Pleural effusions commonly complicate pancreatitis and are usually reactive. Massive pleural effusions are a rare but recognised complication of pancreatitis, the management of which may require surgical intervention. Bishop et al. [1] reported massive pleural effusion secondary to pancreaticopleural fistula in a 4-year-old girl who, following failure of medical management, underwent surgery. Namazi and Mowla [2] also reported a patient with massive pleural effusion secondary to pancreatitis, who underwent drainage of a pancreatic cyst following failure of conservative management. Medical management of massive pleural effusion secondary to pancreatitis is reported to be successful in approximately 40% of adult cases [3]. We report successful resolution following medical management in a 12-year-old girl who presented with a massive right pleural effusion secondary to chronic pancreatitis. A 12-yearold girl presented with poor weight gain, and abdominal and retrosternal chest pain. She underwent a barium meal and an upper and lower gastrointestinal endoscopy. Apart from Enterobius vermicularis infestation resulting in a mild nonspecific proctitis, these investigations were normal. Empirical treatment with Gaviscon and mebendazole resulted in weight gain and symptom resolution. Six months later, she presented with a 2-month history of progressive shortness of breath and poor exercise tolerance. She was noted to be pyrexial and complained of right upper quadrant abdominal and chest pain. Clinical examination revealed no signs of respiratory distress, normal pulse oximetry and respiratory rate. However, there were absent breath sounds over the right lung and a chest X-ray film demonstrated a right pleural effusion (Fig. 1). An ultrasound scan and a chest CT scan confirmed a hyper-echoic fluid collection, total collapse of the right lung with no evidence of septation, mediastinal mass or lymphadenopathy. A Mantoux test was negative. Analysis of pleural fluid obtained after drainage revealed a white cell count of 1.05·10/l, raised amylase of 24777 U/l with a protein content of 32 g/l. Simultaneous serum analysis revealed a serum albumin of 31 g/l and an amylase of 304 U/l. The patient was treated conservatively with chest tube drainage, intravenous antibiotics, and intravenous octreotide (1 lg/kg/h), omeprazole and parentral nutrition. Within 2 weeks her pleural effusion resolved, her plasma amylase normalised and enteral nutrition was reintroduced. A magnetic resonance cholangiopancreatography delineated the pancreas and confirmed a dilated tortuous and beaded pancreatic duct with no evidence of pancreatopleural fistula or pseudocyst (Fig. 2). Further investigation confirmed that the patient and her father both carry the N291 mutation in the PRSS1 hereditary pancreatitis gene explaining her findings of chronic pancreatitis. The patient has remained symptom free with normal plasma amylase levels for 12 months following presentation, and her father has never had symptoms suggestive of pancreatitis. Pleural effusions commonly complicate acute pancreatitis and are usually small, left-sided and reactive. They arise from inflammation of the diaphragm and pleura, the amylase concentration of which may be moderately elevated. Pleural effusions arising from chronic pancreatitis are rare in children and result from either posterior disruption of the pancreatic duct into the retroperitoneal space leading to the formation of a fistulous tract between the pancreas and the pleural cavity through the aortic or oesophageal hiatus, or direct extension of a pancreatic pseudocyst [3]. These effusions tend to be large and recurrent with a dramatically elevated amylase content. M. Lawson (&) AE A. M. Dalzell Department of Paediatric Gastroenterology, Royal Liverpool Children’s Hospital NHS Trust Alder Hey, Eaton Road, L12 2AP Liverpool, UK E-mail: maureenlawson@doctors.org.uk Tel.: +44-151-2525373 Fax: +44-151-2525928
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