AASLD PRACTICE GUIDELINE
Management of Adult Patients With Ascites Due to
Cirrhosis
Bruce A. Runyon
Preamble
These recommendations provide a data-supported ap-
proach. They are based on the following: (1) formal re-
view and analysis of the recently published world
literature on the topic (Medline search); (2) the American
College of Physicians’ Manual for Assessing Health Prac-
tices and Designing Practice Guidelines1; (3) policy guide-
lines, including the American Association for the Study of
Liver Diseases’ Policy Statement on Development and
Use of Practice Guidelines and the American Gastroen-
terological Association’s Policy Statement on the Use of
Medical Practice Guidelines,2,3; and (4) the author’s 22
years of experience in the clinical and laboratory investi-
gation of, and care of patients with, this problem, includ-
ing 7 years’ experience in a liver unit in which
approximately 60% of patients have ascites.
Intended for use by physicians, these recommenda-
tions suggest preferred approaches to the diagnostic, ther-
apeutic, and preventative aspects of care. They are
intended to be flexible, in contrast to standards of care,
which are inflexible policies designed to be followed in
every case. Specific recommendations are based on rele-
vant published information. Cost-effectiveness and cost-
benefit data should be incorporated in the appropriate
setting. In an attempt to characterize the quality of evi-
dence supporting recommendations, the Practice Guide-
lines Committee of the American Association for the
Study of Liver Diseases requires a grade to be assigned and
reported with each recommendation (Table 1).
These guidelines were developed for the care of adult
patients with clinically detectable ascites. Although the
general approach may be applicable to children, the pedi-
atric data base is much smaller and there may be unantic-
ipated differences between adults and children. Patients
with ascites that is detected by imaging modalities but is
not yet clinically evident are not included because of the
lack of published information regarding the natural his-
tory of this entity.
Background
Cirrhosis was the tenth leading cause of death in the
United States, according to a 2000 Vital Statistics Report,
in which data was collected through 1998.4 Ascites is the
most common of the 3 major complications of cirrhosis;
the other complications are hepatic encephalopathy and
variceal hemorrhage.5 Approximately 50% of patients
with “compensated” cirrhosis, i.e., without having devel-
oped one of these complications, develop ascites during
10 years of observation.5 Development of fluid retention
in the setting of cirrhosis is an important landmark in the
natural history of chronic liver disease: approximately
50% of patients with ascites succumb in 2 years.6 Many
patients are referred for liver transplantation after devel-
opment of ascites.
Literature Review
A Medline search from 1966 through 2002 was per-
formed; search terms included ascites, diet therapy, drug
therapy, radiotherapy, surgery, and therapy. The search
involved only papers published in English and involving
humans. A manual search of the author’s files was also
performed. The search yielded 1,867 papers including
411 published since a similar search was performed in
1997 in preparation for writing the previous guideline on
ascites.7
Evaluation and Diagnosis
History
Most patients (approximately 85%) with ascites in the
United States have cirrhosis.8 In about 15% of patients
with ascites, there is a nonhepatic cause of fluid retention.
Successful treatment is dependent on an accurate diagno-
sis of the cause of ascites; e.g., peritoneal carcinomatosis
does not respond to diuretic therapy. Patients with ascites
should be questioned about risk factors for liver disease.
Those who lack an apparent cause for cirrhosis should also
Abbreviations: SAAG, serum-ascites albumin gradient; PMN, polymorphonu-
clear leukocyte; TIPS, transjugular intrahepatic portasystemic stent-shunt; SBP,
spontaneous bacterial peritonitis.
From the Rancho Los Amigos Medical Center, Downey, CA.
Received September 9, 2003; accepted September 17, 2003.
This is a revised and updated guideline based on the previously published version
(HEPATOLOGY 1998;27:264–272).
Address reprint requests to: Bruce A. Runyon, M.D., Chief, Liver Service, Loma
Linda University Medical Center, 11234 Anderson Street, Room 1556, Loma
Linda, CA 92354. E-mail: brunyon@ahs.llumc.edu; fax: 909-558-0274.
Copyright © 2004 by the American Association for the Study of Liver Diseases.
Published online in Wiley InterScience (www.interscience.wiley.com).
