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Dig Dis Sci (2007) 52:3307–3315
DOI 10.1007/s10620-007-9805-5
REVIEW PAPER
An Evidence-Based Manual for Abdominal Paracentesis
Angela McGibbon · Grant I. Chen ·
Kevork M. Peltekian · Sander Veldhuyzen van Zanten
Received: 3 August 2006 / Accepted: 1 February 2007 / Published online: 28 March 2007
C
Springer Science+Business Media, LLC 2007
Abstract The purpose of this study was to provide
evidence-based approaches to detect ascites, perform para-
centesis, order tests, and interpret the results. A Medline
search was performed to identify relevant articles. Of 731
identified articles, 50 articles were used. The most sensi-
tive findings for ascites detection are ankle edema (93%),
increased abdominal girth (87%), flank dullness (84%), and
bulging flanks (81%). Paracentesis is safe, with bleeding
rates and leakage of <1%. An ascitic fluid polymorphonu-
clear cell count ≥250 cells/mm
3
is the most sensitive test
(86%–100%) to diagnose spontaneous bacterial peritoni-
tis. The serum-ascites albumin gradient is the most useful
test in identifying portal hypertension-related ascites. Large-
volume paracentesis is effective in the treatment of refractory
ascites. We conclude that paracentesis is a safe and vital pro-
cedure in patients with new-onset ascites. Once detected,
an algorithmic approach to ordering tests and their inter-
pretation is useful to determine etiology and direct further
management.
Keywords Ascites
.
Paracentesis
.
Diagnosis
.
Review
.
Systematic review
A. McGibbon · G. I. Chen · K. M. Peltekian · S. V. van Zanten
Division of Gastroenterology,
Department of Medicine, Dalhousie University,
Halifax, Nova Scotia, Canada
S. V. van Zanten (
)
Queen Elizabeth II Health Sciences Center,
Victoria General Hospital Site,
Room 928, South Wing, Centennial Building,
Halifax, Nova Scotia B3H 2Y9, Canada
e-mail: Zanten@dal.ca
Introduction
Abdominal paracentesis is the removal of fluid from the
peritoneal cavity. It is an important skill for all internists but
especially for those physicians caring for patients with liver
disease. Abdominal paracentesis is used to help diagnose
the etiology of ascites (diagnostic paracentesis) or as a ther-
apeutic measure whereby a large volume of ascitic fluid is
removed (therapeutic paracentesis). The investigation and
management of patients with ascites have been regularly re-
viewed in the literature [1–4]. Despite the frequency of its
use, the literature is scarce on the technical aspects of ab-
dominal paracentesis.
This manual focuses on the detection of ascites, the in-
dications and contraindications for abdominal paracentesis,
and the risks and complications associated with the proce-
dure. The technique is described, followed by a discussion
of appropriate laboratory tests and their interpretation. This
manual focuses on important questions regarding diagnostic
paracentesis. Issues regarding therapeutic paracentesis are
addressed briefly.
The following questions regarding abdominal paracente-
sis are addressed.
1. Does the patient have ascites?
2. Does the patient need paracentesis?
3. What are the risks and complications?
4. How is paracentesis performed?
5. What tests should be ordered and what do the results
mean?
6. How and when should a therapeutic paracentesis be per-
formed?
Springer
3308 Dig Dis Sci (2007) 52:3307–3315
Methods
English-language articles involving humans were identified
by a Medline search from 1966 to August 2004. The Medi-
cal Subject Headings included ascites, paracentesis, indica-
tions, spontaneous bacterial peritonitis, diagnosis, review,
and guideline, study. Bibliographies of retrieved articles and
textbooks were also searched. The inclusion criteria were
as follows: main focus of article dealt with detection meth-
ods for ascites relevant for clinicians, technique of perform-
ing paracentesis, diagnostic tests on ascitic fluid removed,
and indications for those tests. Relevant evidence-based re-
views (meta-analyses, systematic reviews, topic reviews,
and guidelines) as well as original studies not cited in the
evidence-based reviews were included, as were relevant case
reports if no original studies or evidence-based reviews were
found.
Does the patient have ascites?
Ascites is a pathological increase in fluid in the peritoneal
cavity. The normal peritoneal cavity has a small amount of
free fluid (∼50 ml) [5]. Chronic liver disease with associated
portal hypertension is the most frequent cause of ascites.
Other less common etiologies include malignancy, heart fail-
ure, nephropathy, tuberculosis, and pancreatic disease [6].
Ascites should be suspected in patients with risk factors
or symptoms of chronic liver disease, known liver cirrhosis,
history of congestive heart failure, renal failure, tuberculosis,
pancreatitis, or cancer who present with increasing abdom-
inal girth, ankle edema, or unexplained weight gain. The
accuracy of symptoms elicited from the patient history for
diagnosing ascites has been reviewed using ultrasound as
the “gold standard.” The most sensitive symptoms for as-
cites are ankle edema (93%) and increased abdominal girth
(87%), with specificities of 66% and 77%, respectively [6].
The standard clinical approach to the detection of ascites
includes testing for flank dullness and, if present, proceeding
to testing for shifting dullness and the fluid wave. This is usu-
ally done in patients in whom ascites is suspected, especially
those with liver disease. The presence of ascites is an im-
portant prognostic indicator in patients with liver cirrhosis,
as it is a sign of liver decompensation with an approximate
mortality rate of 50% at 2 years [1]. Once suspected from the
history and physical examination, ascites may be confirmed
by ultrasonography, which can detect as little as 100 ml of
fluid [6].
