Pancreatic ascites managed with a conservative approach: a case report

Abstract

Background:
Pancreatic ascites refers to the massive accumulation of pancreatic fluid in the peritoneal cavity and is a rare entity. Chronic alcoholic pancreatitis is the most common cause. Ascites is commonly seen in patients with alcoholic liver disease and is usually a consequence of portal hypertension. Biliary pancreatitis, pancreatic trauma and cystic duplications of biliopancreatic ducts, ampullary stenosis, or ductal lithiasis are the remaining causes.

Case presentation:
A 53-year-old Chhetri man, a chronic alcoholic, presented with epigastric pain and abdominal distension. He had made several previous visits to a local hospital within the past 6 months for a similar presentation. Serum alkaline phosphatase 248 IU/L, serum amylase 1301 IU/L, and lipase 1311 IU/L were elevated while serum calcium was decreased (1.5 mmol/l). Ascitic fluid amylase was elevated (2801 IU/L). A computed tomography scan of his abdomen revealed features suggestive of acute-on-chronic pancreatitis. The case was managed with a conservative approach withholding oral feedings, starting total parenteral nutrition, paracentesis, octreotide, and pigtail drainage.

Conclusion:
Pancreatic ascites is a rare entity. Diagnosis is suspected with raised ascitic fluid amylase in the presence of pancreatic disease. Such cases can be managed by conservative approach or interventional approach. We managed this case through a conservative approach.

Full text

C A S E R E P O R T Open Access
Pancreatic ascites managed with a
conservative approach: a case report
Raju Bhandari
1*
, Rajan Chamlagain
2
, Saraswati Bhattarai
2
, Eric H. Tischler
3
, Rajesh Mandal
1
and
Ramesh Singh Bhandari
1
Abstract
Background: Pancreatic ascites refers to the massive accumulation of pancreatic fluid in the peritoneal cavity and
is a rare entity. Chronic alcoholic pancreatitis is the most common cause. Ascites is commonly seen in patients with
alcoholic liver disease and is usually a consequence of portal hypertension. Biliary pancreatitis, pancreatic trauma
and cystic duplications of biliopancreatic ducts, ampullary stenosis, or ductal lithiasis are the remaining causes.
Case presentation: A 53-year-old Chhetri man, a chronic alcoholic, presented with epigastric pain and abdominal
distension. He had made several previous visits to a local hospital within the past 6 months for a similar presentation.
Serum alkaline phosphatase 248 IU/L, serum amylase 1301 IU/L, and lipase 1311 IU/L were elevated while serum
calcium was decreased (1.5 mmol/l). Ascitic fluid amylase was elevated (2801 IU/L). A computed tomography scan of
his abdomen revealed features suggestive of acute-on-chronic pancreatitis. The case was managed with a conservative
approach withholding oral feedings, starting total parenteral nutrition, paracentesis, octreotide, and pigtail drainage.
Conclusion: Pancreatic ascites is a rare entity. Diagnosis is suspected with raised ascitic fluid amylase in the presence
of pancreatic disease. Such cases can be managed by conservative approach or interventional approach. We managed
this case through a conservative approach.
Keywords: Pancreatitis, Ascites, Surgical, Medical, Case report
Background
Massive ascites in a chronic alcoholic patient is usually
attributed to hepatic cirrhosis [1]. Pancreatic ascites
should be suspected in patients with chronic alcoholism
and pancreatitis presenting with ascites [2]. The etiology
is probably a pancreatic pseudocyst leakage or ductal
disruption [3]. The diagnosis is based on demonstration
of ascitic fluid amylase (> 1000 U/L). Chronic pancrea-
titis (83%), acute pancreatitis (8.6%), and trauma (3.6%)
are common causes for ductal disruption. Medical treat-
ment includes withholding oral feedings, total parenteral
nutrition (TPN), paracentesis, and administering octreo-
tide [4]. For those not responding to medical therapy,
interventional therapy may be needed which includes
endoscopic transpapillary pancreatic duct stenting or
surgery which includes cystogastrostomy, cystenterost-
omy, pancreatic sphincterectomy, or partial pancreatic
resection [5–7]. We present a case of massive ascites in
a patient with chronic pancreatitis secondary to chronic
alcohol use. The case was successfully managed with a
combination of medical and interventional therapy.
