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Year : 2019  |  Volume : 8  |  Issue : 1  |  Page : 29-31

Pancreatic ascites with 'inflammatory transudate'

1 Department of Medicine, Meenakshi Medical College, Hospital and Research Institute, Kanchipuram, Tamil Nadu, India
2 Department of Medicine, Apollo Institute of Medical Sciences and Research, Chittoor, Andhra Pradesh, India

Date of Web Publication6-Nov-2019

Correspondence Address:
M S Sridhar
Professor, Department of Medicine, Meenakshi Medical College, Hospital and Research Institute, Enathur, Kanchipuram, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCSR.JCSR_26_19

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Pancreatic ascites is not an uncommon condition but requires a high degree of suspicion for prompt diagnosis. Since both hepatic cirrhosis and pancreatitis are related to ethanol abuse, routine investigation of patients with cirrhotic ascites for the rise of ascitic fluid amylase levels will facilitate early diagnosis. The combination of inflammation of pancreas and portal hypertension due to hepatic cirrhosis could give a picture of 'inflammatory transudate'.

Keywords: Ascites, inflammatory transudate, pancreatic ascites

How to cite this article:
Prasad M R, Gopalakrishna P, Madhuri M S, Sridhar M S. Pancreatic ascites with 'inflammatory transudate'. J Clin Sci Res 2019;8:29-31

How to cite this URL:
Prasad M R, Gopalakrishna P, Madhuri M S, Sridhar M S. Pancreatic ascites with 'inflammatory transudate'. J Clin Sci Res [serial online] 2019 [cited 2021 Sep 23];8:29-31. Available from: https://www.jcsr.co.in/text.asp?2019/8/1/29/270384

  Introduction Top

Ascites is excessive and abnormal accumulation of fluid in peritoneal cavity. When this occurs during the course of acute or chronic pancreatitis, it is called 'pancreatic ascites'.[1] It could usually be due to alcohol abuse. Awareness of pancreatic ascites has increased since the early 1950s when it was said to be first reported.[2]

  Case Report Top

A 33-year-old man presented to medicine outpatient service in a teaching hospital with complaints of painful abdominal distension, and breathlessness and left-sided chest pain of 1-month duration. At the age of 8 years, he was treated for pulmonary tuberculosis. There is a history of ethanol and nicotine abuse. Physical examination details are as follows: pulse 82/min, blood pressure 120/70 mmHg in the right arm in the supine position, respirations 28/min and temperature 98.5°F.

There was mild distension of abdomen with tenderness over all the regions; shifting dullness was present. Examination of respiratory system revealed flat note over the left mammary, left infra-axillary and infrascapular regions and reduced to absent breath sounds in the same regions suggesting pleural effusion.

In view of the chronic ethanol abuse, pain abdomen and unilateral shifting dullness, the possibility of chronic liver disease complicated by tuberculosis peritonitis was considered. Ultrasonography of abdomen showed features of cirrhosis of liver, gross ascites, left-sided pleural effusion and mild splenomegaly with splenic collaterals. Contrast-enhanced computed tomography (CECT) of the abdomen showed features of acute pancreatitis with multiple pseudocysts. Upper gastrointestinal endoscopy showed fundic varices with duodenitis. Based on CECT abdomen and other imaging findings, elevated levels of ascitic fluid amylase and the presence of exudative left-sided pleural effusion [Table 1] and [Table 2], the diagnosis of pancreatic ascites was established. The patient was managed conservatively by medical therapy which is the initial treatment recommended; he was discharged at request for treatment at another centre of his choice.
Table 1: Laboratory investigations

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Table 2: Blood/serum, ascitic fluid, pleural fluid analysis

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  Discussion Top

Pancreatic ascites is said to more common among males between ages of 20 and 50. While the abdominal pain is described as 'variable' and abdominal tenderness is notably lacking,[1] both were present in the case of the patient reported. Pancreatic ascites occurs generally against the background of heavy alcohol consumption. Several possible mechanisms of pathogenesis of pancreatic ascites were described. Transdiaphragmatic lymphatic transfer of pancreatic enzymes, intrapleural rupture of mediastinal extensions of pseudocysts and diaphragmatic perforation are some of them. The diagnostic value of pleural fluid amylase levels was recognized. The predilection for left-sided pleural effusion is explained on the anatomical basis of intimate relation of pancreas to the left hemidiaphragm.[3]

The mechanism of ascites and pleural effusion is succinctly described by Cameron[2] as due to disruption of the main pancreatic duct, resulting in an internal fistula between the duct and peritoneal cavity, producing massive ascites and if the duct disruption is posterior, pancreatic secretions can track up into the mediastinum and then escape into one or both pleural spaces, resulting in an internal fistula between the pancreatic duct and pleural space, producing a massive effusion.

The amylase in the ascitic fluid of a patient with pancreatic ascites is always elevated even if the serum levels are normal or slightly elevated as clearance from serum is faster in comparison to that of ascites. In addition, the ascitic fluid protein is usually elevated to the range of 3 g/dL or above. The combination of ascitic fluid protein level in 'exudative' range and serum albumin ascitic fluid albumin gradient (SAAG) in the portal hypertensive range or 'transudative' range gives a picture of 'inflammatory transudate' similar to the observation by Witte et al[4]that peritoneal transudate could be a diagnostic clue to portal system obstruction in patient with intra-abdominal neoplasms or peritonitis. In the present case, though exudative peritoneal fluid is expected, the level of SAAG of 1.3 g/dL suggests the existence of portal hypertension for which imaging and endoscopic findings lend credence. Hence, apart from the traditional concept of transudate and exudates, an additional term inflammatory transudate is also useful so that a wider range of conditions can be considered in the differential diagnosis. Thus, in the evaluation of ascites, the terms, transudate, exudates, serum-to-ascites total protein gradient[5] and SAAG[6] which gives clue whether portal hypertension is present or not and 'inflammatory transudate' form a battery of investigations in the diagnosis of ascites.

In patients with chronic alcoholic liver disease and pancreatitis, the ascitic fluid picture could be misleading. A 'gestalt' of ascitic fluid easily settles the issue. Since the ascitic fluid protein parameters had mixed features, ascitic fluid of the patient reported can be termed as 'inflammatory transudate'.

All patients with ethanol abuse and cirrhotic ascites should be routinely investigated for possible pancreatic ascites. A high degree of suspicion of pancreatic ascites in all patients with alcoholic hepatic cirrhosis without reference to pain abdomen would allow recognition of more number of patients with pancreatic ascites, and proper medical and surgical management can be planned.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Donowitz M, Kerstein MD, Spiro HM. Pancreatic ascites. Medicine (Baltimore) 1974;53:183-95.  Back to cited text no. 1
Cameron JL. Chronic pancreatic ascites and pancreatic pleural effusions. Gastroenterology 1978;74:134-40.  Back to cited text no. 2
Kaye MD. Pleuropulmonary complications of pancreatitis Thora×1968;23:297-306.  Back to cited text no. 3
Witte MH, Witte CL, Davis WM, Cole WR, Dumont AE. Peritoneal transudate. A diagnostic clue to portal system obstruction in patients with intra-abdominal neoplasms or peritonitis. JAMA 1972;221:1380-3.  Back to cited text no. 4
Pillay VK. Diagnostic significance of protein concentration in serous fluids. S Afr Med J 1963;37:379-81.  Back to cited text no. 5
Rector WG Jr., Reynolds TB. Superiority of the serum-ascites albumin difference over the ascites total protein concentration in separation of “transudative” and “exudative” ascites. Am J Med 1984;77:83-5.  Back to cited text no. 6


  [Table 1], [Table 2]


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