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Managing ascites in patients

with chronic liver disease
NS729 Fullwood D, Purushothaman A (2014) Managing ascites in patients with chronic liver disease.
Nursing Standard. 28, 23, 51-58. Date of submission: June 21 2013; date of acceptance: October 29 2013.

Aims and intended learning outcomes

Abstract
This article discusses the pathophysiology of ascites, a complication
associated with chronic liver disease. The diagnosis and grading of
ascites and assessment of patients with the condition are explored. In
addition, the nursing and medical management of ascites is discussed,
and recommendations for interdisciplinary working and education are
suggested. Nursing knowledge of this complication is essential to ensure
that patients with ascites are cared for effectively and that their comfort
is maximised.
Authors
Danielle Fullwood
Lecturer practitioner for hepatology, Kings College Hospital NHS
Foundation Trust, London.
Anan Purushothaman
Practice development nurse, Liver Intensive Care Unit,
Kings College Hospital NHS Foundation Trust, London.
Correspondence to: danielle.fullwood@nhs.net
Keywords
Albumin, ascites, large-volume paracentesis, peritoneal cavity,
transjugular intrahepatic portosystemic shunt
Review
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for plagiarism using automated software.
Online
Guidelines on writing for publication are available at
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search using the keywords above.
This article focuses on the assessment and
management of ascites in patients with chronic
liver disease. After reading this article and
completing the time out activities you should
be able to:
Describe the pathophysiology of ascites.
Discuss the diagnosis of the condition in
patients with chronic liver disease.
Explain the complications that may be
associated with ascites.
Outline the treatments and interventions
used to manage the condition in patients
with chronic liver disease.
Describe the development and treatment
of refractory ascites.
Introduction
Ascites is defined as the accumulation of
fluid in the peritoneal cavity. It is not unique
to liver disease and can be seen in patients
with tuberculosis, peritoneal infection,
pancreatic disease and malignancies
(Rochling and Zetterman 2009). However, it
is a frequent complication of liver dysfunction,
and is observed in approximately 60% of
patients with chronic liver disease (Gins
et al 1987). For the patient, the presence
and experience of ascites causes significant
discomfort and marks the transition from
the liver being able to compensate for the
damage, to a liver that can no longer
perform its functions. This is known as
decompensated liver disease. Once ascites is
present, survival is markedly reduced, with
median survival of approximately two years
(DAmico et al 2006).

