scholarly journals An Unusual Complication and Position 0f Pancreatic Pseudocyst: Gastric Intramural Pseudocyst

2015 ◽  
Vol 2 (3) ◽  
Author(s):  
Filipa Ávila
2008 ◽  
Vol 67 (7) ◽  
pp. 1199-1201 ◽  
Author(s):  
Jeevan Vinod ◽  
Adam Palance ◽  
Gregory Haber

2018 ◽  
Vol 7 (1) ◽  
pp. 65 ◽  
Author(s):  
Yiqi Du ◽  
Yan Chen ◽  
Huiyun Zhu ◽  
Zhendong Jin ◽  
Zhaoshen Li

2021 ◽  
Vol 8 (7) ◽  
pp. 2238
Author(s):  
Spandana Jagannath ◽  
Ashok Kumar

Pleural effusion following rupture of pancreatic pseudocyst into the pleural cavity resulting into pancreaticopleural fistula is an extremely uncommon complication of acute pancreatitis. Pancreaticopleural fistula also results from disruption of a major pancreatic duct usually due to an underlying pancreatic disease (chronic pancreatitis), trauma, or iatrogenic injury. Pleural effusion is predominantly left sided; however, right-sided and bilateral effusion occurs in 19% and 14% of patients respectively. The pleural effusate can be either serous, serosanguinous or black in colour. Analysis of pleural fluid for raised amylase will confirm the diagnosis and investigations like computed tomography (CT), endoscopic retrograde cholangiopancreatography (ECRP) or magnetic resonance cholangiopancreatography (MRCP) may establish the fistulous communication between the pancreas, pseudocyst and pleural cavity. The optimal treatment strategy has traditionally been medical management with thoracocentesis and/or tube thoracostomy and exocrine suppression with octreotide and ERCP stenting of the fistulous pancreatic duct. Surgery, in the current era, is considered in the event patient fails to respond to conservative management or the patient’s condition deteriorates. We report the case of a 24-years-old gentleman who was diagnosed with chronic idiopathic pancreatitis with pseudocyst who developed right sided black pleural effusion.


2000 ◽  
Vol 14 (10) ◽  
pp. 967-967
Author(s):  
A. Pleskovic ◽  
M. Sever ◽  
D. Vidmar ◽  
R. Zorc-Pleskovic ◽  
O. Vraspir-Porenta

1993 ◽  
Vol 70 (05) ◽  
pp. 730-735 ◽  
Author(s):  
P Toulon ◽  
M Lamine ◽  
I Ledjev ◽  
T Guez ◽  
M E Holleman ◽  
...  

SummaryIn human plasma, heparin cofactor II (HCII) is a thrombin inhibitor, whose deficiency has been reported to be associated with recurrent thrombosis. The finding of two cases of low plasma HCII activity in two patients infected with the human immunodeficiency virus (HIV) led us to investigate this coagulation inhibitor in the plasma of a larger population of HIV-infected patients. The mean plasma HCII activity was significantly lower in 96 HIV-infected patients than in 96 age- and sex-matched healthy individuals (0.75 ± 0.24 vs 0.99 ± 0.17 U/ml, p <0.0001). HCII antigen concentration was decreased to the same extent as the activity. The proportion of subjects with HCII deficiency was significantly higher in the HIV-infected group than in healthy individuals (38.5% vs 2.1%). In addition, HCII was significantly lower in AIDS patients than in other HIV-infected patients, classified according to the Centers for Disease Control (CDC) on the basis of an absolute number of circulating CD4+ lymphocytes below 200 x 106/1. The link between HCII and immunodeficiency is further suggested by significant correlations between HCII activity and both the absolute number of CD4+ lymphocytes and the CD4+ to CD8+ lymphocyte ratio. Nevertheless, the mean HCII level was not different in the various groups of patients classified according to clinical criteria, except in CDC IVD patients in whom HCII levels were significantly lower. In addition, no correlation could be demonstrated between HCII and protein S activities, another coagulation inhibitor whose plasma level was also found to be decreased in HIV-infected patients. A similar prevalence of HCII deficiency was also found in a small series of 7 HIV-infected patients who developed thrombotic episodes, an unusual complication of the infection. This suggests that, in HIV-infected patients, HCII deficiency is not in itself the causative factor for the development of thrombosis.


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