DOI 10.1002/hep.20066
1
be questioned about lifetime body weight; nonalcoholic
steatohepatitis has been concluded to be causative in
many of these patients.9 Past history of cancer, heart fail-
ure, or tuberculosis is also relevant. Hemophagocytic syn-
drome can masquerade as cirrhosis with ascites.10 These
patients have fever, jaundice, and hepatosplenomegaly,
usually in the setting of lymphoma or leukemia.10
Physical Examination
The presence of a full, bulging abdomen should lead to
percussion of the flanks. If the amount of flank dullness is
greater than usual (i.e., if the percussed air-fluid level is
higher than normally found on the lateral aspect of the
abdomen with the patient supine), one should test for
“shifting.” Approximately 1,500 mL of fluid must be
present before flank dullness is detected.11 If no flank
dullness is present, the patient has less than a 10% chance
of having ascites.11 The fluid wave and puddle sign are not
useful.11 Ascites due to alcoholic cardiomyopathy can
mimic that due to alcoholic cirrhosis. Jugular venous dis-
tension is present in the former but not in the latter.
The physical examination for detecting ascites in the
obese patient is problematic. An abdominal ultrasound
may be required to determine with certainty if fluid is
present.
The diagnosis of new-onset ascites is suspected on the
basis of the history and physical examinationand usually
confirmed by successful abdominal paracentesis and/or
ultrasound. The diagnosis of the cause of ascites forma-
tion is based on the results of the history, physical, and
ascitic fluid analysis. In general, few other tests are re-
quired. However, the liver is commonly imaged (usually
with ultrasound) to screen for hepatocellular carcinoma,
portal vein thrombosis, and hepatic vein thrombosis.
Abdominal Paracentesis
Abdominal paracentesis with appropriate ascitic fluid
analysis is probably the most rapid and cost-effective
method of diagnosing the cause of ascites.12,13 Fluid due
to portal hypertension can be readily differentiated from
fluid due to other causes.8 Also, in view of the high prev-
alence of ascitic fluid infection at the time of admission to
the hospital, an admission surveillance tap may detect
unexpected infection.14
Although older published series reported a relatively
high morbidity, and even mortality, when trocars were
used for paracentesis, more recent studies regarding para-
centesis complications in patients with ascites docu-
mented no deaths or infections caused by the
paracentesis.15 Complications were reported in only
about 1% of patients (abdominal wall hematomas), de-
spite the fact that 71% of the patients had an abnormal
prothrombin time.15 Although more serious complica-
tions (hemoperitoneum or bowel entry by the paracente-
sis needle) occur,16 they are sufficiently unusual
(�1/1,000 paracenteses) that they should not deter per-
formance of this procedure. It is the practice of some
physicians to give blood products (fresh frozen plasma
and/or platelets) routinely before paracentesis in cirrhotic
patients with coagulopathy. This policy is not data-sup-
ported. The risks and costs of prophylactic transfusions
exceed the benefit.
In the past, the midline was usually chosen as the site
for paracentesis. However, the abdominal wall in the left
lower quadrant, 2 finger breadths cephalad and 2 finger
breadths medial to the anterior superior iliac spine, has
been shown to be thinner and with a larger pool of fluid
than the midline.17 If the fluid is difficult to localize by
examination because of obesity, ultrasonography can be
useful.
There are few contraindications to paracentesis. Co-
agulopathy should preclude paracentesis only when there
is clinically evident fibrinolysis or clinically evident dis-
seminated intravascular coagulation.15 These conditions
occur in less than 1 per 1,000 procedures. There is no
data-supported cutoff of coagulation parameters beyond
which paracentesis should be avoided.15
Recommendations
1. Abdominal paracentesis should be performed and
ascitic fluid should be obtained from inpatients and out-
patients with clinically apparent new-onset ascites.
(Grade II-3)
2. Since bleeding is sufficiently uncommon, the pro-
phylactic use of fresh frozen plasma or platelets before
paracentesis is not recommended. (Grade III)
Ascitic Fluid Analysis
Future outcomes studies are required to determine the
optimal testing strategy. Meanwhile, an algorithm ap-
proach seems preferable to ordering a large number of
tests on most specimens. If uncomplicated cirrhotic as-
cites is suspected, only screening tests (e.g., cell count and
differential, albumin and total protein concentration) are
Table 1. Quality of Evidence on Which a Recommendation Is
Based*
Grade Definition
I Randomized controlled trials
II-1 Controlled trials without randomization
II-2 Cohort or case-control analytic studies
II-3 Multiple time series, dramatic uncontrolled experiments
III Opinions of respected authorities; descriptive epidemiology
*Data from Woolf and Sox.3
2 RUNYON HEPATOLOGY, March 2004
performed on the initial specimen. If the results of these
tests are unexpectedly abnormal, further testing can be
performed on another ascitic fluid sample. Also, many
laboratories save an aliquot of fluid for a few days; this
fluid can be tested if the specimen has been handled prop-
erly. However, since most specimens are consistent with
uncomplicated cirrhotic ascites, no further testing will be
needed in the majority of patients.