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CPD hepatology
Pathophysiology
The liver is supplied with 75% of its blood by
the portal vein, with the remaining 25% of
blood being delivered to the liver by the hepatic
artery. The portal vein brings blood from the
stomach, spleen, umbilicus, and small and
large intestine (Bacon et al 2006), meaning the
blood is rich in nutrients and toxins. The liver
is comprised of millions of lobules, which are
made up of hepatocytes and Kupffers cells.
Each lobule has its own blood supply via a
small branch of the portal vein and hepatic
artery, along with a bile duct that make up
the portal triad (McErlean 2011). About
1,500mL of blood is perfused through the liver
each minute (Wong 2009), making it a highly
vascularised organ.
In a healthy liver, endothelial cells that
line the blood vessels are biologically active
and produce several mediators. Endothelin
and nitric oxide are both produced,
inducing vasoconstriction and vasodilation,
respectively. These mediators work together
to regulate the diameter of and blood
flow through blood vessels at a local level
(Tousoulis et al 2012).
In liver disease, the flow of blood to the
liver and the blood pressure in the blood
vessels change, eventually leading to ascites.
As the liver becomes damaged by the
presence of disease, its architecture changes
and it atrophies and appears shrunken
because more scar tissue is formed and
deposited. Increases in intrahepatic
vasoconstriction agents, such as endothelin,
also occur (Iwakiri and Groszmann 2007).
The blood delivered to the liver, therefore,
starts to meet resistance because of this
change in architecture and intrahepatic
vasoconstriction and pressure rises in the
portal vein starting a process known as
portal hypertension (Garcia-Tsao et al 2007).
In addition, the regulation of mediators
produced by the endothelial cells is altered
and an imbalance occurs. Endogenous
vasodilators such as nitric oxide are
1 When examining produced in excess in the presence of portal
a patients abdomen, hypertension and result in vasodilation of the
palpation, inspection, blood vessels in the splanchnic area, including
percussion and the portal vein and its contributory vessels
auscultation can be used. (Iwakiri and Groszmann 2007, Sargent 2009,
In what order should Dooley et al 2011, Fullwood 2012).
these examinations be This abdominal vasodilation results in
performed by a nurse to blood being redirected away from major
obtain the most accurate organs and an increased blood flow to the
findings, and why? liver, worsening the pressure in the portal
vein. The kidneys, which require a specific
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perfusion pressure to function effectively,
receive a lower perfusion pressure than usual
because the blood is redirected to the dilated
abdominal vessels. This lower perfusion
pressure is sensed and the kidneys activate
the renin-angiotensin-aldosterone system to
increase blood volume to improve their own
blood supply. Renin production is stimulated,
causing angiotensin to be released. This
causes vasoconstriction of the arterial vessels
leading to the kidney in an attempt to increase
the pressure in the glomerulus. Angiotensin
then activates aldosterone secretion and
causes sodium to be reabsorbed in the loop
of Henle, retaining water as a consequence.
This increase in water absorption leads
to an increase in blood volume (Sargent
2009, Dooley et al 2011). However, with
the production of nitric oxide still in excess,
vasodilation of the abdominal vessels
continues as does the fall in blood pressure
to the kidneys. Sodium and water, therefore,
are continuously reabsorbed from the loop
of Henle, making the blood volume increase,
but the blood pressure remains inadequate
(Rosner et al 2006) (Figure 1).
Eventually, the retained water in the
engorged vessels starts to leak out of the
intravascular space and into the lymphatic
system. The amount of fluid exceeds the
lymphatic drainage capacity, and fluid starts
to leak from the lymphatic system into the
peritoneal cavity (Sargent 2009).
Complete time out activity 1
Grading, assessment and diagnosis
The presence of fluid in the peritoneal cavity
can cause abdominal distension. Depending
on the severity of this distension, the ascites
can be graded (European Association for the
Study of the Liver (EASL) 2010) (Table 1).
Inspection of the abdomen should be
performed initially. This involves looking
at the abdomen carefully for signs of injury,
such as bruises or wounds, and the presence
of shiny, taut skin or prominent veins.
The size, distension and symmetry
of the abdomen should be noted along
with the presence of bulging flanks
(Rushing 2005). The abdomen should be
auscultated to detect gurgling or rumbling
reflecting gut peristalsis, and this must be
performed before percussion and palpation
because these examinations can cause
such peristalsis to cease for a short period.
Palpation is performed to detect any pain
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or tenderness, guarding or tensing of the deterioration in health (Sargent 2009).
abdomen followed by percussion. A multidisciplinary team approach to the
Percussion can detect an accumulation of management of patients with ascites is
1,000-1,500mL of fluid in the peritoneal ideal to address mobility issues, optimal
cavity. Percussion is carried out with the medical treatment, patient education and
patient in two positions. First, with the psychological support.
patient in the supine position, free fluid in
the abdomen moves with gravity and will FIGURE 1
collect around the flanks. Percussion,
therefore, reveals dullness in the flanks and Pathophysiology of ascites
tympanic sounds at the top of the abdomen
where air has accumulated. Second, the Increased pressure
patient is positioned on his or her side. Now in the portal vein
the fluid moves with gravity to the front of the
abdomen, allowing the air to be percussed
at the top by the flank. This is known as the
assessment of shifting dullness (Rushing Sodium and water Production of nitric
2005) (Figure 2), and can be done by a retention oxide causing dilation of
the abdominal vessels
nurse with advanced assessment skills or
a medical practitioner.
Once fluid has been detected and the
ascites graded, it is important to confirm
that the ascites is occurring as a result of Renin-angiotensin- Increased blood flow in
liver dysfunction. As previously mentioned, aldosterone activation the abdominal vessels
there are other causes of ascites and it is
important to rule these out before treatment
options are considered.
A 30mL sample of ascitic fluid should be Reduced blood flow
to major organs
aseptically obtained by a medical practitioner,
10mL of which should be tested for white
and red blood cell counts and albumin
concentration. Table 2 shows the rationale TABLE 1
for testing these parameters. The remaining
20mL of ascitic fluid is sent for culture and Grading of ascites
sensitivity testing. If infection is present, this Grade Detection technique Abdominal distension
will indicate which organism is responsible and
1 Ultrasound Absent (<500mL of fluid)
the appropriate antibiotic therapy.
2 Inspection, palpation Moderately distended
and percussion
Psychological effects 3 Inspection, palpation Grossly or markedly
The psychological needs of patients with and percussion distended
ascites are important yet are often neglected (Adapted from European Association for the Study of the Liver 2010)
because of the prioritisation of medical
needs. The complications of and treatments
for chronic liver disease can lead to lethargy, FIGURE 2
depression and reduced quality of life (Mucci
Assessment of shifting dullness
et al 2013). The complications of end-stage
JO CAMERON

