Teaching Case

A 27-year-old chronic alcoholic male patient came with complaints of epigastric pain. He also had dyspnoea at rest. The patient has had a history of pancreatitis before with last episode of epigastric pain 6 months back

US (done in different institution) revealed chronic pancreatitis with a large pseudocyst arising from the pancreas and left-sided pleural effusion.

CECT thorax and upper abdomen done in our institution revealed atrophic pancreas with a large thick-walled pseudocyst (12 x 10 x 8 cm) arising from the body and tail of pancreas. The pseudocyst was noted to extend anterosuperior into the lesser sac and push the stomach anteriorly. Superiorly the pseudocyst was noted to extend into the mediastinum through the oesophageal hiatus via a fistula anterior to the aorta and communicate with the bilateral pleural cavity with left massive pleural effusion causing complete collapse of the underlying lung parenchyma. Right mild pleural effusion was also noted. There was peripancreatic inflammation noted.

Thoracocentesis was done which revealed blood-stained collection with high amylase and lipase levels.

Pleural effusion can be seen in both acute and chronic pancreatitis. In acute pancreatitis, the effusions are usually left-sided, small and self-limiting likely of reactive, lymphatic or sympathetic origin.[1]. These show normal amylase activity and albumin concentration [2]. The second type of pleural effusion is due to the presence of pancreaticopleural fistula (PPF) associated with chronic pancreatitis which is usually large, recurrent and has high level of amylase above 1000 U/L and protein above 3 g/dl.[2][3]. PPF may gain access to the pleural cavity through the sternocostal triangle, the aortic/oesophagal hiatus or directly through the diaphragm [4]. PPF is considered a rare pathology with incidence estimated at 0.4% in patients with pancreatitis and 4.5% in those presenting with a pancreatic pseudocyst[4].

PPF usually involves males in their late 40s having chronic pancreatitis due to excessive alcohol abuse. These patients usually present to the emergency room with breathing difficulty and abdominal symptoms are usually absent.[5].

In patients with PPF, chest radiograph usually demonstrates unilateral or bilateral pleural effusion, with the left side being more common. Thoracocentesis is usually done for symptom relief. Laboratory analysis of the pleural fluid reveals amylase levels greater than 1000 IU which may be suggestive for PPF in the absence of malignant cells [5].

In our patient, the initial USG revealed a large pancreatic pseudocyst. CECT  imaging of thorax and upper abdomen showed the fistulous communication between the cyst and the pleural cavity via the oesophageal hiatus. Previous studies state that CT imaging can diagnose fistula only in 33–47% of cases while ERCP can demonstrate PPF in 46–78% of cases[4]. Magnetic resonance cholangiopancreatography (MRCP) is considered a method of choice for suspected PPF [4,5,6]. However with a high index of suspicion CT findings when combined with pleural fluid amylase and lipase can help us diagnose PPF comfortably. Following our diagnosis thoracocentesis was done and patient was planned for surgery.

So it is important to keep in mind the possibility of PPF in a patient with chronic pancreatitis who presents with respiratory symptoms as all pleural effusions are not reactive in nature. It must be made a common practice to look at the diaphragmatic hiatus is all patients with pancreatitis and large pleural effusions.