Case presentation
A 53-year-old, Chhetri man with a history of 10–12 years
of chronic alcoholism presented to our hospital with
the chief complaints of weight loss of 18 kg over the
past 6 months, as well as epigastric pain and vomiting
for the past month. Otherwise, there was no docu-
mented history of fever, yellowish discoloration of skin,
gastrointestinal bleeding, melena, dark-colored urine or
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* Correspondence: rbiom27@gmail.com
1
Department of General and GI Surgery, Tribhuvan University Teaching
Hospital, Kathmandu, Nepal
Full list of author information is available at the end of the article
Bhandari et al. Journal of Medical Case Reports (2020) 14:154
https://doi.org/10.1186/s13256-020-02463-0
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pale stool. His past medical or surgical history was not
significant. He had been admitted to a local hospital on
several occasions in the past 6 months with similar
complaints and was diagnosed as having acute mild
pancreatitis, which was managed conservatively. His
current pain was moderate to severe in intensity, radiat-
ing to his back, and it was aggravated by meals and re-
lieved on stooping forward. He had associated
symptoms of non-projectile, non-bloody, and non-
bilious vomiting, only containing water and food con-
tents. Furthermore, he also complained of respiratory
discomfort that was concurrent with pain episodes. On
examination, he was ill appearing and had the following
vital signs: pulse of 124 beats per minute, temperature
37 ºC (98.6 ºF), and blood pressure of 110/70 mm Hg.
An abdominal examination revealed marked general-
ized abdominal tenderness. Bowel sounds were normal.
Other systemic examinations were not significant.
With regards to laboratory values, total cell and differ-
ential counts, electrolytes, bilirubin, serum glutamic-
oxaloacetic transaminase (SGOT)/serum glutamic-pyruvic
transaminase (SGPT), lactate dehydrogenase (LDH),
serum protein, serum albumin, and urine and stool ana-
lysis were within normal limits at the time of admission.
However, serum alkaline phosphatase (ALP; 248 IU/L),
amylase (1301 IU/L), and lipase (1311 IU/L) were elevated
while serum calcium was decreased (1.5 mmol/l). Tumor
markers CA 19-9 and carcinoembryonic antigen (CEA)
were within normal limits. Arterial blood gas analysis
revealed respiratory alkalosis: pH = 7.48, partial pressure
of carbon dioxide (pCO
2
) 28 mmHg, and bicarbonate
(HCO
3
) 21.3 mmol/l. Ultrasonography (USG) of his abdo-
men and pelvis revealed features suggestive of complicated
acute pancreatitis with loculated peripancreatic collection
extending to the bilateral perinephric space; however, it
was noted to be more prominent on the left side. He was
admitted with the diagnosis of acute pancreatitis and
treated conservatively. He was kept nil by mouth with the
initiation of TPN, octreotide infusion, intravenous fluid
(Ringer’s lactate solution; RL), morphine, and paracetamol.
A central venous catheter was inserted.
On the third day of admission, he developed abdom-
inal distension with pain and maximal fever of 37.8 ºC
(100.1 ºF). USG-guided diagnostic tapping of ascitic fluid
was performed. Ascitic fluid analysis revealed white
blood cell count of 1740 cells/mm
3
with 60% granulo-
cytes, total protein of 3.6 g/dl, and albumin of 1.8 g/dl.
Blood culture was negative at that time. On subsequent
days, leukocyte counts decreased to 13,000/mm
3
from
17,000/mm
3
. Ascitic fluid amylase was 2801 IU/L and
adenosine deaminase was 11 U/ml. Serum ascites albu-
min gradient (SAAG), the difference in serum and ascitic
fluid albumin level, was 1.0 g/dl signifying non-portal
cause. A computed tomography (CT) scan of his
abdomen and pelvis revealed decreased pancreatic bulk
with mildly prominent pancreatic duct and a small cystic
area in the uncinate process with adjacent peripancreatic
and retroperitoneal collection extending to bilateral
pararenal space, which suggested acute-on-chronic pan-
creatitis (Fig. 1).
On the tenth day of admission, a 10F pigtail drainage
was inserted in his right pelvic cavity in paracolic gutter
which drained approximately 472 ml. Previously, the
drainage from the same site at first day was 3000 ml and
20 ml on eighth day. Meanwhile, abdominal girth re-
duced from 78 cm to 68 cm during the same duration.
He improved clinically and symptomatically and was dis-
charged on the 22nd day of admission. On a follow-up
clinic visit 1 week later, our patient was noted to have
marked improvement in abdominal distension and
discomfort.
