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Albumin infusion in liver cirrhotic patients

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 REVIEW ARTICLE
Albumin Infusion in Liver Cirrhotic Patients
Ni Made Renny A. Rena, I Dewa Nyoman Wibawa
Department of Internal Medicine, Faculty of Medicine, University of Udayana-Sanglah Hospital. Jl. PB. Sudirman,
Denpasar Bali, Indonesia.
Correspondence mail to: pipfkui@yahoo.com
ABSTRACT
Albumin infusions have been used for many years in
the management of patients with decompensated cirrhosis
in an attempt to reduce the formation of ascites, to improve
circulatory and renal function, or in SBP patients. While
some of these indications for albumin infusions are
supported by the results of randomised studies, others are
based on clinical experience and have not been proved in
prospective investigations. Therefore, the use of albumin
infusions in patients with cirrhosis is still controversial.
However, despite the controversies, the use of albumin at
least has been proven to be safe. Some guidelines
recommended the use of albumin infusion in
decompensated cirrhosis with spontaneous bacterial
peritonitis, hepatorenal syndrome, large volume
parecentesis and decompensated cirrhosis with
complications.
Key words: albumin, liver cirrhotic.
162
INTRODUCTION
Liver cirrhosis, especially in the presence of
decompensation, is characterized by significant
hemodynamic changes. These changes consist of
systemic arterial vasodilatation, and effective arterial
underfilling, which stimulate the renin aldosteron
angiotensin system and associated with renal retention
of sodium and water, and ascites is one of their clinical
manifestations. In addition, patients with liver cirrhosis
are susceptible to sepsis, especially bacterial infections.
Once infection develops, renal failure, shock and
encephalopathy can follow, all of which adversely
affect survival and increase mortality.
Albumin is the most abundant protein in the
circulation, which has multiple function that can be used
in cirrhotic patients with those complications mention
above. The main physiologic function of albumin is to
maintain intravascular volume and colloid osmotic
pressure. The other physiologic functions of albumin
include ligand binding and transport of various
molecules, such as hormones, lipid and drugs. In
addition to having antioxidant and antiinflammatory
actions, and stabilizing effect on the endothelium.1-4
The use of albumin for many of these indications is
controversial, some studies support it based on the
decreasing of mortality rate of these patients. The other
indication for albumin use in cirrhotic patients is
extracorporeal albumin dialysis, which has shown
promise for the treatment of hepatic encephalopathy.
Some studies debate this mostly because of the cost of
albumin infusions, the lack of clear-cut benefits for
survival, and for fear of transmitting unknown viruses
such as hepatitis B, hepatitis C and also HIV adding to
the controversy, allthough some studies say it is safe.1,5
Finally, it still requires further discussion, studies and
evidences for administration albumin in cirrhotic
patients.
Vol 42 • Number 3 • July 2010
ALBUMIN
In healthy individuals, albumin is the most
abundant plasma protein, accounting for 55-60% of the
measured serum protein. It consists of a single
polypeptide chain of 585 amino acids with a molecular
weight of 66 500 Da. The mature, circulating molecule
is arranged in a series of α-helices, folded and held by
17 disulphide bridges.2
The serum albumin concentration is a function of
its rate of synthesis and degradation and its distribution.
