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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 4  |  Issue : 2  |  Page : 218-221

Pancreatic pleural effusion: A diagnosis not to be missed!


1 Department of Internal Medicine, Tata Main Hospital, Tata Steel, Jamshedpur, Jharkhand, India
2 Department of Pulmonary Medicine, Tata Main Hospital, Tata Steel, Jamshedpur, Jharkhand, India

Date of Web Publication20-Dec-2016

Correspondence Address:
Sangita Kamath
Department of Internal Medicine, Tata Main Hospital, Tata Steel, Jamshedpur, Jharkhand
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2321-4848.196206

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  Abstract 

Pleural effusion as a consequence of acute pancreatitis is transient, usually left-sided; straw colored and accounts for 1% of all the cases. Rarely, it may be right-sided and hemorrhagic causing difficulty in establishing the diagnosis, especially if the chest symptoms are disproportionately more than the abdominal symptoms. We present a case of a young alcoholic male patient with a history of inadequately treated tuberculosis in the past, who presented with massive right pleural effusion, ascites, and right hydrocele and was overtly symptomatic for 1 week before hospital admission. Evaluation of pleural fluid revealed hemorrhagic, lymphocyte predominant exudate with low Adenosine Deaminase (ADA) and high amylase level. Ascitic fluid too showed similar characteristics. His serum amylase level was also elevated which prompted us to make a clinical diagnosis of pancreatic pleural effusion with ascites. Further radiological investigations confirmed the diagnosis of acute pancreatitis. Early pleural fluid amylase testing will certainly avoid a delay in the timely diagnosis.

Keywords: Amylase, hemorrhagic pleural effusion, pancreatitis, pseudocyst


How to cite this article:
Kamath S, Samanta RP, Rao BS. Pancreatic pleural effusion: A diagnosis not to be missed!. Arch Med Health Sci 2016;4:218-21

How to cite this URL:
Kamath S, Samanta RP, Rao BS. Pancreatic pleural effusion: A diagnosis not to be missed!. Arch Med Health Sci [serial online] 2016 [cited 2017 Mar 23];4:218-21. Available from: http://www.amhsjournal.org/text.asp?2016/4/2/218/196206


  Introduction Top


Acute pancreatitis generally causes transient, mild to moderate left-sided pleural effusion. The underlying pancreatic disease especially if asymptomatic, the diagnosis can be missed. We report a rare case of a young male alcoholic patient with acute on chronic pancreatitis who developed massive hemorrhagic right pleural effusion and ascites with high amylase concentrations.


  Case Report Top


A 38-year-old man presented to our hospital with progressively increasing breathing difficulty and abdominal distension of 3 weeks duration. He would become breathlessness on walking a few steps and going to bathroom 1 week before admission. He had a dry cough on lying down partly relieved by sitting up. There was loss of appetite, nausea but no vomiting. Four weeks before the development of the above complaints, he had upper abdominal pain with fever for 4–5 days which had subsided with medication taken from a local doctor. There was no history of trauma to the chest and abdomen. He was not a smoker but had been a chronic alcoholic for past 12 years and would consume alcohol almost daily till the onset of his disease. He had taken anti-TB therapy (DOTS) for 2 months for pulmonary tuberculosis 6 months back and had stopped treatment on his own. His sputum was 1+ positive for acid fast Bacillus (AFB) then.

On admission, he was lean, coherent, febrile, had mild pallor, no lymphadenopathy, clubbing, cyanosis, icterus, pulse was 98/min, regular, adequate volume, and blood pressure was 110/70 mm Hg. Signs of chronic liver disease, such as palmar erythema, spider nevi, and parotid glands enlargement, were not detected. The examination of respiratory system revealed tachypnea (respiratory rate 28/min), stony dull note, absent vocal fremitus, and absent breath sounds on the right with tracheal and mediastinal shift to the left. Abdominal examination revealed diffuse tenderness and massive ascites. Liver span was normal. Examination of rest of the systems was normal.