Discussion
Pancreatic ascites refers to the massive accumulation of
pancreatic fluid in the peritoneal cavity. The prevalence
rate of pancreatic ascites is only 1%; it is more common
in men than in women (male:female ratio 2:1) and be-
tween 20 and 50 years of age [8]. Ascites is commonly
seen in patients with alcoholic liver disease and is usu-
ally a consequence of portal hypertension. Biliary pan-
creatitis, pancreatic trauma and cystic duplications of
biliopancreatic ducts, ampullary stenosis, or ductal lithia-
sis account for the remainder of cases [9]. It occurs in
approximately 4% of patients with chronic pancreatitis
and 6–14% of patients with pancreatic pseudocysts. It
may also occur after an incidence of acute pancreatitis
or blunt abdominal trauma causing duct dehiscence.
The diagnosis should be considered in patients with
chronic ascites with a history of alcoholism, chronic
pancreatitis, or abdominal trauma [8]. In 80% of cases,
pancreatic ascites results from leakage from a pseudocyst
in communication with the ductal system; ductal disrup-
tion in the absence of pseudocyst accounts for the
remaining 20% of cases [5].
Patients with pancreatic ascites often present with
symptoms of mild abdominal pain, decreased appetite
and sense of fullness, weight loss, and progressive asci-
tes. They often present with a history of chronic pan-
creatitis, a recent episode of acute pancreatitis, or with
new-onset ascites. However, these symptoms may be ab-
sent in alcoholics and the diagnosis may be falsely attrib-
uted to cirrhosis. Diagnosis can be made by paracentesis
and analysis of the fluid for protein and amylase content.
Pancreatic ascites is an exudative ascites characterized
by high amylase concentration in ascitic fluid (usually
over 1000 IU/L) and protein concentration over 3 g/dl,
which differentiates it from cirrhosis, tuberculosis, or
carcinomatosis. Rarely, the origin is indeterminate in
Bhandari et al. Journal of Medical Case Reports (2020) 14:154 Page 2 of 5
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10% of cases. In addition to ascites, pleural effusion may
be seen in such cases [10].
Once the diagnosis has been established, abdominal
CT should be done to rule out pseudocysts. The use of
endoscopic retrograde cholangiopancreatography
(ERCP) has been suggested to help localize ductal ob-
struction or the site of leakage for stenting when pos-
sible. Magnetic resonance cholangiopancreatography
(MRCP) can delineate the anatomy of pancreatic duct
and any abnormalities present and can be considered for
candidates who cannot undergo ERCP [11]. However,
the role of MRCP in the diagnosis of pancreatic ascites
is not clear due to a paucity of data.
Therapy for pancreatic ascites is controversial [8].
There are no randomized control studies regarding ther-
apy due to the rarity of the condition. A patient with
Fig. 1 Computed tomography scan of the abdomen and pelvis showing decreased pancreatic bulk and small cystic area in uncinate process
with adjacent peripancreatic and retroperitoneal collection extending to bilateral pararenal space
Bhandari et al. Journal of Medical Case Reports (2020) 14:154 Page 3 of 5
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pancreatic ascites may be managed conservatively with-
holding oral feedings and starting TPN. These minimize
pancreatic secretions. One third of patients usually im-
prove with this conservative approach while some may
require treatment with octreotide or other somatostatin
analogs, diuretics, and repeated paracentesis. Segal et al.
conducted a prospective study to evaluate the efficacy of
a long-acting somatostatin analogue called Sandostatin
(octreotide) among 18 patients with either pancreatic as-
cites or external pancreatic fistulas (12). The ascites re-
solved in nine out of ten patients in a mean period of
22 days (+/−3 days). The external fistulas were all high-
output fistulas and resolved in seven out of eight pa-
tients. These results indicate the value of conservative
patient management [12].
The total duration of therapy is unknown and a trial
of 4–6 weeks is suggested with a consideration for inter-
ventional therapy if the condition does not resolve. This
approach led to healing in less than 50% of patients and
overall mortality of 15% and 15–25% recurrence [9].
Fortunately, our patient improved with conservative
management. Patients who fail conservative therapy
require interventional therapy which can be either endo-
scopic or surgical. ERCP is a valuable tool in the evalu-
ation of patients with pancreatic ascites to locate the site
of disruption and, subsequently, placement of a transpapil-
lary stent to bypass the obstruction in addition to large-
volume paracentesis. In addition, patients can undergo
concomitant endoscopic or percutaneous pseudocyst
drainage [8].