There are several physical examination techniques that
are used to detect the presence of ascites. These include in-
spection for bulging flanks while supine, percussion dullness
in the flanks, testing for shifting dullness, and the presence of
a fluid wave [6, 7]. Two less common methods are ausculta-
tory percussion and the puddle sign [6, 7]. These techniques
are briefly described in Table 1. The most sensitive physical
examination maneuvers for ascites are flank dullness (84%)
and the presence of bulging flanks (81%), both of which have
a specificity of 59%. The most specific test is the presence
Table 1 Physical exam
maneuvers for the detection of
ascites
Maneuver Description
Bulging flanks/distended
abdomen
Inspect the abdominal contours for a protuberance of the abdomen
anteriorly and bulging of the flanks laterally while the patient is supine.
Flank dullness Percuss the abdominal wall starting at the periumbilical region and then
going outward to the dependent areas (flanks). If ascites is present, there
is a change from tympany to dullness.
Shifting dullness Note the level of change from tympany to dullness. Position the patient in
the right lateral decubitus position and percuss the abdomen, starting on
the left side and then going toward the right side. If ascites is present, the
level at which tympany turns to dullness will have shifted.
Fluid wave Assistance is required to perform this test. With the patient in the supine
position, the ulnar side of an assistant’s hand and forearm is placed
firmly in the midline of the anterior abdominal wall, in line with the
patient. The examiner’s two hands are then placed on either side of the
abdomen. While one hand strikes the abdomen, the other hand feels for
an impulse of a fluid wave.
Ausculatory percussion With the patient standing, auscultate just above the symphysis pubis while
percussing (using single finger flicks) from the costal margin down to the
pelvis. In normal individuals, there is a sharp transition from quiet to
loud at the pelvic border. With ascites, the transition occurs higher up.
Puddle sign The patient is put on the hands and knees. After the patient has been in
that position for several minutes, the periumbical region is percussed for
dullness to determine the presence of fluid.
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Dig Dis Sci (2007) 52:3307–3315 3309
of a fluid wave (90%), although its sensitivity is poor (62%)
[6].
More recently, Chongtham et al. performed a study of
66 patients comparing the accuracy of physical examination
compared with ultrasound as a gold standard in the detection
of ascites. Those with a history of ascites or therapeutic para-
centesis, or in whom ascites was detected by shifting dullness
or fluid wave, were excluded. They found that ausculatory
percussion was the most sensitive maneuver (66%), followed
by flank dullness (57%). The fluid wave sign was found not
to be sensitive (20%) but to be very specific (100%) [8].
Does the patient need paracentesis?
Paracentesis aids in determining the etiology of the ascites
(most commonly chronic liver disease or malignancy) and
the presence of infection, and will often give temporary relief
of dyspnea, chest and abdominal discomfort, and anorexia in
patients with tense ascites when a therapeutic (large-volume)
paracentesis is performed [1].
As discussed later, ascites due to chronic liver disease
with portal hypertension results in a high serum-to-ascites
albumin gradient (formerly referred to as a “transudate”),
in contrast to nonportal hypertensive causes of ascites (i.e.,
malignancy), which result in a low serum-to-ascites albumin
gradient (formerly referred to as an “exudate”) [9].
Spontaneous bacterial peritonitis (SBP) refers to the in-
fection of previously sterile ascitic fluid with no apparent
intra-abdominal source, in contrast to secondary bacterial
peritonitis due to a perforated viscus or intra-abdominal ab-
scess. SBP is thought to result from translocation of bacteria
from the intestinal lumen to the systemic circulation in the
setting of impaired immunological defences due to liver dis-
ease. There is subsequent hematologic seeding of the peri-
toneal fluid leading to the infection [10, 11]. The incidence
of ascitic fluid infection is 10%–30% in patients admitted to
hospital with ascites and cirrhosis [10]. SBP may not always
present with signs of peritoneal irritation. In a series of pa-
tients with SBP, the most common presenting features were
fever (67%), abdominal pain (60%), and confusion (57%)
while 74% had an elevated white cell count. Peritoneal irri-
tation on physical examination was present in only 42% of
patients [11]. Therefore, a high index of suspicion should be
maintained in patients with chronic liver disease who present
with clinical deterioration [1]. Table 2 lists the indications
for a diagnostic paracentesis.
Distinguishing spontaneous from secondary bacterial
peritonitis is critical, as the management is different. SBP
is treated with antibiotics, as it is associated with a sig-
nificant mortality rate (30% in hospital and 50% at 1 year)
[12]. Secondary bacterial peritonitis requires further imaging
and possible surgical intervention in addition to antibiotics
Table 2 Patients who should undergo diagnostic paracentesis
Patients with new-onset ascites
Hospitalized patients with ascites
Patients with known ascites and at least one of the following:
Fever
Leukocytosis
Abdominal pain
Peritoneal findings
Increasing ascites volume
Unexplained encephalopathy
Deteriorating liver function
Renal failure
[1]. Table 3 summarizes the features that help differenti-
ate between spontaneous bacterial peritonitis and secondary
bacterial peritonitis [1, 10, 13].
