MODIFICATION OF THE PFEFFER PANCREONECROSIS MODEL FOR ASSESSING PANCREATIC SECRETION IN THE ACUTE PERIOD OF DISEASE

A preliminary experimental study: Measurement of exocrine pancreatic secretion was performed on Wistar rats after an induction of acute pancreatitis by ‘closed duodenal loop’ (CDL) method (total number of animals = 39). After 24 hrs duration of AP the CDL content was evacuated by syringe and tested for amylase level (IU/ml). A near normal output remained in most animals (1987,35 ± 558,26, n = 12); moderately decreased output was 264,67 ± 162,74 (n = 9), and cessation of the output in n = 3 (0,6 ± 0,3) (q < 0,01 for each group). So, in our series the exocrine pancreatic output was found diverging largely with a normal secretion prevailing. Further study is warranted for some conclusive results to obtain.

Role of the ducktal secretion dysfunction in the pathogenesis of chronic pancreatitis

The review presents an analysis of current scientific data on the role of ductal secretion disorders in the pathogenesis of chronic pancreatitis. It is shown that under the influence of alcohol or other provoking factors, the CFTR transport mechanism of duct cells undergoes damage, which leads to the decrease in the bicarbonate and fluid secretion. Dehydration and acidification contribute to the hyperconcentration of protein and mucous components of pancreatic secretion and to the change in its rheological properties, which complicates further transport through the ductal system. Current conditions are favorable for the formation of mucoprotein plugs and the ductal obstruction that may have an important role in the pathogenesis of chronic pancreatitis at the early stage of development of the disease.

Changes in the ducts of the pancreas with pancreatic necrosis

The article presents data on the development in the lumen of the pancreatic duct of condensed protein masses in people who died from the development of severe acute pancreatitis. 10 pancreas (areas of the head, body and tail, ductal system of the pancreas) of people who died of acute pancreatitis were subjected to histological examination. The material was fixed in 10% formalin solution, carried out in alcohols of increasing strength and enclosed in celloidin. The sections were stained with hematoxylin and eosin. A histological examination revealed that the condensed masses were represented by heterogeneous protein formations, cells of desquamated ductal epithelium, blood elements, fibrin threads. They completely filled the lumen of the pancreatic ducts and stopped the movement of pancreatic secretion. The data on the treatment of severe pancreatitis in experimental studies using the method of bougie and washing the pancreatic ducts with a novocaine-contrical mixture are presented. Two methods are proposed for restoring the permeability of the pancreatic duct in pancreatic necrosis in humans. Possible ways of the formation of fistulas and cysts are suggested, as a complication in the severe course of acute pancreatitis.

Successful postoperative pancreatic fistula treatment with the use of somatostatin infusion after duodenal gastrointestinal stromal tumor resection

Introduction. According to the International Study Group on Pancreatic Fistula, a postoperative pancreatic fistula is defined as every case of fluid leak on the third (or later) postoperative day, in which the level of amylase in the collected fluid is at least three times higher than the serum amylase level. Depending on the stage and the designated management, pancreatic fistulas are divided into the following three categories: A (mild), B, and C (severe). Regardless of favorable conditions, exocrine pancreatic secretion is the key factor in fistula formation. The decrease in pancreatic secretion caused by somatostatin and its analogues combined with parenteral nutrition is a well-established treatment method in pancreatic fistula management. Case outline. The case of a 69-year-old patient who had undergone a resection of a duodenal gastrointestinal stromal tumor located directly above the major duodenal papilla is presented. Excessive drainage of amylase-rich fluid was observed in the postoperative period. Treatment comprised continuous infusion of somatostatin and parenteral nutrition. Fistula closure was accomplished on postoperative day 14, confirmed by a radical decrease in the volume of drainage and low amylase levels in the collected fluid. The patient remained in a good clinical state and was discharged from hospital on postoperative day 20. Conclusion. This is an example of the early diagnosis of a postoperative pancreatic fistula, treated conservatively with the use of somatostatin. Post-surgery clinical awareness of the importance of direct contact between the stromal tumor and pancreatic tissues, in connection with routine amylase level assessment, led to a quick diagnosis of pancreatic fistula and the therapy led to an uneventful outcome.