Surgical therapy is recommended when there is no re-
sponse to conservative therapy in 3–4 weeks. The choice
of surgery depends on the site of leakage and associated
pancreatic abnormality as demonstrated by ERCP and
contrast-enhanced CT. Pseudocysts are usually treated
by distal pancreatectomy when the leak is in the pancre-
atic tail or drained by cystogastrostomy, cystojejunost-
omy, or cystoduodenostomy. Studies have shown that
internal pancreatic drainage is the ideal surgical treatment
for patients with pancreatic ascites and/or pleural effusion
that do not respond to medical treatment. When this is
not feasible, external drainage can be used as an alterna-
tive to pancreatic resection [7]. Fistulas in the pancreatic
duct are usually drained to a Roux-en-Y jejunal loop. Re-
currence rates from 50 to 64% have been reported in pa-
tients undergoing surgical intervention without ERCP [8].
Mortality rates have been reported to be similar with sur-
gical and medical therapies (15–25%) [8].
We successfully managed our patient with a conserva-
tive approach. Our case highlights a few important mes-
sages. First, we often label the ascites as cirrhotic or
secondary to portal hypertension given its high preva-
lence; it is important to also consider pancreatic ascites
as part of the differential. As a clinician, it is important
not to miss cases of pancreatic ascites. Past history or re-
cent history of pancreatitis, recurrent admissions to an
emergency room due to abdominal pain in chronic alco-
holics, or history of blunt abdominal trauma may pro-
vide important guidance in diagnosing such cases.
Furthermore, evaluation of the SAAG can be accurately
measured to narrow the diagnosis. Paré et al. reported
that SAAG calculation offers the best diagnostic discrim-
ination between ascites caused by liver disease and asci-
tes caused by a neoplasm [13]. Second, such cases are
typically rare, and if diagnosed can be managed with
medical and/or interventional therapy.
Conclusion
Alcoholic chronic pancreatitis is the most common
cause of pancreatic ascites; it is a rare entity. Biliary pan-
creatitis, pancreatic trauma and cystic duplications of
biliopancreatic ducts, ampullary stenosis, or ductal lithia-
sis account for the remainder of cases. Diagnosis is usu-
ally clinched by raised ascitic fluid amylase (> 3 times
that of plasma), raised total ascitic protein level (> 3 g/dl)
and low SAAG (< 1.1 g/dl) in the presence of pancreatic
disease, and such cases can be managed by a conserva-
tive approach.
Abbreviations
TPN: Total parenteral nutrition; CEA: Carcinoembryonic antigen;
CT: Computed tomography; ERCP: Endoscopic retrograde
cholangiopancreatography; MRCP: Magnetic resonance
cholangiopancreatography; HCO
3
: Bicarbonate; LDH: Lactate dehydrogenase;
ALP: Alkaline phosphatase; pCO
2
: Partial pressure of carbon dioxide;
RL: Ringer’s lactate solution; SGOT: Serum glutamic-oxaloacetic transaminase;
SGPT: Serum glutamic-pyruvic transaminase; USG: Ultrasonography;
SAAG: Serum ascites albumin gradient
Acknowledgements
Not applicable.
Authors’contributions
RB was involved in treating the patient, manuscript writing, and reviewing. RC
was involved in manuscript writing and reviewing. SB was involved in treating
the patient and manuscript reviewing. EHT was involved in reviewing the
manuscript. RM and RSB were involved in treating the patient and reviewing
the manuscript. The authors read and approved the final manuscript.
Funding
No funding was required for this work.
Availability of data and materials
All data are within the article.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent for publication of this case report and
accompanying images was obtained from the patient. A copy of the written
consent is available for review by the Editor-in-Chief of this journal.
Competing interests
None of the authors have any conflict of interest to disclose. We confirm
that we have read the Journal’s position on issues involved in ethical
publication and affirm that this case report is consistent with those
guidelines.
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Author details
1
Department of General and GI Surgery, Tribhuvan University Teaching
Hospital, Kathmandu, Nepal.
2
Tribhuvan University, Institute of Medicine,
Maharajgunj, Kathmandu, Nepal.
3
Department of Orthopedic Surgery and
Rehabilitation Medicine, State University of New York, Downstate Medical
Center, Brooklyn, New York, USA.
Received: 1 June 2020 Accepted: 27 July 2020
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