What are the risks and complications?
Earlier literature reported the use of paracentesis with tro-
cars that were associated with a high morbidity and even
mortality [1]. However, with current techniques, diagnostic
paracentesis is considered a safe procedure, with no reported
deaths or infections [14]. The only absolute contraindica-
tions to paracentesis are clinically evident fibrinolysis or
disseminated intravascular coagulation. Relative contraindi-
cations to blind paracentesis (performed without the aid of
ultrasound) include pregnancy, severe bowel distension, and
previous extensive abdominal/pelvic surgery. If a relative
contraindication is present, an ultrasound-guided paracente-
sis should be considered. A study of 27 patients requiring
paracentesis showed that the success of blind paracentesis is
directly related to the amount of ascitic fluid present (44%
with 300 ml and 78% with 500 ml). The site of accumulation
of ascitic fluid depends on the quantity of ascites, its etiology,
and the presence of peritoneal adhesions [15]. Therefore, ul-
trasound not only confirms the presence of ascites, but also
Table 3 Features of spontaneous and secondary bacterial peritonitis
[1, 10, 13]
Feature
Spontaneous
bacterial peritonitis
Secondary bacterial
peritonitis
Clinical
Fever
±+
Peritoneal findings
±+
Free intraperitoneal air −
+
Ascitic fluid
LDH >225 U/L −
+
Total protein >1.0 g/dl
±+
Glucose <50 mg/dl −
+
Gram’s stain/culture −/monomicrobial
+/polymicrobial
Note. LDH, lactate dehydrogenase.
Springer
3310 Dig Dis Sci (2007) 52:3307–3315
is used to locate the best site to perform a successful para-
centesis, especially when dealing with smaller volumes of
fluid.
The risks of a diagnostic paracentesis include bleeding,
visceral perforation, local infection or peritonitis, and a per-
sistent leak. Each of these risks is addressed separately.
Bleeding risk
Bleeding related to paracentesis manifests as either an ab-
dominal wall hematoma or a hemoperitoneum. The risk of
transfusion-requiring abdominal wall hematoma is less than
1% as shown in two studies, one a retrospective analysis of
242 consecutive diagnostic paracenteses and one a prospec-
tive study of 229 diagnostic paracenteses [14, 16].
Two larger retrospective studies, of 608 and 4729 para-
centeses, showed a very low risk of bleeding complications
in patients with coagulopathy and/or thrombocytopenia of
varying severities. The results between the studies are con-
sistent with a significant bleeding rate of about 0.2% [17,
18]. In one of the studies, patients who were prophylactically
transfused fresh-frozen plasma did not show a decreased rate
of bleeding compared with those who were not transfused
[17]. The amount of blood loss was also similar among those
with mild to moderate coagulopathy compared with no co-
agulopathy. In both studies, significant renal impairment was
associated with an increased bleeding rate, likely related to
a qualitative platelet defect from uraemia [17, 18]. How-
ever, closer monitoring rather than prophylactic transfusion
of platelets is advocated in these patients [17].
There have been case reports of significant bleeding from
paracentesis performed in the midline related to puncture
of intra-abdominal varices [19] and a recanalized umbilical
vein [20]. A laparoscopic study found that the peritoneal side
of the subumbilical midline is frequently vascular in patients
with portal hypertension [21].
Bowel or bladder puncture
The risk of bowel or bladder puncture is decreased by ensur-
ing that the patient has an empty bladder and avoiding areas
of scarring where there may be underlying adherent bowel.
Ultrasound-guided removal of the ascites is recommended
when there is a concern regarding localization of fluid [15].
Local infection or peritonitis
There is a theoretical risk of introducing infection into the
ascitic fluid with the paracentesis procedure [22].Thisriskis
minimized by the use of sterile technique and the precautions
taken, which are described later. A prospective study, using
a technique similar to the one described here, did not find
this complication [14].
Persistent leak at the site of puncture
Less than 1% of patients may develop a persistent small
volume leak at the site of paracentesis. The risk appears to
be greatest in those with tense ascites. Various techniques
have been used in anecdotal reports to minimize the risk
including the use of small-gauge needles and the “Z-tract”
technique, which consists of misaligning puncture sites of
skin, fascia, and muscle with skin traction [23]. Persistent
ascitic fluid leaks despite the use of the Z-tract method can
be remedied by using a purse-string stitch and having the
patient lie on the side opposite the puncture site [3]. There
has been a reported case of using an adhesive glue, 2-octyl
cyanoacrylate [24].
How is paracentesis performed?
Once an indication for paracentesis has been identified and
the presence of any contraindications (absolute or relative)
have been considered and addressed adequately, the proce-
dure needs to be explained to the patient. The discussion
should include the reasons for doing the procedure and the
risks discussed above. Once informed consent has been ob-
tained, the appropriate equipment should be assembled (see
Table 4). There are no studies examining specific aspects
of technique (i.e., patient positioning, needle puncture site).
The standard technique is as follows.
1. Position the patient comfortably: in the supine (large vol-
umes) or lateral decubitus (small volumes) position.