Albumin synthesis takes place only in the liver, with
the rate of synthesis 197 mg/kg body weight/day or
about 12-25 g of albumin per day. Albumin is not stored
by the liver but secreted into the portal circulation as
soon as it is manufactured. Physiologically, the liver
can increase albumin synthesis to only 2-2.7 times
normal. Some factors required for the albumin
synthesis are suitable nutritional, hormonal and osmotic
environment. The colloid osmotic pressure (COP) of
the intertitial fluid bathing the hepatocyte is the most
regulator of albumin synthesis. Some factors to modify
albumin metabolism are on Table 1.1,2,6
Table 1. Factors that modify albumin metabolism2
Reduced albumin synthesis
Decrease gene Trauma, sepsis, inflammation (cytokines)
transcription
Hepatic disease
Diabetes
Decrease growth hormone
Decrease corticosteroids (in vitro)
Ribosome Fasting, especially protein depletion
disaggregation
Each day, the total body albumin pool measure
about 3.5-5.0 g/kg body weight or about 250-300 g for
a healthy 70 kg adult. Distribution of albumin to the
intravascular compartment is about 42%, and the rest
being in extravascular compartment. Most of albumin
in extravascular space is recovered back into the
circulation by lymphatic drainage. Albumin lost into the
intestinal tract about 1 g, and only few grams (about
10-20 mg/day) pass through the kidney as urinary loss.2
Albumin degradation in a 70 kg adult every day is
around 14 g or 5% of daily whole body protein turn
over. Albumin is broken down mostly in muscle and
skin (40-60%) and other organs in the body such as
liver, kidney and gastrointestinal tract.2
Albumin being extensively studied and well
established has numerous functions used in many
clinical situations, including:1,2,7
• Maintaining colloidal osmotic pressure
Albumin Infusion in Liver Cirrhotic Patients
• Ligand binding of numerous endogenous and
exogenous compounds
• Effective as plasma buffer
• Antioxidant effects
• Endothelial stabilization
• Anti coagulant
HYPOALBUMINEMIA IN LIVER CIRRHOTIC
PATIENTS
Liver cirrhotic is a protein catabolic disease, which
at the advanced stages is usually associated with loss
of lean body mass and decreased albumin concentra-
tion. Moriwaki, et al in 2001 found that 40% with
protein malnutrition, 10% with energy malnutrition, 30%
with protein-energy malnutrition and 20% with normal
nutritional state. Other study by Merli, et al in 1996
found malnutrition is strongly associated with the
deterioration of liver function, and considered as a
dependent risk factor for mortality in cirrhotic patients.4,8
Hypoalbuminemia in liver cirrhotic patients is due
to:4,9
1. Decrease of albumin synthesis in the liver
2. Increase of albumin catabolism
3. Vascular leakage due to increase of membarane
permeability such as ascites and oedem.
4. Capillary leakage, such as sepsis and shock.
ALBUMIN INFUSION IN LIVER CIRRHOTIC PATIENTS
The indication of giving albumin in liver cirrhotic
patients are:
Spontaneous Bacterial Peritonitis (SBP)
Spontaneous bacterial peritonitis (SBP) is a
common and often fatal complication of cirrhosis with
high mortality rate. Mortality in patients with SBP is
caused by gastrointestinal bleeding, liver failure and
around 30-40% fall into Hepato Renal Syndrome.1,4
In patients with SBP, there is a risk that their
systemic hemodynamic parameters can deteriorate,
with further arterial and splanchnic vasodilatation.
These patients are, therefore, at high risk of develop-
ing renal insufficiency. Peritonitis and the release of
high level of vasoactive cytokines in sepsis are
considered as the patophysiological explanation for the
association between SBP and renal insufficiency. Va-
soactive cytokine worsens the arterial vasodilatation
and results in secondary activation of neurohormonal
system. Therefore, the use of albumin is to maintain
intravascular volume and to repair renal perfussion.1,3,4
Pau Sort, et al. at 1999, have done a randomized
study in 7 hospitals in Spain and found that the
163
Ni Made Renny A. Rena
administration of albumin prevents renal impairment
and reduces mortality in patients with cirrhosis and
spontaneous bacterial peritonitis. The incidence of
renal impairment was significantly lower among
patients treated with cefotaxime and albumin than
among patients treated with cefotaxime alone, which