His blood parameters on admission showed hemoglobin of 9.8 g/dl, mean corpuscular volume 88 fl, total leukocyte count of 7700/cu mm with 58% neutrophils, 9% monocytes and 22% lymphocytes, 10% eosinophils and platelet count 3.67 lakhs/cu mm. His biochemical tests showed blood urea 44 mg/dl, serum creatinine 0.6 mg/dl, serum sodium 137 mmol/L, serum potassium 4.1 mmol/L, serum calcium 8.4 mg/dl, serum thyroid-stimulating hormone 1.96 µIU/ml, serum amylase 641.6 U/L, serum lipase 1352.8 U/L, and serum lactate dehydrogenase (LDH) 386.4 U/L. His liver function test revealed serum bilirubin 0.57 mg/dl, alanine transaminase 20.5 U/L, aspartate transaminase 116.8 U/L, alkaline phosphatase 134.2 U/L, total proteins 5.58 g/dl, serum albumin 2.4 g/dl, serum globulin 3.18 g/dl and INR 1.82. His lipid profile was within normal limits except for low high-density lipoprotein cholesterol (HDL-c) which was 31.6 mg/dl. His urine routine examination was normal, and culture was sterile. His viral markers (hepatitis B surface antigen, anti-hepatitis C virus antibodies, anti-HIV l and ll antibodies) were nonreactive. His antinuclear antibody and rheumatoid arthritis tests were negative. Stool for occult blood was negative. X-ray chest showed massive right pleural effusion with tracheal and mediastinal shift to the left. The left lung was normal [Figure 1]. Sputum on Ziehl–Nelson staining did not show AFB. No pathogenic organisms were isolated on the culture of sputum.
Figure 1: Chest X-ray showing massive right pleural effusion.

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His pleural fluid examination revealed uniformly hemorrhagic fluid [Figure 2]a with a total cell count of 380/cu mm with 30% neutrophils, 40% lymphocytes, plenty of red blood cells (RBCs), and 30% reactive mesothelial cells. Malignant cells were not found in all three samples. Microorganisms, AFB, and fungal elements were not found. Biochemical analysis showed exudative fluid with total proteins 3.15 g/dl, albumin 1.5 g/dl (serum ascites albumin gradient 0.9 which is <1.1), LDH 486.7 U/L, glucose 82 mg/dl, and Adenosine Deaminase (ADA) 15.3 U/L (>30 U/L significant). Pleural fluid cultures were sterile for aerobic and anaerobic organisms while lipase was 5956.8 U/L. Ascitic fluid also was uniformly hemorrhagic [Figure 2]b with a total cell count of 450/cu mm with 25% neutrophils, 45% lymphocytes, plenty of RBCs and 30% reactive mesothelial cells. Biochemical analysis showed exudative fluid with total proteins 3.75 g/dl, albumin 2 g/dl, LDH 566.7 U/L, glucose 88 mg/dl, and ADA 12.3 U/L (>30 U/L significant). Malignant cells were not found in all three samples. His ascitic fluid lipase was 5451.6 U/L. Microorganisms, AFB, and fungal elements were not found.
Figure 2: (a) Hemorrhagic pleural fluid. (b) Hemorrhagic ascitic fluid.

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Ultrasound examination of abdomen and pelvis showed gross ascites with echogenic fluid, increased echotexture of liver, obscured pancreas, Grade 1 renal parenchymal disease and echogenic fluid in the right tunica vaginalis. Upper gastrointestinal (GI) endoscopy was normal except for mild diffuse gastritis. Contrast enhanced computerized tomography (CECT) of chest showed massive right pleural effusion [Figure 3]a and [Figure 3]b with compressive lung collapse while that of abdomen confirmed the findings of ultrasound, in addition, it showed hypoechoic bulky body and tail of the pancreas, mild dilatation of the main pancreatic duct, specks of calcification suggestive of acute on chronic pancreatitis [Figure 4]a and [Figure 4]b. There was no evidence of pseudocyst or stricture. A working diagnosis of acute on chronic pancreatitis (probably ethanol-induced) with pancreatic right pleural effusion, ascites and hydrocele and ethanol-induced liver disease was made.
Figure 3: (a and b) Computerized tomography of thorax showing massive right pleural effusion.

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Figure 4: (a and b) Computerized tomography abdomen showing bulky pancreas with speckles of calcification suggestive of acute on chronic pancreatitis.

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During the hospital stay, 4 L of ascitic fluid and 1 L of pleural fluid were tapped, on the 2nd day, only to find rapid re-accumulation by the 5th day [Figure 5]. Again 3.5 L of ascitic fluid and 1.5 L of pleural fluid were tapped on the 5th day. In view of rapid accumulation, injection octreotide 50 mcg subcutaneously 3 times, a day was started and right-sided underwater seal intercostal drainage tube was inserted after consulting chest physician and gastroenterologist. He received octreotide for 2 weeks, in addition to piperacillin-tazobactam 4.5 g thrice a day intravenously. His intercostal tube drainage gradually decreased to 300 ml to 400 ml/day from the initial 1.5–1.8 L/day. A Magnetic Retrograde Cholangio Pancreaticography was planned. However, patient refused and on the 20th day of admission, left the hospital against medical advice due to financial constraint.
Figure 5: Fluid reaccumulated by 5th day after tapping.

