Pancreaticopleural Fistula with Bilateral Plural Effusion

PANCREATICOPLEURAL FISTULA WITH BILATERAL PLEURAL EFFUSION

JAYSHRI MAKHIJANI*, SANDRA DRAGO**, AJ PAIDHUNGHAT***,HARDIK SHAH****, VISHAL JAYKAR****
*Lecturer; **Associate Professor; ***Professor in Medicine; ****Resident, Department of Medicine, TN Medical College and BYL Nair Ch. Hospital, Mumbai Central, Mumbai 400 008, India.

A case of pancreaticopleural fistula with bilateral pleural effusion is presented.

INTRODUCTION

Inflammatory disease of pancreas is associated with a number of complications like pancreatic abscess, pseudocyst formation and various metabolic abnormalities. These are well documented sequelae seen with acute attacks. Chronic pancreatitis can result in exocrine insufficiency with steatorrhoea and endocrine insufficiency resulting in diabetes. Here we document a case of pancreaticopleural fistula which has been a well recognized complication of chronic pancreatitis.

CASE REPORT

A 30 year old male was admitted to the hospital complaining of sudden onset breathlessness and left sided chest pain. He had attacks of severe epigastric pain for several months radiating to the back but not related to meals. Patient was a chronic alcoholic. On examination, patient was afebrile and haemodynamically stable. Rest of general examination was normal. Examination of respiratory system revealed a stony dull note on percussion and absent air entry in the left hemithorax. On abdominal system examination there was evidence of hepatomegaly with tenderness in epigastric region. Rest of systemic examination was unremarkable. Based on history and clinical findings, a provisional diagnosis of left sided pleural effusion with pancreatitis was made. Chest X-ray (Fig. 1) showed homogeneous opacification of left hemithorax suggestive of massive left sided pleural effusion. Paracentesis of pleural fluid produced 1200 ml of haemorrhagic fluid with protein content of 3.7 g/ml, white blood cell count of 100/cumm, red blood cell count of 2000/cumm and no organisms on Gram staining. The amylase content of pleural fluid was 1780 IU/ml, whereas the serum amylase was only 668 IU/ml. Ultrasonography of abdomen revealed pancreatic calcification suggestive of chronic pancreatitis with bilateral pleural effusion. Despite repeated thoracocentesis, radiography of chest showed refilling of fluid in pleural space. Computed tomography of abdomen (Fig. 2) was done which revealed right pancreaticopleural fistula with right sided pleural effusion. Also calcification of head, body and tail of pancreas was noted with phlegmon formation. Patient was started on conservative management, kept nil by month, put on continuous Ryle tube drainage and patient was started on somatostatin and intravenous antibiotics. Intercostal drainage tube was inserted and drainage was 800-1000 ml/day for initial 3 days. The intercostal tube was removed after 6 days as drainage was minimal. The amylase content of the pleural fluid and serum gradually diminished and was 38 IU/ml and 62 IU/ml after 7 days. Right pleural effusion being small, did not require intercostal drainage. Patient was subjected to endoscopic retrograde pancreaticography (Fig. 3) which revealed stricture of pancreatic duct at junction of head-body of pancreas and a leak from pancreatic duct into right pleural space was also visualized. The rest of pancreatic duct could not be seen since guide wire could not be negotiated beyond the stricture and the second leak into the left pleural space was therefore not appreciated. Stenting of the pancreatic duct was done proximal to the stricture. The recovery was uneventful and the patient was then discharged and advised to follow up regularly in the out patient department.

Fig 1 : Chest X-ray shows homogeneous opacification of left hemithorax suggestive of massive left sided pleural effusion.

Fig 2: Computed tomography of abdomen reveals calcification of head, body and tail of pancreas with phlegmon formation

DISCUSSION

Pancreaticopleural fistula is an uncommon sequalae of pancreatitis.[1] Pleural effusions in the course of acute pancreatitis develop in 3-17% of patients and are believed to represent a sympathetic, chemically induced diaphragmatic pleural inflammation. The pancreatic enzyme activity of the pleural fluid is low and the effusion tends to resolve along with the pancreatitis.[2,3] Large recurrent effusions demonstrating a high amylase content in the pleural aspirate relative to serum are a hallmark of pancreaticopleural fistula as in our patient.

Fig 3: Edoscopic retrograde pancreaticography reveals structure of pancreatic duct at junction of head-body of pancreas and a leak from pancreatic duct into right pleural space.

Pancreaticopleural fistula is commonly associated with both disruption of main pancreatic duct and pseudocyst formation. The fistula develops either by direct passage of a pseudocyst through a natural diaphragmatic hiatus (e.g. Oesophageal or aortic) or by direct fistulation through the dome of diaphragm.[2] Pleural effusion and nonspecific thoracic symptoms such as pain, dyspnoea, cough, sputum production etc. may dominate the clinical status of the patient, whereas the abdominal symptoms are only mild. The condition is therefore often elusive, as respiratory rather than abdominal symptoms usually predominate as noted in this case.[4] Biochemical analysis of pleural fluid is another important diagnostic tool. The amylase is always markedly elevated, often in thousands and the albumin is usually 3 g/dl as observed in our patient. The albumin is presumably elevated be cause of subacute inflammatory response of serosal surface. If albumin is not elevated, this usually indicates that patient is severely malnourished and hypoalbuminaemic. The elevation of serum amylase does not indicate active inflammatory disease that occurs as a result of passive absorption of amylase from parietal surfaces. A normal serum does not eliminate the diagnosis of an internal pancreatic fistula.[5]

Ultrasonography, Computed Tomography and endoscopic retrograde pancreaticography may localize the origin of internal fistulas by identifying the duct pathology and defining the pathway of extension of pancreatic secretions to the thoracic cavity, thus allowing an exact classification.[6]

Initial treatment should be directed towards control of the pleural effusion. Intercostal tube drainage, parenteral nutrition and somatostatin analogue octreotide achieved a 48% fistula closure rate over a two-three week period with conservative management.[2] Persistence or recurrence of an effusion is an indication for pancreatic surgery. Even when conservative treatment is successful, the underlying cause, i.e. chronic pancreatitis may need addressing. In our patient, stenting of pancreatic duct was done proximal to the stricture. If obstruction to the duct system is present, surgical decompression with or without excision of involved portion of obstructed pancreas may be required. It is unnecessary to resect fistulous tract if pancreatic duct obstruction is dealt with adequately. Surgical procedures have an operative mortality of 3-5% and a good long term outcome in 80-95% cases.[1]

REFERENCES

1.Wakefield S, Tulty B, Britton J. Pancreaticopleural fistula : Rare complication of chronic pancreatitis. Post Grade Med J 1996; 48 : 115-6.

2. Cameron JL. Chronic pancreatic ascites and pancreaticopleural effusions. Gastroenterology 1978; 74 : 134-40.

3. Cameron JL, Kieffer RS, Anderson WJ, et al. Internal pancreatic fistulas : pancreatic ascites and pleural effusions. Ann Surg 1976; 184 : 587-93.

4..Izbicki JR, Wilker DK, Waldner H, Rueff FI, Schweiberer L. Thoracic manifestations of Internal pancreatic fistulae : Report of five cases. Ann and Gastroenterol 1989; 84 : 265-71.

5. Lipsett PA, Cameron JL. Internal pancreatic fistula. Ann J Surg 1992; 163 : 216.

6.Satake K, Cho K, Sowa M, et al. Demonstration of a pancreatic fistula by endoscopic pancreaticography. In a patient with Chronic pleural effusion. Ann J Surg 1978; 136 : 390-2.

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