Table 4 Equipment used for abdominal paracentesis
Sterile gloves
Mask (optional)
10% povidine iodine solution or 70% alcohol for skin preparation
Sterile gauze and drapes
Local anesthetic (1% xylocaine)
Syringes: 5 and 50 ml
Needles
18-gauge needle for drawing up local anesthetic
25-gauge, 1.5-in. needle for applying anaesthetic
20- or 22-gauge, 2.5-in. needle for diagnostic paracentesis
14- or 16-gauge, 2.5-in. angiocatheter or 15-gauge Caldwell
needle/cannula
a
18- or 22-gauge, 3.5-in. spinal needle for obese patients
Two blood culture bottles (one aerobic, one anaerobic)
Hematology, chemistry, and microbiology sample tubes or bottles
4 ×4-in. gauze and bandage
Noncollapsible intravenous tubing
a
Drainage system (typically vacuum bottles)
a
a
For therapeutic paracentesis.
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Dig Dis Sci (2007) 52:3307–3315 3311
2. Percuss the abdominal wall to determine the level of dull-
ness. Choose the puncture site: either midline (2 cm be-
low umbilicus) or in the lower quadrant, 2–3 cm lateral
to the anterior rectus muscle border. The correct site for
the puncture is not exact, but the far lateral sites, areas of
superficial infection or previous scarring, and engorged
veins need to be avoided. Ultrasound to mark the optimal
site for paracentesis should be used, if necessary.
3. Observe universal precautions with regard to handling of
needles and body fluids.
4. Prepare skin around and at site selected for puncture with
providine or alcohol solution using sterile gauze. Drape
the puncture site to form a sterile field.
5. Draw up local anesthetic and administer subcutaneously
and into the soft tissue at the puncture site using a 5-ml sy-
ringe and 25-G needle. Always aspirate while advancing
the needle deeper into the soft tissue.
6. With the longer 22-G needle and a 50-ml syringe, enter the
frozen puncture site at a perpendicular angle. Slowly ad-
vance the needle through the soft tissue, aspirating while
advancing. Traction may be applied on the skin with one
hand while the other hand handles the syringe. The trac-
tion causes the puncture holes through the skin, muscle,
and fascia not to overlap (Z-tract), which may lessen the
risk of a persistent leak. As the needle enters the peritoneal
cavity, a “give” will be felt and fluid should be aspirated
into the syringe.
7. Continue to aspirate 20–50 ml of fluid for evaluation.
8. When the desired amount of fluid is obtained, remove
the needle swiftly while aspirating and remove the skin
retraction once the needle is completely out. Apply pres-
sure to the puncture site for a short period, if necessary,
to ensure no excessive bleeding or fluid leakage. Apply
bandage to puncture site.
9. If diagnostic paracentesis is being performed, the ascitic
fluid should be sent for the appropriate tests (see Table 5).
Table 5 Ascitic fluid tests
Routine
Cell count and differential
Albumin, total protein (with new-onset ascites)
If infection suspected
Gram’s stain
Cultures (inoculate blood culture bottles at the bedside)
Lactate dehydrogenase, glucose (if secondary peritonitis
considered)
Miscellaneous tests (depending on pretest probability of suspected
condition in italics)
Pancreatic disease: amylase
Malignancy: cytology
Tuberculosis: acid-fast bacillus smear and culture
Lymphatic leak/obstruction: triglyceride
Biliary leak: bilirubin
Other
10. Ensure that a blood sample for albumin is sent along with
other tests (i.e., lactate dehydrogenase [LDH], glucose,
etc.) as warranted by clinical suspicion.
What tests should be ordered and what
do the results mean?
Tests of the ascitic fluid help to establish the etiology of the
ascites and to rule out infection. The ascitic fluid cell count
and differential should always be ordered, while albumin
should also be ordered in every case of newly diagnosed
ascites [1]. Additional tests are ordered depending on the
clinical circumstances and are discussed here.
Cell count and differential
The cell count and differential are used to diagnose sponta-
neous bacterial peritonitis (SBP). The utility of ascitic fluid
cell count in the diagnosis of SBP was initially examined
in several studies that used a positive bacterial ascitic fluid
culture as the “gold standard.” These studies had varying
results for sensitivity and specificity and used different cut-
off levels for ascitic fluid polymorphonuclear (PMN) count.
Overall, an ascitic fluid PMN count ≥500 cells/mm
3
has a
sensitivity of 70%–100%, with a specificity of 86%–100%.
The current diagnostic standard is an ascitic fluid PMN count
≥250 cells/mm
3
which has a sensitivity of 80%–100% and
a specificity of 86%–100% [10]. Ascitic leukocyte (or neu-
trophil) count is not influenced by peripheral leukocytosis
(or neutrophilia) [25]. Several studies have examined the use
of urine dipsticks to detect neutrophils in ascitic fluid at the
bedside [26–30]. In aggregate, they have shown a sensitivity
of 83%–100%, a specificity of 89%–100%, a positive pre-
dictive value of 91%–100%, and a negative predictive value
of 98%–100% compared with an ascitic fluid PMN count
≥250 cells/mm
3
as the gold standard for the diagnosis of
SBP. High ascitic fluid lymphocyte counts are seen with tu-
berculosis, fungal infections, and peritoneal carcinomatosis,
following diuresis, and, rarely, in hematological malignan-
cies [31].