liver disease, including ascites, have been

shown to reduce mobility, limit physical
activity and reduce patients health-related
quality of life (Cox-North et al 2013). Nurses Tympany
should be sensitive to the psychological Tympany
needs of these patients and refer them to
available support as appropriate. Referral Dullness
Dullness
to a counselling team may benefit these
patients with ascites, particularly as they
may experience loss of independence and

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CPD hepatology

Complications Hyponatraemia may be dilutional in nature,

There are complications associated with ascites
that affect both the morbidity and mortality of
patients. Fluid accumulating in the peritoneal
cavity reduces the space available for lung
expansion and can lead to shortness of breath,
particularly when in a supine position. The
stomach can be compressed, leading to a
reduced appetite, nausea and vomiting.
When large volumes of fluid are present, the
pressure can compress the bowel and reduce
blood supply to abdominal organs. Reduced
gut function and renal perfusion are possible
consequences (Garcia-Tsao 2011). A list of
further complications is shown in Table 3.
It is important that healthcare professionals
are able to assess the presence of ascites and
commence treatment in a timely manner
to limit the risk of complications. It is also
important that healthcare professionals are able
to monitor patients with ascites for signs of any
complications and to commence appropriate
treatments as soon as possible.
Nursing care
While patients with grade 1 ascites may not
require immediate treatment, measures should
be taken to prevent the development of grade
2 or 3 ascites (Table 1). Patients with grade
2 or moderate ascites can be treated at home
with follow up, unless other complications of
cirrhosis are also present. Treatment is aimed
at reducing sodium intake and increasing renal
sodium excretion (Garcia-Tsao 2011). This
reduces the formation of ascites by reducing
the amount of sodium and water retained by
the kidneys (Sargent 2009). Advising a reduced
sodium diet may seem conflicting when
hyponatraemia is a potential complication.
caused by the excessive retention of salt and
therefore water, which follows salt to form
ascites. If less salt is consumed then less water
will be reabsorbed, thus reducing ascites
formation (Bacon et al 2006).
According to Garcia-Tsao (2011), salt
should be restricted to 70-90mmol/day.
This equates to a non-added salt diet rather
than the more traditional recommendation
of a low salt diet of 22-40mmol/day. The
traditional regimen has been found to
compromise protein and calorie intake in a
patient group that is already experiencing
malnutrition as a result of chronic liver
disease (Garcia-Tsao 2011), and therefore
it is no longer recommended.
Any patient prescribed a reduced salt diet will
benefit from referral to a dietician for both a
formal nutritional review and education (Moore
and Aithal 2006). Relatives or those cooking
for the patient should also attend any patient
education sessions to aid compliance with
this treatment regimen. The need for nursing
education is evident as nurses should be able to
promote this treatment and to educate patients
about high salt content foods to be avoided. An
awareness of medications that are high in salt is
also required so that these may be avoided.
Alcohol abstinence is a vital component
in the treatment of ascites caused by
alcohol-related liver disease. Early
abstinence may reverse portal hypertension
and sodium retention (Runyon 2009).
Referral to a specialist nurse is, therefore,
beneficial and recommended in patients with
alcohol or substance misuse issues (National
Institute for Health and Care Excellence
(NICE) 2011).
Complete time out activity 2