is 29%, by contrast, the group treated with cefotaxime
and albumin was only 10%. However, this study
received many criticisms because of unblind random-
ization study and without the insertion of CVP lines in
all the patients in order to know the relationship with
the disorder of renal function. Besides, this study also
didn’t make comparison between albumin and others
plasma expanders.10,11
Study in 2005 by Fernandez, et al. compared the
role of albumin and hydroxyethyl starch (HES) to
prevent renal failure in SBP patients, found that
albumin has it’s superiority than HES.12 Another study
compared albumin, crystalloid fluid and artificial
colloid give the same result.13 Although albumin has a
significant role in SBP patients with severe disturbance
of liver and renal function, but it’s use is still debated
because of the high cost. 3,14,15 Other opinion says
patients with sepsis have an increase vascular
permeability, therefore albumin as well as other
molecule may became far less efficient in maintaining
effective plasma volume for longer period because of
rapid leakage from circulation. It still need to do
further study.3 The third phase of study has been
done until now about the role of human albumin in
cirrhotic patients with infection other than SBP. This
study was held in February 2008.16
The other practice guidelines to follow are
regarding to recommendation of American Associa-
tion for the Study of Liver Diseases (AASLD) and
Indonesian Association for the Study of the Liver. It
suggested that patient clinical suspected of SBP should
receive albumin 1,5 g/kg body weight within 6 hours of
detection and should be given lower dose 1 g/kg body
weight on day 3.4,14,17
Hepato Renal Syndrome
Hepatorenal syndrome (HRS) is a dreaded
complication of advanced cirrhosis. HRS is defined as
the development of renal failure in patients with
advanced liver failure (acute or chronic) in the absence
of any identifiable causes of renal pathology. Untreated
type 1 HRS carries a grim prognosis and high mortal-
ity as 80% in second week and only 10% of patients
survived more than 3 months. The prognosis can be
assessed by CHILD-PUGH and MELD (Model of
End-Stage Liver Disease) as an independent predictor
164
Acta Med Indones-Indones J Intern Med
of death which is with score of 20 or more being only
1 month compared with 8 months in those with a MELD
score <20. By contrast, patients with type 2 HRS have
a much better median survival, approximately 6
months.18
The hallmark of HRS is renal hypoperfusion, which
is caused by reduction renal blood flow result from
condition of systemic arterial vasoconstriction. The
effective arterial underfilling is caused by splanchnic
vasodilatation. Renal vasoconstriction occurs as the
result of both active renal vasoconstriction and
reducing systemic vasodilator factor such as
prostaglandine, Nitric Oxyde (NO) and natriuretic
peptide as the compensated action due to systemic
arterial vasodilatation.4,18
The goal of treatment in SHR is to reduce
systemic vasodilatation and increase renal blood flow.
Besides renal transplantation and hemodialysis,
pharmacotherapies have been recommended in
systemic vasoconstrictors as vasopressin analogs or
α-adrenergic agonists. The use of albumin to improve
arterial underfilling is also recommended in
combination with vasoconstrictors, ocreotide or
midodrine. Some authors believe that albumin can
improve the efficacy of vasoconstrictors therapy.
Angeli et al. in 2003 reported the superiority of
administration dopamin together with albumin at non
intensive ward in type 1 HRS.19 Another pilot study
done by Duvoux, et al. using norepinephrine plus
albumin, reports 83% success in reversing type 1 HRS.
American Association for the Study of Liver Diseases
(AASLD) recommended that albumin infusion plus
administration of vasoactive drugs such as ocreotide
and midodrine should be considered in the treatment
of type 1 HRS (level II-1). Indonesian Association for
the Study of the Liver also recommended that albumin
infusion given to prevent HRS in SBP patients
combined with cefotaxime can decrease mortality and
frequency of HRS. Other study shows it can improve
renal function to 60-70%. The dose given is 1 g/kg
intravenously in day 1 and followed by 20-40 g/day for
5-15 days or stopped when CVP >18 cm H 2O.