Hemorrhagic ascites is defined as an ascitic red blood
cell count >50,000/mm
3
. This is most commonly due to a
“traumatic tap,” although it also occurs with cirrhotic ascites,
malignancy, peritoneal carcinomatosis, or congestive heart
failure. In order to correct the PMN count in bloody ascitic
fluid, 1 PMN can be subtracted from the total for every 250
red blood cells in the ascitic fluid [32].
Albumin
Ascitic fluid albumin determination is crucial in determin-
ing the etiology of the ascites. The serum-ascites albumin
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3312 Dig Dis Sci (2007) 52:3307–3315
Liver Cirrhosis
Alcoholic hepatitis
Budd-Chiari syndrome
Portal Vein Thrombosis
Veno-occlusive Disease
Fulminant Hepatic
Failure
Liver metastases
Myxedema
SAAG
≥ 1.1 g/dL
< 2.5 g/dL
Total Ascitic Fluid Protein
Normal or ↓
High
Cardiac Failure
Constrictive Pericarditis
Pulmonary
Hypertension
Protein-losing Enteropathy
Nephropathy
Malnutrition
Malignancy
Peritoneal carcinomatosis
TB peritonitis
Pancreatic ascites
Serositis
Secondary Peritonitis
Jugular Venous Pressure
< 1.1 g/dL
≥ 2.5 g/dL
Mixed Ascites*
Fig. 1 Algorithm for
determining the etiology of
ascitic fluid. SAAG,
serum-ascites albumin gradient.
∗
Portal hyptensive and
non-portal hypertensive cause
for ascites (high serum/ascites
albumin gradient with variable
amounts of total ascitic fluid
protein)
gradient (SAAG) has been shown to be superior to the
exudate-transudate concept (using total ascitic fluid protein)
for classifying ascitic fluid [9]. The SAAG is the absolute
difference between the serum albumin and the ascitic albu-
min level. The SAAG has been shown to be directly related
to an elevation of portal venous pressure [33]. Therefore, it
is used to distinguish between sinusoidal portal hypertensive
and non-portal hypertensive causes of ascites (Fig. 1). A high
SAAG (≥1.1 g/dl) identifies ascites due to sinusoidal portal
hypertension 97% of the time [9]. Once the cause has been
established, it is not necessary to repeat the test for albumin
in subsequent paracentesis unless clinically warranted.
Gram’s stain and culture
There are typically low numbers of organisms in the ascitic
fluid with SBP, which may explain why Gram’s stain is only
positive in 7%–10% of early SBP [10, 34]. However, Gram’s
stain is still recommended if infection is a consideration,
as it may identify secondary peritonitis due to a perforated
viscus in which multiple organisms are seen. In patients with
an ascitic fluid PMN count ≥250 cells/mm
3
, ascitic fluid
cultures are positive in only 50% (by the method of delayed
inoculation of culture medium in the lab), compared with
∼80% if the fluid is inoculated directly into blood culture
bottles at the bedside [1, 34]. Outside the context of clinical
trials, the real-world yield is closer to 50% [10].Themost
common organisms implicated in SBP are Escherichia coli,
Klebsiella pneumoniae, and pneumococci [1].
Ascites can be classified based on the culture and cell
count result as follows [10].
1. SBP: Ascitic fluid PMN count ≥250 cell/mm
3
and/or pos-
itive culture with a single organism. Treatment with an-
tibiotics should be initiated.
2. Culture-negative neutrocytic ascites: Ascitic fluid PMN
count ≥250 cells/mm
3
with a negative culture. This is
considered a variant of SBP (same natural history as SBP)
and should be treated as SBP.
3. Monomicrobial nonneutrocytic bacterascites: PMN count
<250 cells/mm
3
and culture positive for a single organ-
ism. Since a significant minority of these patients will
progress to SBP, it is recommended that a repeat para-
centesis be performed within 24 hr. Treatment is recom-
mended for symptomatic patients, those who have per-
sistent bacterascites, and those who show evidence of an
extraperitoneal infection.
4. Polymicrobial bacterascites/secondary bacterial peritoni-
tis: Multiple organisms are cultured. Treatment with
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Dig Dis Sci (2007) 52:3307–3315 3313
antibiotics with additional investigations (ascitic fluid glu-
cose, protein, LDH, and imaging) is required.
Total protein
The ascitic total protein concentration is a reflection of the
serum protein concentration and portal pressure [33].Tra-
ditionally, an ascitic fluid total protein level ≥2.5 g/dl was
considered an exudate, while total protein <2.5 g/dl was
considered a transudate. This method was only 56% accu-
rate in classifying the cause of ascites [9]. While it is not
a useful test to distinguish between portal hypertensive and
non-portal hypertensive causes of ascites, it is a useful ad-
junctive test for elucidating the cause of ascites in the absence
of portal hypertension (Fig. 1).
A low ascitic total protein (<1.0 g/dl) has been associated
with a higher risk of spontaneous bacterial peritonitis [35].
However,a consensus has not been reached on the routine use
of prophylactic antibiotics to prevent SBP in this setting, as
a main concern has been the selection of antibiotic-resistant
organisms [1, 10]. High total protein levels (>1.0 g/dl) in
ascitic fluid are commonly seen in secondary peritonitis
(Table 2).
Glucose and lactate dehydrogenase
These tests should not be ordered routinely on ascitic fluid.