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  Discussion Top


Pleural effusion often occurs as a complication of pancreatic disorders such as acute pancreatitis, pancreatic abscess, pseudocyst, and chronic pancreatitis.[1] The incidence of pleural effusion with acute pancreatitis in older reports was about 3–7%,[2] but it is nearing 50% in recent reports based on pleural fluid detection by CT.[3] Pancreatic pathologies can be complicated by two types of pleural effusion. The first is usually a small left-sided effusion,[4] reactive, often mild to moderate and characterized by normal amylase activity (below 100 U/L) and low protein concentration (<3 g/dl); this type is associated with acute pancreatitis and resolves during recovery. The second type of pleural effusion is related to the presence of pancreaticopleural fistula (PPF) in the course of chronic pancreatitis; this effusion is usually large, single-sided, recurrent, contains a high level of amylase above 1000 U/L and protein above 3 g/dl.[5],[6] It rapidly accumulates and is refractory to drainage procedures. Right-sided effusions account for 20% of the cases while 15% are bilateral.[7]

Alcoholism is the most common cause of acute pancreatitis in males accounting for 90% of the cases.[7] Pleural effusion is commonly observed in men than women with chronic alcoholism.[7] The pathogenic mechanism involved in the formation of the pleural effusion include direct contact of pancreatic enzymes with the diaphragm, hematogenous transfer of pancreatic enzymes into pleura,[8] transfer of pancreatic secretions through transdiaphragmatic lymphatics and formation of pleuropancreatic fistula which results in direct communication of pancreatic pseudocyst with pleural cavity.[3],[8] Rarely, there may spontaneous rupture of the pseudocyst into the pleural cavity causing massive pleural effusion.[9] PPFs have been noted in 2.3–4.5% of patients presenting with pancreatic pseudocyst.[10] If the pancreatic duct disruption occurs posteriorly, an internal fistula may develop between the pancreatic duct and the pleural space, producing a pleural effusion (PPF) that is usually left-sided. If the pancreatic duct disruption is anterior, amylase- and lipase-rich peritoneal fluid accumulate (pancreatic ascites).[8] Sometimes pancreatic fluid tracks through the aortic or esophageal hiatus into the mediastinum. Occasionally, secretions are contained within the mediastinum presenting as a mediastinal pseudocyst.[10]

Once fluid enters the pleural space, the PPF is likely to result in a massive chronic pleural effusion.[11] If therapeutic thoracentesis is performed, the pleural effusion re-accumulates rapidly. These effusions are generally serosanguinous, hemorrhagic and of exudative type. Hemorrhagic pleural effusion is also seen in cases of thoracic trauma, tuberculosis, intrathoracic malignancy, bleeding diathesis, and rarely uremic pleural effusions.[12],[13]

That the massive pleural effusion and ascites were secondary to pancreatitis (acute on chronic) was by established by elevated pleural fluid amylase and lipase level when compared to that in serum, which may also be seen in tuberculosis, malignancy and oesophageal rupture. Tubercular pleural effusion was ruled out by not finding mycobacterium in the cultures of pleural fluid and sputum. Contrast CT thorax also did not show evidence of pulmonary tuberculosis. Malignancy was ruled out with pleural fluid and ascitic fluid cytologic studies (done 3 times) and was supported by CECT thorax. Oesophageal rupture was not considered based on the clinical picture and was also supported by upper GI endoscopy and radiological investigations.

When the chest symptoms dominate the clinical picture, and with no previous history of pancreatic disease, diagnosis becomes difficult as the pancreatic condition remains completely or partly in the background. Many patients go through extensive pulmonary evaluation before the pancreas is identified as the site of primary pathology. In one series of 113 patients from Japan, 42 complained of dyspnea and 29 complained of chest and back pain, while only 23 complained of upper abdominal pain.[7] As the underlying pancreatic disease may be asymptomatic, pleural fluid amylase should be measured in any case of recurrent exudative pleural effusion of unknown etiology. It is the best screening test for diagnosing pancreatic pleural effusion. It is markedly elevated, usually over 1000 U/L, even when the serum amylase may be mildly elevated. CT chest as well as abdomen and endoscopic retrograde cholangiopancreatography (ERCP) are required for confirmation of diagnosis and planning surgery.

