurs in patients with steatorrhoea (pale,

fatty stool), increased energy expenditure,

decreased mobility and alcohol consumption
(Vintro et al 2002, McCullough 2006).
There are many consequences of malnutrition
including increased vulnerability to infection,
delayed wound healing, impaired respiratory and
cardiac function, decreased muscle strength and
depression. About 40 per cent of patients with
non-alcoholic liver disease have fat soluble
vitamin deficiency. These vitamin deficiencies
have a higher prevalence in patients with
alcoholic liver disease and are caused by loss of
hepatic function, diminished reserves and
malabsorption. Patients with alcohol-induced
liver disease are at risk of developing Wernickes
encephalopathy (confusion, ataxia and ocular
disturbances) caused by thiamine deficiency.
These patients should be given twice daily IV
B vitamins (Pabrinex), followed by a course of
oral thiamine to prevent the development of this
syndrome.
It is also important that patients are referred
for dietetic advice and have a nutritional
assessment as early as possible for correct
guidance on dietary and vitamin supplements,
and to determine patients who may benefit from
enteral feeding. The use of patient meal charts is
valuable in establishing actual dietary intake.
One of the misconceptions about patients with
liver cirrhosis and hepatic encephalopathy is the
need to restrict dietary protein intake. However,
the current guidelines of the European Society of
Parenteral and Enteral Nutrition (Plauth et al
1997) advocate patients with chronic liver disease
should receive 35-40kcal/kg/day of non-protein

References
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NURSING STANDARD

(Last accessed: November 10 2006.)

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Page 56

include the division of a liver for two transplant

recipients, living donor transplantation and the use
of non-heart beating donors (Abt et al 2004).

learning zone hepatology

energy with 1.5g/kg/day as protein (calculated
using ideal body weight) and, therefore, there is
no justification for protein restriction.

Liver transplantation
Since the first pioneering liver transplant in the
1960s, refinements in organ preservation,
surgical techniques and immunosuppressive
therapy have enabled liver transplantation to
become an acceptable life-saving treatment for
patients with liver cirrhosis, with good
documented survival outcomes and
improvements in patients perceived quality of
life (Sargent and Wainwright 2006).
Therefore, once a patient has been identified as
having liver cirrhosis or having a chronic liver
disease that is likely to progress to cirrhosis, the
possibility of liver transplantation should be
considered (Habib et al 2001). However, continual
increases in the number of patients with liver
disease and cirrhosis are reflected in the rise in
patients listed for a transplant. Despite the
increased demand for this life-saving treatment, the
overall number of liver transplants in the UK fell by
7 per cent in 2005-2006. This has resulted in longer
waiting times and increased numbers of patients
being suspended or removed from the active list
(United Kingdom Transplant 2006). To address
this deficit, several new concepts of transplantation
have been expanded or implemented which

Conclusion
Liver disease is a growing healthcare problem in
the UK. While most therapies aim at reducing
the progression or development of cirrhosis and
subsequent end-stage liver disease, for many
patients liver transplantation is the only survival
option. This article has illustrated the
complexity of health problems and multiple
therapies that arise as a consequence of patients
developing liver cirrhosis and portal
hypertension. Effective knowledge of both the
physical and psychological needs of patients is
vital to optimise nursing care NS

Time out 6
Now that you have completed the
article, you might like to write a practice
profile. Guidelines to help you are on page 60.

USEFUL INTERNET SITES

British Liver Trust: www.britishlivertrust.org.uk
British Society of Gastroenterology: www.bsg.org.uk
The British Transplantation Society: www.bts.org.uk
United Kingdom Transplant Services:
www.uktransplant.org.uk
(Last accessed: November 10 2006.)

References continued
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Moore K, Thursz M, Mirza DF
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et al (1997) ESPEN guidelines for

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Vintro AQ, Krasnoff JB, Painter P

(2002) Roles of nutrition and
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NURSING STANDARD