Their value lies in the diagnosis of secondary bacterial
peritonitis [13]. The scitic glucose concentration is low in
secondary peritonitis and peritoneal carcinomatosis. Ascitic
LDH is nonspecific, as its level fluctuates with infection and
malignancy. The normal LDH ratio (ascites/serum LDH) is
0.4 and typically approaches 1.0 with SBP and malignancy
[36].
Amylase
Pancreatic ascites is suspected in patients with new-onset as-
cites and a history of pancreatic disease or trauma. The ascitic
amylase levels are often >1000 IU/L, with the ascitic/serum
amylase ratio increasing up to 6.0, indicating leakage of pan-
creatic enzymes into the peritoneal cavity [37].
Triglycerides
The presence of milky-colored ascitic fluid suggests chy-
lous ascites (lymphatic fluid within the peritoneal cavity)
and should prompt a test for triglyceride levels. This occurs
in 0.5%–1% of cirrhotic patients with ascites and is due to
rupture of lymphatic channels within the peritoneal cavity,
which are dilated from high lymph flow [38]. Chylous ascites
is defined by an ascitic fluid triglyceride level >200 mg/dl.
The most common causes in the adult population are malig-
nancy (i.e., retroperitoneal lymphoma, ovarian carcinoma),
cirrhosis, and infections (i.e., filariasis, tuberculosis). An as-
citic fluid cholesterol level >48 mg/dL has an accuracy of
92% for distinguishing malignant from cirrhotic ascites [38].
Bilirubin
In the deeply jaundiced patient, the ascites may be brown,
which is a reflection of the elevated bilirubin concentration.
Usually, the ascitic bilirubin concentration is approximately
40% of the serum level. However, choleperitoneum (bile in
the peritoneal cavity due to a bile leak) is characterized by an
ascitic bilirubin level >6 mg/dl or an ascitic/serum bilirubin
ratio >1.0 [39].
Cytology
Ascitic fluid cytology is ordered when malignancy is sus-
pected. The overall sensitivity of cytology for malignant as-
cites is 57%–67% [40]. The sensitivity for peritoneal carci-
nomatosis is 96.7%, while it is much lower (6.7%–13.3%)
in ascites due to hepatocellular carcinoma, liver metastases,
or chylous ascites with lymphoma [41].
Other tests
If there is a high pretest probability of peritoneal tuberculosis
(extraperitoneal tuberculosis, immunocompromised patient,
and/or patient from an endemic area), the ascitic fluid may
be sent for acid-fast bacillus smear and culture, although
the sensitivity for both of these tests is low (33%–50%) [1
,
42]. Measurement of adenosine deaminase activity of ascitic
fluid has been shown not to be useful in a North American
population [43]. Ascitic fluid tuberculosis PCR has shown
some promise [44]. Ultimately, the most sensitive test is
direct peritoneal biopsy via laparoscopy [1].
The utility of measuring tumor markers such as carci-
noembryonic antigen (CEA) and cancer antigen 125 (CA-
125) in ascitic fluid has not been established. CA-125 is
commonly elevated in patients with liver cirrhosis and it is
related to the presence of ascites but does not relate to the
etiology of cirrhosis or ascites [45]. Tests that should not be
ordered are pH and lactacte, as they are both insensitive and
nonspecific [1, 10].
How and when should a therapeutic
paracentesis be performed?
The technique of therapeutic or large-volume paracentesis
(LVP) is identical to that of the diagnostic paracentesis de-
scribed previously except that a larger-bore needle (angio-
cath needle or Caldwell needle/cannula) is used. Once the
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3314 Dig Dis Sci (2007) 52:3307–3315
ascitic fluid flows from the peritoneal cavity into the syringe,
the catheter is held in place and the inner needle/cannula is
removed. The catheter is then attached to vacuum bottles via
intravenous tubing. The vacuum ensures continuous flow of
ascitic fluid. Both the catheter and the patient may need to
be repositioned during the procedure to allow optimal flow
of ascitic fluid. The 15-G Caldwell needle/cannula (CNC), a
multifenestrated metal cannula with a removable inner stylet,
has been shown to be more successful (faster and requiring
less punctures) than the 14-G angiocath needle in LVP [46].
A detailed discussion of the management of ascites due
to liver cirrhosis and the role of large-volume paracentesis
is beyond the scope of this article. These issues have been
addressed in several recent review articles [1–4, 10, 47].
The main safety concern with LVP has been regarding
hemodynamic changes that may occur with removal of a
large volume of fluid from the peritoneal cavity. The Amer-
ican Association for the Study of Liver Diseases (AASLD)
practice guideline suggests that serial LVP should only be
used in refractory ascites and that, for a therapeutic paracen-
tesis of >5 L, albumin infusion of 8–10 g/L fluid removed
should be considered, while this is not recommended for
volumes of <5L[1].
Hemorrhagic complications of LVP occur slightly more
often than in diagnostic procedures (1%–3%) and may be
seen up to a week after the procedure [48–50]. This compli-
cation is likely related to pressure changes within the por-
tal system seen with LVP, which increase the likelihood of
bleeding from mesenteric collaterals [50].
