Case Report
Chronic Pancreatitis Presenting as Recurrent Pleural Effusion
Authors
Sunil Kumar, Associate Professor, SK Diwan,
Professor, Milind Dekate, Lecturer,
Department of Medicine, Jawahar Lal Nehru Medical College,
DMIMS, Sawangi, Wardha, Maharashtra, India.
Address for Correspondence
Dr. Sunil Kumar, Associate Professor, Department of Medicine, Jawahar Lal Nehru Medical College,
DMIMS, Sawangi, Wardha,
Maharashtra, India.
E-mail:
sunilkumarmed@gmail.com
Citation
Kumar S, Diwan SK, Dekate M. Chronic Pancreatitis Presenting as Recurrent Pleural Effusion. Online J Health Allied Scs.
2013;12(2):22. Available at URL:
http://www.ojhas.org/issue46/2013-2-22.html
Open Access Archives
http://cogprints.org/view/subjects/OJHAS.html
http://openmed.nic.in/view/subjects/ojhas.html
Submitted: Jun 25,
2013; Accepted: Jul 5, 2013; Published: Aug 25, 2013 |
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Introduction:
Pleural effusion is an uncommon complication of pancreatitis. It is often left sided and
associated with acute pancreatitis. Development of massive and recurrent haemorrhagic pleural effusion on one side followed by
effusion on the opposite side after a relatively symptom free interval in a patient with no clinical evidence of pancreatic
disease has been reported rarely.1 This article reports recurrent hemorrhagic pleural effusion as the sole
manifestation of pancreatitis in a 40 years old tribal male patient.
Case Report
A 40 years old tribal man from rural Wardha in Maharashtra presented to this hospital with
cough and breathlessness since fifteen days. He also complained of left sided dull chest pain radiating to the back,
cough with minimal mucoid expectoration, loss of weight over last 6 months. He also had pain in upper abdomen. There was no
history of injury and any abdominal discomfort or pain. He was a non-smoker and chronic alcoholic probably consumed alcohol
daily for the preceding eight years, but he stopped taking this since last 6 months. He gave history of taking anti-TB therapy
for 6 months for right sided pleural effusion from outside hospital six month back. On examination, there was mild pallor, no
lymphadenopathy and no hepatosplenomegaly. There was neither ascitis nor pericardial effusion. He had signs of massive pleural
effusion on left side.
His liver function tests were normal. Hemoglobin was 9.8 g%, total leukocyte count 9,400/cumm, ESR
26mm in lst hour, fasting blood sugar level 102mg%. His X-ray chest revealed massive pleural effusion (L) with mediastinal
shift to the opposite side (Fig. 1) and thoracentesis revealed hemorrhagic effusion with: amylase: 9940 U/L (serum amylase:
818 U/L), protein: 2.5 mg/dL (serum albumin: 4.1 mg/dL) and lactate dehydrogenase (LDH): 227 U/L (serum LDH: 335 U/L).
Acid fast staining of pleural fluid and culture for Tuberculosis were negative. Mantoux test to 1 TU was 6mms. Bronchoscopy
was normal and washings were negative for malignant cells and AFB. Due to markedly elevated serum and pleural fluid amylase
abdominal CT scan was done. The imaging showed multiple calcifications with pseudocyst formation in the tail region extending
towards left hemidiaphram.(Fig-2) Abdominal ultrasonography revealed a small septated cystic structure in the head of the
pancreas which was edematous and suggestive of pseudocyst of acute pancreatitis. Intercostals drainage with Chest tube was done,
during this period the clinical symptoms such as dyspnea and chest pain improved. The daily drain output was about 350cc at the
first day of chest tube insertion but it decreased gradually. Patient was referred to surgical unit for possible ERCP or
Magnetic resonance cholangio pancreatography (MRCP) for management of the calcification and pseudocyst. Patient refused to
do so because of financial non affordability. We also lost follow up. The cause of pancreatitis could be alcohol in this case.
He may be treated with antitubercular drugs for previous pleural effusion because tuberculosis is most common cause of
effusion in India.
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Fig 1: Chest X-ray shwing massive pleural effusion (L) with mediastinal
shift |
Fig 2: CT Scan showing multiple calcifications with pseudocyst formation in the tail region |
Discussion
Association of pleuropulmonary complication like hemorrhagic pleural effusion with pancreatitis
is well known but relatively uncommon. Common causes of hemorrhagic pleural effusion include Tuberculosis, trauma, Intrathoracic
neoplasms, or bleeding diathesis2. The mechanisms for hemorrhagic effusions in pancreatitis may include
transdiaphragmatic transfer of fluid via lymphatics, diaphragmatic perforation of pseudocyst and mediastinal extension and a
fistula connecting a pancreatic pseudocyst with pleural cavity.3,4 If the pancreatic duct disruption is posterior,
an internal fistula may develop between the pancreatic duct and the pleural space, producing a pleural effusion
(pancreaticopleural fistula) that is usually left-sided and often massive. If the pancreatic duct disruption is anterior,
amylase- and lipase-rich peritoneal fluid accumulate (pancreatic ascites).5
Cause of pancreatitis in this case may be alcohol induced and reports have shown that pleural
effusion with a very high pancreatic enzymes activity most frequently occurs in patients with alcoholic pancreatitis.5
Pleural effusions due to pancreatic diseases are mostly reactive with slightly elevated amylase levels. Very high levels of
amylase in the pleural fluid are rare and can only be explained by pancreatitis or rupture of a pancreatic pseudocyst with
perforation into the pleural cavity such as by drainage of pancreatic fluid into the pleural cavity.6 The other causes
of pleural effusions with an increased amylase include esophageal rupture, malignancy, ruptured ectopic pregnancy.2
In this case no such diaphragmatic perforation of pseudocyst or esophageal rupture was noted on CT scan of abdomen, though ERCP
was not done due to non affordability. Possibility of high amyalase content massive recurrent pleural effusion may be due to
transdiaphragmatic transfer of fluid via lymphatics in our case.
In most cases, the pleural effusion occurs concomitantly with the signs and symptoms of
pancreatitis, but may occur even after the acute abdominal symptoms have subsided. Considerable diagnostic problems may be
encountered in cases in which the clinical picture is dominated by the pleuro-pulmonary symptoms, and the pancreatic condition
remains completely or partly in the background.7 An early and rapid diagnosis can be made by the examination of the
pleural fluid for elevated amylase.
Conclusion
Pancreatitis should be taken into consideration when hemorrhagic pleural effusion occurs,
especially when it is recurrent. Treatment with drainage by a chest tube, with concomitant conservative treatment of the
pancratitis, is usually effective in massive pancreatic pleural effusions. Morbidity and mortality are reduced when a definite
diagnosis is established and appropriate therapy rendered.
Reference
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