TABLE 2
Ascitic fluid analysis
Parameter Rationale Explanation

2 Aldosterone
antagonists and loop
diuretics are two groups
of diuretics commonly
used in the treatment
of grade 2 ascites. Can
you name at least one
diuretic that falls in each
category and outline
their specific mode of
action?
White cell count Presence of >250 white blood
cells/mm3 indicates infection.
Red cell count Presence of red blood cells
indicates bleeding within the
peritoneal cavity.
Albumin content Comparing the serum albumin
with the ascitic albumin
content indicates the cause of
ascites.
(Moore and Aithal 2006, Runyon 2013)
If the fluid is drained when infection is
present, septicaemia may occur.
Fluid in the abdomen can tamponade
bleeding. If the fluid is drained, the bleeding
point may haemorrhage further as the
pressure pushing against it would decrease.
Serum ascites albumin gradient >11g/L
(>1.1g/dL) indicates the ascites is present
because of liver disease.

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TABLE 3
Complications of ascites
Complications Symptoms Treatments
Spontaneous Abdominal pain, fever. May be asymptomatic. Antibiotic administration. Large-volume paracentesis
bacterial peritonitis should be withheld until infection is treated effectively.
Dilutional Increased peripheral oedema and Fluid restriction may be instigated if sodium is
hyponatraemia re-accumulation of ascites. <130mmol/L, but should be used with caution.
Hepatorenal Reduced renal function, raised creatinine in the Administration of the vasoconstrictor terlipressin in
syndrome absence of infection, shock or use of nephrotoxic combination with albumin. Liver transplantation.
drugs.
Pleural effusion Shortness of breath, increased respiratory rate, Chest drains are contraindicated for this cause of
reduced air entry. pleural effusion. First-line treatment includes diuretic
administration and reduced sodium diet.
Umbilical hernia Swelling of the area around the umbilicus. May require surgical intervention depending on the
May be associated with abdominal pain or severity of the hernia.
discomfort.
(Adapted from European Association for the Study of the Liver 2010, Garcia-Tsao 2011, Runyon 2013)

Diuretics are used in conjunction with a reduced
salt diet to increase the excretion of sodium via
the kidneys. Aldosterone antagonists are more
effective than loop diuretics in the management
of ascites because they treat the pathophysiology
of the accumulation of ascites as well as
preserving potassium levels. Patients with a first
episode of ascites should receive an aldosterone
antagonist such as spironolactone at doses of
between 100mg and 400mg daily (Rosner et al
2006). The maximum recommended weight
loss during diuretic therapy should be 0.5kg
daily in patients without peripheral oedema and
1kg daily in patients with peripheral oedema
(EASL 2010). In patients who do not respond
to aldosterone antagonists, which means a
reduction of body weight of less than 2kg per
week, or if the patient develops hyperkalaemia
or recurrent ascites, a loop diuretic such as
furosemide should be added to the treatment
regimen at a dose of 40-160mg daily (Runyon
2013). Patients should be monitored frequently
for clinical and biochemical parameters,
particularly during the first month of treatment.
Side effects of diuretics include renal failure,
hepatic encephalopathy, electrolyte disorders,
gynaecomastia and muscle cramps (British
National Formulary 2013). Monitoring should,
therefore, include electrolyte balance, renal
function and assessment for signs of hepatic
encephalopathy.
Bed rest with legs elevated is advocated by
Alexander et al (2006) as the most comfortable
position and is likely to reduce peripheral
oedema. The adoption of an upright position
has been linked with activation of the
renin-angiotensin-aldosterone system,
a reduction in sodium excretion and a
reduced response to diuretics (Bacon et al
2006). However, there is no evidence to
support the relationship between bed rest
and the effectiveness of diuretics; therefore,
complications of bed rest must be considered
(Moore and Aithal 2006). Bed rest may lead
to muscular atrophy, constipation, increased
risk of deep vein thrombosis and prolonged
hospital stay.
Fluid restriction as a standard treatment
is not advisable, and there are no studies
proving its efficacy in the management of
ascites (Runyon 2013). Fluid restriction
may exacerbate the severity of central
hypovolaemia, which may increase the
secretion of antidiuretic hormone and result in
a further deterioration in renal function. Fluid
restriction may be recommended if dilutional
hyponatraemia of less than 130mmol/L is
present; however, it must always be used with
caution (Garcia-Tsao 2011).
Large-volume paracentesis is the insertion
of a catheter into the peritoneal cavity to drain
the fluid and is the first-line therapy in patients
with large or grade 3 ascites. It is usually
performed by a medical practitioner and can be
undertaken in an outpatient setting; however,
ascites may re-accumulate quickly and require
further drainage. There is no indication
that coagulation or platelet count should be
corrected before this procedure because the risk
of bleeding is low (Pache and Bilodeau 2005).
Large-volume paracentesis should be
performed using an aseptic technique by pulling
the skin down, holding it firmly and inserting
the paracentesis catheter the Z-track technique