If ascitic fluid infection is suspected (fever, abdominal
pain, or unexplained encephalopathy), bacterial culture in
blood culture bottles should be performed. Use of a urine
dipstick to detect neutrophils in ascitic fluid takes only 90
seconds to 2 minutes; if confirmed by other studies, this
may become a routine method of providing early suspi-
cion of infection.18,19 Automated cell counting has been
shown to be accurate; the result is rapidly available and
thus may replace the manual cell count.20 Additional test-
ing, e.g., total protein, lactate dehydrogenase, and glucose
to assist in differentiating spontaneous from secondary
bacterial peritonitis, can be performed on the initial spec-
imen based on clinical judgment.21 An ascitic fluid carci-
noembryonic antigen greater than 5 ng/mL or ascitic fluid
alkaline phosphatase greater than 240 units/L has also
been shown to be accurate in detecting gut perforation
into ascitic fluid.22
The serum-ascites albumin gradient (SAAG) has been
proved in prospective studies to categorize ascites better
than the total-protein-based exudate/transudate concept
and better than modified pleural fluid exudate/transudate
criteria.8,23 Calculating the SAAG involves measuring the
albumin concentration of serum and ascitic fluid speci-
mens obtained on the same day and subtracting the ascitic
fluid value from the serum value. If the SAAG is greater
than or equal to 1.1 g/dL (11g/L), the patient has portal
hypertension, with approximately 97% accuracy.8 Pa-
tients who have portal hypertension plus a second cause
for ascites formation also have a SAAG greater than or
equal to 1.1g/dL.
Patients undergoing serial outpatient therapeutic para-
centeses probably should be tested only for cell count and
differential (the author has detected 8 episodes of sponta-
neous bacterial peritonitis in approximately 400 paracen-
teses in a paracentesis clinic in 2 years [Zeid Kayali, Reza
Khoshini, B.A.R., outpatient management of refractory
ascites, unpublished observations, 2003]). Bacterial cul-
ture is not necessary in asymptomatic patients undergoing
serial large-volume paracenteses.24,25
The most expensive tests are the cytology and smear
and culture for mycobacteria; these tests should probably
be ordered only when there is a high pretest probability of
occurrence of the disease under consideration. The ascitic
fluid cytology is positive only in the setting of peritoneal
carcinomatosis.26 The sensitivity of cytology in detecting
peritoneal carcinomatosis is 96.7% if 3 samples are sent
and processed promptly; the first sample is positive in
82.8% and at least 1 of 2 samples is positive in 93.3%.26
In this study, 50 mL of fresh warm ascitic fluid were
hand-carried to the laboratory for immediate processing.
Patients with peritoneal carcinomatosis usually have a his-
tory of a breast, colon, gastric, or pancreatic primary car-
cinoma. The sensitivity of smear for mycobacteria is
approximately 0%; the sensitivity of fluid culture for my-
cobacteria is approximately 50%.27 Only patients at high
risk for tuberculous peritonitis (e.g., recent immigration
from an endemic area or acquired immunodeficiency syn-
drome)28 should have testing for mycobacteria on the first
ascitic fluid specimen. Laparoscopy with biopsy and my-
cobacterial culture of tubercles are the most rapid and
accurate methods of diagnosing tuberculous peritonitis.
Multiple prospective trials have shown that bacterial
growth occurs in only about 50% of instances when as-
citic fluid with a polymorphonuclear leukocyte (PMN)
count greater than or equal to 250cells/mm3 (0.25 �
109/L) is cultured by older methods as compared to ap-
proximately 80% if the fluid is inoculated into blood
culture bottles at the bedside.29,30
Recommendations
3. The initial laboratory investigation of ascitic fluid
should include an ascitic fluid cell count and differential,
ascitic fluid total protein, and SAAG. (Grade II-2)
4. If ascitic fluid infection is suspected, ascitic fluid
should be cultured at the bedside in blood culture bottles.
(Grade II-2)
5. Other studies can be ordered based on pretest
probability of disease (Table 2). (Grade III)
Differential Diagnosis
Although cirrhosis is the cause of ascites formation in
most patients, approximately 15% have a cause other than
liver disease, including cancer, heart failure, tuberculosis,
or nephrotic syndrome.8 Approximately 5% of patients
with ascites have 2 or more causes of ascites formation,
i.e., “mixed” ascites.8 Usually, these patients have cirrhosis
plus 1 other cause, e.g., peritoneal carcinomatosis or peri-
toneal tuberculosis. Many patients with enigmatic ascites
are eventually found to have 2 or even 3 causes for ascites
formation (e.g., heart failure, diabetic nephropathy, and
cirrhosis due to nonalcoholic steatohepatitis). In this set-
ting, the sum of predisposing factors leads to sodium and
water retention when each individual factor might not be
severe enough to cause fluid overload.