In our case also the diagnosis was initially overlooked as a patient gave a history of predominantly chest symptoms with few abdominal symptoms and that too on direct interrogation. The initial working diagnosis was tubercular pleural effusion with ascites in view of history of tuberculosis incompletely treated tuberculosis in the past. The massive right pleural effusion and ascites were probably due to PPF, which may be difficult to demonstrate. CT imaging can diagnose fistula only in 33–47% of cases while ERCP can demonstrate PPF in 46–78% of cases.[6] The pseudocyst may rupture into the pleural cavity and on ultrasonography or CT abdomen, pseudocyst may not be seen in the pancreas thus, probably explaining why pseudocyst was not seen in our case.

Treatment with drainage by an intercostal chest tube, with concomitant conservative treatment of pancreatitis to decrease pancreatic exocrine secretion (nasogastric suction, total parental nutrition, somatostatin analogs), is usually effective in massive pancreatic pleural effusions.[5] If drainage by a chest tube fails after 2–3 weeks, percutaneous catheter drainage of the abdominal pseudocyst can be considered, or gastrocystostomy can be done for pseudocyst. Some patients who have PPF in head or body on ERCP can be successfully treated by placing stents in the pancreatic duct.[14] Surgery is usually resorted to when medical or endoscopic therapy fails.


  Conclusion Top


Right-sided pleural effusion in the setting of pancreatitis is rare and occurring in association with ascites and hydrocele and being hemorrhagic in nature is further extremely rare. Pancreatitis should be taken into consideration when hemorrhagic pleural effusion occurs, especially when it has elevated amylase level. Lack of awareness can result in a delay in the diagnosis and morbidity. This case is, hence, presented to make the physicians aware of this rare presentation.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
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2.
Lankisch PG, Dröge M, Becher R. Pleural effusions: A new negative prognostic parameter for acute pancreatitis. Am J Gastroenterol 1994;89:1849-51.  Back to cited text no. 2
    
3.
Bedi RS. Massive pleural effusion due to asymptomatic pancreatic disease. Lung India 2006;23:163-4.  Back to cited text no. 3
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Aswani Y, Hira P. Pancreaticopleural fistula: A review. JOP 2015;16:90-4.  Back to cited text no. 4
    
5.
Rockey DC, Cello JP. Pancreaticopleural fistula. Report of 7 patients and review of the literature. Medicine (Baltim) 1999;69:332-44.  Back to cited text no. 5
    
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Sontakke A, Tayade BO. Case series of pancreatic pleural effusion with pancreatico-pleural fistula. JIACM 2014;15:245-8.  Back to cited text no. 6
    
7.
Uchiyama T, Suzuki T, Adachi A, Hiraki S, Iizuka N. Pancreatic pleural effusion: Case report and review of 113 cases in Japan. Am J Gastroenterol 1992;87:387-91.  Back to cited text no. 7
    
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Kumar S, Diwan SK, Dekate M. Chronic pancreatitis presenting as recurrent pleural effusion. Online J Health Allied Sci 2013;12:22.  Back to cited text no. 8
    
9.
Marwah S, Shivaran K, Guruwalia JP. Spontaneous rupture of pseudopancreatic cyst causing massive pleural effusion. Int J Case Rep Med 2013;2013:4.  Back to cited text no. 9
    
10.
Moorthy N, Raveesha A, Prabhakar K. Pancreaticopleural fistula and mediastinal pseudocyst: An unusual presentation of acute pancreatitis. Ann Thorac Med 2007;2:122-3.  Back to cited text no. 10
[PUBMED]  Medknow Journal  
11.
Wakefield S, Tutty B, Britton J. Pancreaticopleural fistula: A rare complication of chronic pancreatitis. Postgrad Med J 1996;72:115-6.  Back to cited text no. 11
    
12.
Porcel JM, Vives M. Etiology and pleural fluid characteristics of large and massive effusions. Chest 2003;124:978-83.  Back to cited text no. 12
    
13.
Raghu MB, Balasubramanian S, Balasubramanyam G. Hemorrhagic pleural effusion – sole manifestation of pancreatitis. Indian J Pediatr 1992;59:767-9.  Back to cited text no. 13
    
14.
Safadi BY, Marks JM. Pancreatic-pleural fistula: The role of ERCP in diagnosis and treatment. Gastrointest Endosc 2000;51:213-5.  Back to cited text no. 14
    


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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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