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CPD hepatology

for intramuscular injection (Rochling and

Zetterman 2009). This technique reduces the risk
FIGURE 3
of ascitic fluid leaking from the insertion site once Z-track technique
the paracentesis catheter is removed (Figure 3). a) Displace tissues

JO CAMERON
The nurse should be present to ensure the patient
is comfortable and understands the procedure.
Vital signs monitoring must be performed before
the procedure to establish a baseline and then
every 15-30 minutes to assess cardiovascular
stability (Sargent 2009). A complication of
large-volume paracentesis is post-paracentesis
circulatory dysfunction, which manifests as a
low blood pressure, a high heart rate (Salerno
et al 2010) and rapid re-accumulation of ascites
(EASL 2010).
The fluid is then drained via the catheter
continuously over four to six hours. The drain
should not be clamped during this time because
of the increased risk of infection (Sargent
2009). Fluid replacement is required to
prevent cardiovascular complications.
Studies have examined the most effective b) Place paracentesis catheter
fluid to administer for paracentesis, and a
meta-analysis of randomised controlled trials
found that albumin was the most effective
plasma expander in this patient population
(Bernardi et al 2012). Albumin should be
administered at a ratio of 100mL 20% human
albumin solution for every 2-3L of ascites
drained (Moore and Aithal 2006, EASL
2010). In patients undergoing large-volume
paracentesis of 5L or less of ascites, the risk
of developing post-paracentesis circulatory
dysfunction is low and, therefore, evidence
suggests that volume replacement is not
required (Moore and Aithal 2006, EASL
2010). In clinical practice, however, albumin
is often administered for every 2-3L of ascites
drained regardless of the total volume drained
to minimise cardiovascular complications. c) Release tissues
Once the paracentesis catheter is removed,
a dry dressing can be applied over the insertion
site if there is no fluid leaking. If the Z-track
method of insertion is not used, a stoma
collection bag is often required because of
persistent leakage of ascitic fluid from the
paracentesis site (Sargent 2009).
Complete time out activity 3

After large-volume paracentesis, patients

should receive the minimum dose of diuretics
to prevent the re-accumulation of ascites
(Dooley et al 2011). Patients need to have
their blood results monitored for electrolyte
abnormalities and renal impairment. A fluid
balance chart will give an accurate account of
the volume of fluid drained and replaced, and