However, for the preventive dose is 1,5 g/kg body
weight in day 1 and 1 gram / kg body weight in the
next 48 hours.3,4,14,17,18
A prospective, randomized, controlled study shows
that Molecular Adsorbent Resirculating System
(MARS), an extracorporeal albumin dialysis, can
improved clinical and biochemical parameters in type
1 HRS patients. The advantage of using MARS in HRS
relies on the assumption that removing albumin-bound
Vol 42 • Number 3 • July 2010
toxins which have a detrimental effect on hepatocytes
and other organs, including the kidney, will stabilize liver
function and improve other end organ damage.18
Moreau et al. in 2002 doing the largest
retrospective study on the use of terlipressin for HRS
did not find any difference in patient outcomes
irrespective of whether they received albumin infusions
as well as terlipressin. However, Uriz et al. in 2000
found that terlipressin combined with albumin was
effective for type 1 HRS. Other study found one thirds
patients with ischemia as side effect from using
ornipressin and albumin.1,13,16-18
Tabel 2. Definition of refractory ascites20
Diuretic-resistant ascites
Ascites that cannot be mobilized with dietary sodium restriction
(50mEq/day) and intensive diuretic treatment (spironolactone
400 mg/day plus furosemide 160 mg/day) for at least 1 week or
which recurs early despite the above measures.
Diuretic-intractable ascites
Ascites that cannot be mobilized or prevented from recurring,
due to the development of diuretic-induced complications,
that precludes the usage of an effective diuretic dosage.
Plasma Expansion in Large Volume Paracentesis
The circulatory disturbances seen in advanced
cirrhosis lead to the development of ascites, which can
become refractory to diet and medical therapy.
Approximately 10-20% of patients with ascites
have adequate natriuresis and clinical response to
dietary sodium restriction alone, and the majority of
the remaining patients respond to diuretic therapy.
However, around 10% of patients do not respond to
the above measures, or develop complications to
diuretic therapy, and these patients are classified as
having refractory ascites. Prognosis for this subgroup
of patients is poor, with a 50% 1-year mortality. The
International Ascites Club recently redefined
refractory ascites.20
One of the management of refractory ascites is
Large Volume Paracentesis (LVP). Some studies
concluded that serial therapeutic paracentesis can be
performed safely and effectively with volume less than 5
litres.17,20-22 Circulatory dysfunction can develop after
large-volume paracentesis. This is caused by
exaggerated systemic arterial vasodilatation, effective
intravascular volume depletion, and elevated renin and
aldosterone levels. Clinically it’s recognized as renal
impairment and electrolyte imbalance, particularly
hyponatremia.1
Albumin infusion seems to be the most appropriate
way to prevent this complication of paracentesis. The
Albumin Infusion in Liver Cirrhotic Patients
argument against albumin infusion in conjunction with
paracentesis use is further fuelled by the finding that a
5l paracentesis without albumin infusion was not
associated with any changes in central blood volume,
serum sodium levels or renal function. However some
consensus still recommended albumin infusion in
LVP. 1,23-27
American Association for the Study of Liver
Diseases (AASLD) recommended that albumin
infusion should be given with dose 6-8 g/1 litre ascites
fluid removed for paracentesis volumes of greater than
5-6 litres. Fifty percents should be given in the first 1
hour (maximum 170 mL/hr) and the remain in the next
6 hours.14,15
The uses of albumin led to studies investigating
substitute fluid for albumin that can prevent circula-
tory failure after paracentesis. It’s found mannitol has
the same effectivity as albumin, but not others plasma
expanders like dextran and polygelyne. Hydroxyethyl
starch (HES) is still controversy, it concluded there the
use was no significantly differences than albumin. It
can be tolerated by liver cirrhotic patients, but it still
need further investigation about lower weight loss
compare to albumin.28-31
Albumin Level <2.5 g/dL in Liver Cirrhotic Patients
with Complications
Some complications can occur in liver cirrhotic
patients, the low level of albumin leads them into worst
condition. Therefore, Indonesian Association for the
Study of the Liver in 2003 suggest albumin infusion for
those conditions. The dose is different albumin level in
every kg body weight.4
Other complications such as electrolyte
abnormalities, especially hyponatremia and
hyperkalemia, are common in patients with advanced
cirrhosis. These abnormalities can occur spontaneously,
or more often follow the use of diuretics. Hyponatremia
is usually the result of overactivity of vasopressin, in
response to a reduction in the effective arterial blood
volume Diuretic-induced electrolyte abnormalities and
blood-volume contraction can also lead to the
development of hepatic encephalopathy in patients with
cirrhosis. In a study conducted in cirrhotic patients with
diuretic-induced hepatic encephalopathy by Jalan R et
al., showed infusion of a 4.5% albumin solution was
comparably effective to infusion of a colloid solution in
relation to increasing plasma volume. Both treatments
caused similar reductions in plasma ammonia
concentrations, and increased in urinary ammonia
excretion. The improvement of hepatic encephalopa-
thy grade, although it was only sustained at 72 h in the
165
Ni Made Renny A. Rena Acta Med Indones-Indones J Intern Med

group who received albumin infusions, and was
associated with a reduction in plasma malondialdehyde,
which suggested a reduction in oxidative stress.7
As the use of albumin in liver cirrhotic patients is
still controversial, not only because of lack of clear cut
benefits for survival, but also because of the high cost
of albumin infusion. Therefore, many studies done to
compare effectivity between albumin and other fluids
in SBP patients and ascites patients whose done LVP
is shown in Table 3.