HEPATOLOGY, Vol. 39, No. 3, 2004 RUNYON 3
Treatment of Ascites
Appropriate treatment of patients with ascites depends
on the cause of fluid retention. SAAG can be helpful
diagnostically as well as in decision-making regarding
treatment. Patients with low SAAG ascites usually do not
have portal hypertension and, with the exception of ne-
phrotic syndrome, do not respond to salt restriction and
diuretics.13 In contrast, patients with a high SAAG have
portal hypertension and usually are responsive to these
measures.13
The remainder of this guideline is applicable only to
patients with cirrhosis as the cause of their ascites. Im-
provement in the outcome of patients with nonportal-
hypertension-related ascites depends on successful
treatment of the underlying disorder.
Alcohol-induced liver injury is perhaps the most re-
versible cause of liver disease that leads to high albumin
gradient ascites.13 One of the most important steps in
treating ascites in this setting is to treat the underlying
liver disease by convincing the patient to stop drinking
alcohol. In a period of months, abstinence can result in
dramatic improvement in the reversible component of
alcoholic liver disease. One recent study demonstrates
that patients who have Child-Pugh C cirrhosis due to
alcohol and who stop drinking have an approximately
75% 3-year survival, but all those who continue to drink
die in 3 years.31 Ascites may resolve or become more re-
sponsive to medical therapy with abstinence and time.
Nonalcoholic liver diseases are less reversible; by the time
ascites is present, these patients may be better candidates
for liver transplantation than protracted medical therapy.
The mainstays of treatment of patients with cirrhosis
and ascites include (1) education regarding dietary so-
dium restriction (2000 mg per day [88 mmol per day])
and (2) oral diuretics.12,13 More stringent dietary sodium
restriction can speed mobilization of ascites. Fluid loss
and weight change are directly related to sodium balance
in patients with portal-hypertension-related ascites. It is
sodium restriction, not fluid restriction, which results in
weight loss; fluid follows sodium passively.32 Measure-
ment of urinary sodium excretion is a helpful parameter
to follow when rapidity of weight loss is less than de-
sired.12,13 Random urinary sodium concentrations are of
value when they are 0 mmol/L or greater than 100
mmol/L but are much less helpful when they are interme-
diate because of lack of uniformity of sodium excretion
during the day and lack of knowledge of total urine vol-
ume, which may vary from 300 mL to greater than 3000
mL. Twenty-four-hour collections of urine for determi-
nation of sodium excretion are much more informative
than random specimens; however, full-day collections are
cumbersome. Providing patients with verbal and written
instructions, a container, and a lab order slip to turn in
with the completed specimen helps insure compliance.
Completeness of collection of the 24-hour specimen can
be assessed by measurement of urinary creatinine. Cir-
rhotic men should excrete more than 15 mg of creatinine
per kilogram of body weight per day, and women should
excrete more than 10 mg/kg per day.33 Less creatinine is
indicative of an incomplete collection. Total nonurinary
sodium excretion is less than 10 mmol per day in afebrile
cirrhotic patients without diarrhea.34 One of the goals of
treatment is to increase urinary excretion of sodium so
that it is greater than 78 mmol per day (88 mmol intake
per day� 10 mmol nonurinary excretion per day). Only the
10% to 15% of patients who have spontaneous natriuresis
greater than 78 mmol per day can be considered for dietary
sodium restriction alone (i.e., without diuretics). However,
when given a choice, most patients would prefer to take some
diuretics and have a more liberal sodium intake than take
no pills and have a more severe sodium restriction.
A random “spot” urine sodium concentration that is
greater than the potassium concentration correlates with a
24-hour sodium excretion greater than 78 mmol per day
with approximately 90% accuracy.35 This urine sodium/
potassium ratio may replace the cumbersome 24-hour
collection.
Fluid restriction is not necessary in treating most pa-
tients with cirrhosis and ascites. The chronic hyponatre-
mia usually seen in cirrhotic ascites patients is seldom
morbid. Attempts to rapidly correct hyponatremia in this
setting with hypertonic saline can lead to more complica-
Table 2. Ascitic Fluid Laboratory Data*
Routine Optional Unusual Unhelpful
Cell count and differential Culture in blood culture bottles AFB smear and culture pH
Albumin Glucose Cytology Lactate
Total protein Lactate dehydrogenase Triglyceride Cholesterol
Amylase Bilirubin
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