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daily weights will also show the volume of fluid
lost. It is important that patients are weighed
at the same time each day with the same
clothes to obtain accurate readings. Pain scores
should be obtained before draining ascites
and reassessed throughout the procedure. In
addition, patients should be encouraged to
report any abdominal discomfort or bleeding
around the paracentesis site.
Complete time out activity 4
Contraindicated drugs
Non-steroidal drugs are contraindicated
in patients with ascites because of the
increased risk of developing further sodium
retention, hyponatraemia, and renal failure
(Hampel et al 2001). Drugs that decrease
arterial pressure or renal blood flow such as
angiotensin-converting enzyme inhibitors and
angiotensin-II receptor antagonists should be
avoided because of the increased risk of renal
impairment (Hampel et al 2001). The use
of aminoglycoside antibiotics, for example
gentamicin, is associated with an increased
risk of renal failure (Garcia-Tsao 1998) and
should be used with caution and in association
with regular monitoring of creatinine levels in
patients with ascites.
Management of refractory ascites
Refractory ascites refers to ascites that does
not respond to medical management or
re-accumulates immediately after treatment,
or in patients for whom medical treatment cannot
be given because of untoward side effects such as
muscle cramps or severe electrolyte imbalance.
Treatment options available for refractory
ascites include large-volume paracentesis
with administration of albumin, transjugular
intrahepatic portosystemic shunt (TIPSS),
implanted automated pump system insertion
and liver transplantation.
Transjugular intrahepatic portosystemic shunt
A TIPSS is the insertion of a mesh stent between
the portal vein and the hepatic vein. This
assists in reducing the pressure in the portal
vein and reduces the accumulation of ascites
(Sargent 2009). The TIPSS has been found to
be successful at controlling refractory ascites
in 75% of cases (Riggio et al 2008). It has
also been linked to a decrease in activation of
the renin-angiotensin-aldosterone system and
improved nutritional state because of reduced
pressure on the stomach and gastrointestinal
tract (Riggio et al 2008). However, although
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the TIPSS has been found to be more effective
than large-volume paracentesis in preventing
recurrence of ascites in randomised comparative
trials, it is associated with a much higher risk of
severe encephalopathy (Riggio et al 2008).
A stent reduces the pressure in the portal
vein but also reduces the amount of blood
passing through the liver for detoxification.
Some blood will, therefore, return to the
heart with raised levels of toxins from the
gut, including ammonia. This is one of the
hypothesised causes of hepatic encephalopathy
(Houlston and ONeal 2009) and raised levels
in the blood can lead to neurological changes
associated with hepatic encephalopathy.
Despite the relative success of the TIPSS, it
may not be suitable for all patients (Moore and
Aithal 2006).
Implanted automated pump system
The automated pump system is surgically
implanted subcutaneously, and it draws
ascitic fluid from the abdominal cavity to
the bladder where it is excreted through
normal urination (Bellot et al 2013). Excess
abdominal fluid is drawn automatically and
continually into the bladder. The speed and
quantity of fluid removal may be adjusted
to the clinical and social requirements of
the individual patient. This system helps to
reduce the need for repeat paracentesis.
A study of 40 patients with refractory ascites
who received an implanted pump showed 3 As the nurse caring
that 90% of ascites was removed and the for a patient undergoing
need for large-volume paracentesis was large-volume
reduced. However, there were a large number paracentesis, what
of complications associated with both the observations would
insertion procedure and the system itself, you make to ensure the
for example infection and bladder catheter patients comfort and
dislocation (Bellot et al 2013). There safety, and why?
are larger studies underway looking
at the efficacy of the implanted 4 Drugs that impair
automated pump system in comparison renal function should
to large-volume paracentesis. be avoided in patients
with ascites because
Liver transplantation the kidneys may become
Patients with refractory ascites should be injured as a result of the
considered for liver transplantation because constant need to retain
their median survival is approximately six salt and water and
months (EASL 2010). At this advanced stage the reduced perfusion
of liver disease, transplantation is the only pressure. Make a list
option. Garcia-Tsao (2011) recommended of the drugs commonly
early assessment, before further complications used in your clinical area
cause deterioration in the patients condition, and find out if any of
which may limit his or her suitability these have nephrotoxic
for surgery. Because ascites marks the side effects.
change from compensated liver disease to
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CPD hepatology

decompensated liver disease, transplant susceptibility to infection, and respiratory and

5 Now that you have
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you might like to write
a practice profile.
Guidelines to help you
are on page 62.
assessment may be suggested when this
complication arises as a result of the reduced
survival associated with it (DAmico
et al 2006).
Conclusion
Ascites is a common complication of chronic
liver disease, marking the point where the
liver is no longer able to function effectively
because of the degree of damage present. The
fluid in the peritoneal cavity causes significant
discomfort to patients and increases their
renal dysfunction. Healthcare professionals
should have an understanding of the
treatments and interventions available for
managing ascites. Interdisciplinary working is
important in the management of these patients
to ensure their physical and psychosocial
needs are met.
There are treatments available for patients
with refractory ascites; however, these can have
adverse complications. Liver transplantation is
the optimal treatment and should be considered
for patients when ascites is first identified NS
Complete time out activity 5

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