The debate about the use of albumin in the
critically ill patients has been stimulated by the
publication of a meta-analysis which reviewed 32
randomized controlled trials published between 1975
and 1998, in which albumin was used in treatment of
hypovolemic, burnt or hypoalbuminaemic patients. The
data suggested that the use of albumin in these groups
resulted in six additional deaths per 100 patients. The
controversy seems to have centred on the validity of
the conclusions drawn from such a heterogenous group
of studies, samples of the studies were small, and there
were few deaths. Some of the responses suggested
that capillary leakage may explain the increased
mortality, and presented data showing that albumin
leakage was greater in critically ill patients than in
patients after major surgery. Thus, infusion of albumin

Table 3. A summary of studies to date that have compared the use of albumin versus
various colloids for the management of complications of cirrhosis1
Study Colloid Patient population Outcome
Moreau et al Albumin vs Ascitic patient undergoing Albumin group: significantly fewer
(2006) 3,5% LVP (Alb n=30; liver-related complications
polygeline Polygeline n=38) adjusted per 100 patient days and
lower hospital costs. No
difference in survival
Fernandez Albumin vs Ascitic patients with SBP Albumin group: improved
et al (2005) HES (Albumin group, n = 10 systemic hemodynamics, and
200/0.5 Starch group, n = 10) decreased endothelial activation
with no further increase in nitric
oxide derivatives
Garcia- Albumin vs Ascitic patients undergoing No significant difference in the
Compean et dextran 40 LVP (Albumin group, development of complications
al. (2002) n = 48. Starch group, related to LVP, ascites recurrence
n = 48) and survival. Dextran 40® was
not as efficacious as albumin in
the prevention of paracentesis-
induced circulatory dysfunction
Altman et al Albumin vs Ascitic patients undergoing No significant difference between
(1998) HES LVP (Albumin group, the groups in the prevention of
n = 33. Starch group, n = complications related to LVP
27)
Gines et al Albumin vs Ascitic patients undergoing Albumin was significantly better
(1996) dextran 70 total paracentesis (Albumin than dextran 70® and polygeline
& polygeline group, n = 33. Starch in the prevention of paracentesis-
group, n = 27) induced circulatory dysfunction
which was associated with
shorter time to readmission and
shorter survival
Fassio et al Albumin vs Ascitic patients undergoing No significant difference between
(1992) dextran 70 LVP (Albumin group, the groups in the development of
n = 21. Starch group, complications related to LVP,
n = 20) hospital readmission and survival.
The cost of using dextran 70®
was significantly lower.
Salerno et Albumin vs Ascitic patients undergoing No significant difference between
al (1991) hemaccel total paracentesis (Albumin the groups in the development of
group, n = 27.Hemaccel complications related to total
group, n = 27) paracentesis, hospital
readmission and survival.