Summary
Abdominal paracentesis is a skill that all physicians car-
ing for patients with ascites should master. Paracentesis has
two critical roles in patient care: the classification of ascites
(which directs further investigation, diagnosis, and manage-
ment) and the relief of dyspnea, anorexia, and abdominal
discomfort in patients with tense ascites. Paracentesis is a
safe procedure. Using evidence-based approaches to diag-
nosing ascites and abdominal paracentesis should reduce in-
appropriate testing and unnecessary administration of blood
products.
References
1. Runyon BA (2004) Management of adult patients with ascites due
to cirrhosis. Hepatology 39:841–856
2. Garcia-Tsao G (2001) Current management of the complications
of cirrhosis and portal hypertension: variceal hemorrhage, ascites,
and spontaneous bacterial peritonitis. Gastroenterology 120:726–
748
3. Moore KP, Wong F, Gines P, Bernardi M, Ochs A, Salerno F, Angeli
P, Porayko M, Moreau R, Garcia-Tsao G, Jimenez W, Planas R,
Arroyo V (2003) The management of ascites in cirrhosis: Report
on the consensus conference of the International Ascites Club.
Hepatology 38:258–266
4. Gines P, Cardenas A, Arroyo V, Rodes J (2004) Management of
cirrhosis and ascites. N Engl J Med 350:1646–1654
5. Boey JH (1994) Peritoneal cavity. In: Way LW (ed). Current surgi-
cal diagnosis and treatment, 10th ed. Appleton & Lange, Norwalk,
CT, p 453
6. Williams JW, Simel DL (1992) Does this patient have ascites? How
to divine fluid from the abdomen. JAMA 267:2645–2648
7. Seidel HM, Ball JW, Dains JE, Benedict GW (1999) Mosby’s guide
to physical examination, 4th ed. Mosby, St. Louis
8. Chongtham DS, Singh MM, Kalantri SP, Pathak S, Jain AP (1998)
Accuracy of clinical manoeuvres in detection of minimal ascites.
Indian J Med Sci 52:514–520
9. Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving
MA, McHutchison JG (1992) The serum-ascites albumin gradient
is superior to the exudate-transudate concept in the differential
diagnosis of ascites. Ann Intern Med 117:215–220
10. Rimola A, Garcia-Tsao G, Navasa M, Piddock LJ, Planas R,
Bernard B, Inadomi JM (2000) Diagnosis, treatment and prophy-
laxis of spontaneous bacterial peritonitis: A consensus document.
International Ascites Club. J Hepatol 32:142–153
11. Hoefs JC, Runyon BA (1985) Spontaneous bacterial peritonitis.
Dis Mon 31:1–48
12. Altman C, Grange JD, Amiot X, Pelletier G, Lacaine F, Bodin F,
Etienne JP (1995) Survival after a first episode of spontaneous bac-
terial peritonitis. Prognosis of potential candidates for orthotopic
liver transplantation. J Gastroenterol Hepatol 10:47–50
13. Akriviadis EA, Runyon BA (1990) Utility of an algorithm in differ-
entiating spontaneous from secondary peritonitis. Gastroenterol-
ogy 98:127–133
14. Runyon BA (1986) Paracentesis of ascitic fluid: A safe procedure.
Arch Intern Med 146:2259–2261
15. Bard C, Lafortune M, Breton G (1986) Ascites: Ultrasound guid-
ance or blind paracentesis? CMAJ 135:209–210
16. Mallory A, Schaefer JW (1978) Complications of diagnostic para-
centesis in patients with liver disease. JAMA 239:628–630
17. McVay PA, Toy PT (1991) Lack of increased bleeding after para-
centesis and thoracentesis in patients with mild coagulation abnor-
malities. Transfusion 31:164–171
18. Pache I, Bilodeau M (2005) Severe haemorrhage following abdom-
inal paracentesis for ascites in patients with liver disease. Aliment
Pharmacol Ther 21:525–529
19. Qureshi WA, Harshfield D, Shah H, Netchvolodoff C, Banerjee B
(1992) An unusual complication of paracentesis. Am J Gastroen-
terol 87:1209–1211
20. Aagaard J, Jensen LI, Sorensen TI, Christensen U, Burcharth F
(1982) Recanalized umbilical vein in portal hypertension. Am J
Radiol 139:1107–1110
21. Oelsner DH, Caldwell SH, Coles M, Driscoll CJ (1998) Subumbili-
cal midline vascularityof the abdominal wall in portal hypertension
observed at laparoscopy. Gastrointest Endosc 47:388–390
22. Conn HO (1979) Bacterial peritonitis: Spontaneous or paracen-
tetic? Gastroenterology 77:1145–1146
23. Runyon BA (2002) Ascites and spontaneous bacterial peritonitis.
In: Feldman M, Friedman LS, Sleisenger MH (eds). Sleisenger
& Fordtran’s gastrointestinal and liver disease, 7th ed. Saunders,
Philadelphia, pp 1519–1521
24. Hale BR Jr, Girzadas DV Jr (2001) Application of 2-octyl-
cyanoacrylate controls persistent ascites fluid leak. J Emerg Med
20:85–86
25. Antillon MR, BA Runyon (1991) Effect of marked peripheral
leukocytosis on the leukocyte count in ascites. Arch Intern Med
151:509–510
26. Castellote J, Lopez C, Gornals J, Tremosa G, Farina ER, Baliellas
C, Domingo A, Xiol X (2003) Rapid diagnosis of spontaneous
Springer
Dig Dis Sci (2007) 52:3307–3315 3315
bacterial peritonitis by use of reagent strips. Hepatology 37:893–
896
27. Thevenot T, Cadranel JF, Nguyen-Khac E, Tilmant L, Tiry C,
Welty S, Merzoug N (2004) Diagnosis of spontaneous bacterial
peritonitis in cirrhotic patients by use of two reagent strips. Eur J
Gastroenterol Hepatol 16:579–583
28. Vanbiervliet G, Rakotoarisoa C, Filippi J, Guerin O, Calle G,
Hastier P, Marine-Bajoan E, Schneider S, Piche T, Broussard JF,
Dor JF, Benzaken S, Hebuterne X, Rampal P, Tran A (2002) Di-
agnostic accuracy of a rapid urine-screening test (Multistix8SG)
in cirrhotic patients with spontaneous bacterial peritonitis. Eur J
Gastroenterol Hepatol 14:1257–1260
29. Butani RC, Shaffer RT, Szyjkowski RD, Weeks BE, Speights LG,
Kadakia SC (2004) Rapid diagnosis of infected ascitic fluid using
leukocyte esterase dipstick testing. Am J Gastroenterol 99:532–
537
30. Sapey T, Mena E, Fort E, Laurin C, Kabissa D, Runyon BA,
Mendler MH (2005) Rapid diagnosis of spontaneous bacterial peri-
tonitis with leukocyte esterase reagent strips in a European and in
an American center. J Gastroenterol Hepatol 20:187–192
31. Hoefs JC (1981) Increase in ascites white blood cell count and
protein concentrations during diuresis in patients with chronic liver
disease. Hepatology 1:249–254
32. DeSitter L, Rector WG Jr (1984) The significance of bloody ascites
in patients with cirrhosis. Am J Gastroenterol 79:136–138
33. Hoefs JC (1983) Serum protein concentration and portal pressure
determine the ascitic fluid protein concentration in patients with
chronic liver disease. J Lab Clin Med 102:260–273
34. Siersema PD, de Marie S, van Zeijl JH, Bac DJ, Wilson JH (1992)
Blood culture bottles are superior to lysis-centrifugation tubes for
bacteriological diagnosis of spontaneous bacterial peritonitis. J
Clin Microbiol 30:667–669
35. Runyon BA (1986) Low-protein-concentration ascitic fluid is pre-
disposed to spontaneous bacterial peritonitis. Gastroenterology
91:1343–1346
36. Runyon BA, Hoefs JC (1985) Ascitic fluid chemical analysis be-
fore, during and after spontaneous bacterial peritonitis. Hepatology
5:257–259
37. Runyon BA (1987) Amylase levels in ascitic fluid. J Clin Gastroen-
terol 9:172–174
38. Cardenas A, Chopra S (2002) Chylous ascites. Am J Gastroenterol
97:1896–1900
39. Runyon BA (1987) Ascitic fluid bilirubin concentration as a key to
choleperitoneum. J Clin Gastroenterol 9:543–545
40. DiBonito L, Falconieri G, Colautti I, Bonifacio D, Dudine S
(1993) The positive peritoneal effusion. A retrospective study of
cytopathologic diagnoses with autopsy confirmation. Acta Cytol
37:483–488
41. Runyon BA, Hoefs JC, Morgan TR (1988) Ascitic fluid analysis
in malignancy-related ascites. Hepatology 8:1104–1109
42. Muneef MA, Memish Z, Mahmoud SA, Sadoon SA, Bannatyne
R, Khan Y (2001) Tuberculosis in the belly: a review of forty-six
cases involving the gastrointestinal tract and peritoneum. Scand J
Gastroenterol 36:528–532
43. Hillebrand DJ, Runyon BA, Yasmineh WG, Rynders GP (1996)
Ascitic fluid adenosine deaminase insensitivity in detecting tuber-
culous peritonitis in the United States. Hepatology 24:1408–1412
44. Uzunkoy A, Harma M, Harma M (2004) Diagnosis of abdominal
tuberculosis: Experience from 11 cases and review of the literature.
World J Gastroenterol 10:3647–3649
45. Xiao WB, Liu YL (2003) Elevation of serum and ascites cancer
antigen 125 levels in patients with liver cirrhosis. J Gastroenterol
Hepatol 18:1315–1316
46. Shaheen NJ, Grimm IS (1996) Comparison of the Caldwell nee-
dle/cannula with Angiocath needle in large volume paracentesis.
Am J Gastroenterol 91:1731–1733
47. Gines P, Guevara M, De Las Heras D, Arroyo V (2002) Review
article: Albumin for circulatory support in patients with cirrhosis.
Aliment Pharmacol Ther 16(Suppl 5):24–31
48. Webster ST, Brown KL, Lucey MR, Nostrant TT (1996) Hemor-
rhagic complications of large volume abdominal paracentesis. Am
J Gastroenterol 91:366–368
49. Arnold C, Haag K, Blum HE, Rossle M (1997) Acute
hemoperitoneum after large-volume paracentesis. Gastroenterol-
ogy 113:978–982
50. Martinet O, Reis ED, Mosimann F (2000) Delayed hemoperi-
toneum following large-volume paracentesis in a patient with cir-
rhosis and ascites. Dig Dis Sci 45:357–358
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