Planas, et al Albumin vs Ascitic patients undergoing No significant difference between
(1990) dextran 70 total paracentesis (Albumin the groups in the development of
group, n = 43. Starch complications related to LVP,
group, n = 45) hospital readmission and survival.
Albumin was more efficacious in
the prevention of paracentesis-
induced circulatory dysfunction

166
Vol 42 • Number 3 • July 2010
in the critically ill patients would not increase the
intravascular albumin concentration, and would
exacerbate interstitial oedema.2, 32
Further explanations of why albumin might not work
is because of the beneficial effects of albumin in the
circulation, such as the binding of toxins, heavy metals
and drugs, are detrimental outside of the circulation,
given the increase in capillary permeability during critical
illness. There may also be the adverse immunological
effects of albumin transfusion that could explain the
increase in mortality suggested by this meta analysis.2,
32
Arroyo and Gines in 2000 wrote a controversial
article about whether there is still a need for albumin
infusions to treat patients with liver disease. There is a
strong body of evidence indicating that renal functional
abnormalities and ascites formation in cirrhosis are the
final consequence of circulatory dysfunction,
characterized by marked splanchnic arterial vasodila-
tation causing a reduction in effective arterial blood
volume and homeostatic activation of vasoconstrictor
and antinatriuretic mechanisms.In contrast, there is no
evidence to support a role for reduced vascular oncotic
pressure due to hypoalbuminaemia in the pathogenesis
of ascites.33
Saline Versus Albumin Evaluation (SAFE) study, a
randomized clinical trial in Australia and New Zealand
included a heterogeneous population of nearly 7000
critically ill patients requiring intravascular fluid
resuscitation. The Australian and New Zealand
Intensive Care Society Clinical Trials Group set out to
determine the safety of fluid resuscitation with 0.9%
normal saline versus 4% human albumin on a number
of patient outcomes. There were no significant
differences between the groups with respect to 28-
day mortality, incidence of organ failure, intensive care
unit or hospital length of stay, or duration of mechanical
ventilation or renal replacement therapy.34
Indonesian Association for the Study of the Liver
suggested that infusion of albumin 20% with maximum
rate is 1 mL/minute, and for albumin 5% is 2-4 mL/
minute. Some complications can occur after giving
albumin infusion such as heart decompensated, lung
oedema, increasing of risk of bleeding like the rupture
of esophageal variceal, drugs/metals/hormones
accumulation in intestitial space, increasing of
nitrogen bodies, and also some studies found viral
transmission after albumin infusion.4 It’s important to
monitor hemodynamic status including vital sign,
coagulation (Prothrombin Time and Activated Partial
Thromboplastin Time), renal function test and level of
albumin serum after transfusion.4
Albumin Infusion in Liver Cirrhotic Patients
CONCLUSION
Liver cirrhosis, especially in the presence of
decompensation, is characterized by significant
hemodynamic changes. These changes consist of
systemic arterial vasodilatation, and effective arterial
underfilling associated with renal retention of sodium
and water which is shown as ascites, hepato renal
syndrome, and spontaneous bacterial peritonitis.
Albumin, with its multiple physiological effects of
volume expansion, anti oxidation and endothelial
protection, would seem to be the ideal treatment
solution for patients with cirrhosis, especially those
with complications. The use of albumin in patients with
cirrhosis is controversial; there is evidence to support
its use in the management of complications of
cirrhosis, but there are also arguments against its use
in cirrhosis, especially since albumin infusions are costly
and survival has not been shown to be improved with
this treatment.
Despite this controversies, safety of the use of
albumin at least has been proven. Some guidelines
recommended by American Association for the Study
of Liver Diseases (AASLD) and Indonesian
Association for the Study of the Liver suggested the
use of albumin infusion in decompensated cirrhosis with
spontaneous bacterial peritonitis, hepato renal
syndrome, large volume parecentesis and cirrhosis with
complication. Future efforts still need to define the
other indications for albumin use, dose of albumin
required and predictors of response, so that patients
gain the maximum benefit from its administration.
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