Migration of biliary plastic stents: experience of a tertiary center

Background and study aims  Stent migration occurs in about 5–10% of patients undergoing biliary stenting. The aim of this study was to analyze the risk factors for stent migration in patients with benign and malignant strictures. Patients and methods  We retrospectively analyzed records of 524 biliary plastic stent placement procedures. Details noted included the cause and localization of stricture, characteristics and number of stents, direction of stent migration, presentation of patient with migrated stent, and the methods used for retrieval of migrated stents. Results  Two hundred and four (38.9%) of the procedures were performed for benign biliary strictures (BBS) and 320 (61.1%) for malignant biliary strictures (MBS). Thirty-four patients had 45 migrated biliary stents. The rate of migration was 8.58% (proximal 4.58% and distal 4.00%). Migration frequency was higher in BBS compared with MBS (13.7% versus 5.3%, p = 0.001). In BBS, the rate of stent migration was higher in cases with one (19.3%) and two stents (20.9%) when compared with cases with multiple stents (2.7%) (p = 0.001; p = 0.001, respectively). Migration occurred more frequently (10.9%) in cases with two stents when compared both to cases with one stent (3.0%) and those with multiple stents (0%) in MBS (p = 0.008; p = 0.020, respectively). In BBS, short stents migrated more frequently proximally (77%) and long stents more frequently distally (73%) (p = 0.008). In BBS, migration in cases with proximal stricture occurred more frequently distally (76.9%), while in those with distal stricture, migration was more frequently proximal (73.3%) (p = 0.008). All of the proximally migrated stents could be successfully retrieved endoscopically. Conclusions  The risk of stent migration is higher in BBS compared with in MBS. The cases with multiple stents had significantly lower stent migration. In BBS, long stent, proximal and postcholecystectomy strictures were associated with distal migration, while short stent, distal and non-postcholecystectomy strictures were associated with proximal migration.     

Second-Look Operation for Unresectable Pancreatic Ductal Adenocarcinoma at a High-Volume Center

Background The value of re-exploration for pancreatic ductal adenocarcinoma after the initial diagnosis of unresectability is unclear. Methods In this study, we analyzed 33 patients who were re-explored after an initial diagnosis of unresectability. Results At the time of reoperation, a resectable tumor was found in 18 patients: therefore, 15 pancreaticoduodenectomies, two total pancreatectomies and one left resection were performed with three vascular resections. Morbidity and mortality rates for the cohort were 6/33 and 1/33, without significant differences between resectable and nonresectable patients. Length of stay, duration of operation, and blood loss were significantly increased in the resection group. Kaplan–Meier survival analysis demonstrated increased median survival for resected patients (1078 days after the initial operation versus 547 days in the group of unresectable patients; p = 0.018). Analysis of the reasons against initial resection showed that, if the patients had been sent to a tertiary referral center for pancreatic surgery, a different decision in favor of resection would probably have been made in 14 out of 33 patients. A review of 10 published reports on reoperation for pancreatic cancer revealed results comparable to our study in terms of low morbidity and mortality as well as a survival benefit. Conclusions Reoperation for pancreatic ductal adenocarcinoma that is initially deemed unresectable can be safely performed in a selected group of patients by experienced surgeons, supporting the concept of patient centralization in pancreatic surgery. Resection at the second operation may confer a survival benefit even when the initial findings preclude a potentially curative approach.     

The role of posterior instrumentation and fusion after anterior radical debridement and fusion in the surgical treatment of spinal tuberculosis: experience of 127 cases

Long periods of immobilization, progressive kyphosis and graft failure are the major postoperative problems encountered after anterior radical surgical treatment for tuberculosis of the spine. Posterior fusion and instrumentation can be an effective solution for these problems. Effectiveness of posterior fusion and instrumentation was investigated in this study on the basis of the cases with anterior procedure only, and with combined anterior-posterior procedures. One hundred twenty-seven cases of tuberculosis of the spine were surgically treated between 1987 and 1995. All had either 1 or more of conditions such as spinal cord compression and neurological deficit, vertebral body collapse and kyphosis, or wide paravertebral abscess unresponsive to medical treatment. Of these, 57 had only anterior radical procedure between the years 1987 and 1993. Seventy cases had posterior instrumentation and fusion after the anterior procedure between the years 1991 and 1995. In about two third of the patients (81) autogenous iliac strut graft and in one third of them (40) autogenous fibular strut graft (cases with more than 2 level involvement) was used along with rib grafts after debridement. Twenty-one of the 57 patients who had only anterior procedure demonstrated a postoperative increase of kyphosis of more than 10 degrees. Increased kyphosis was due to graft slippage in 3, resorption in 2 and subsidence in 16 patients. No such increase or graft failure was noted in cases of combined anterior-posterior procedure. The difference in terms of kyphosis was found to be statistically significant (P=0.047). Anterior radical debridement and strut graft is the golden standard in the surgical treatment of spinal tuberculosis, but it should always be accompanied by posterior instrumentation and fusion to shorten the immobilization period and hospital stay, obtain good and long lasting correction of kyphosis, and prevent further collapse and graft failure.     

The role of pancreatic stellate cells in pancreatic cancer

Since conventional and targeted therapies aiming at cancer cells have largely failed to prolong survival in pancreatic cancer, targeting the infrastructure of the tumor, hence its stroma is a novel strategy. It is believed that fibrotic and hypovascular stroma forms a barrier around cancer cells, hindering effective delivery of chemotherapy. Theoretically, antifibrotic therapy should reduce the compactness of the stroma and reduce the interstitial pressure, allowing better delivery of chemotherapy. This approach has worked successfully in a genetically engineered mouse model but failed in humans, paradoxically increasing mortality in the treatment arm. Normally, stromal cells deposit extracellular matrix as an innate defensive reaction to form a barrier between what is harmful and the rest of the body. Despite the significant amount of in vitro data suggesting the pro-tumorigenic roles of activated stellate cells, there is no reason to believe that stellate cells around genetically mutated cells are from the beginning there to support carcinogenesis. Such a stromal activation is also observed around PanIN lesions (which harbor genetically mutated cells) in chronic pancreatitis, where no cancer develops. In pancreatic cancer, the selection pressure created by the fibrotic and hypoxic stroma eventually leads to the evolution of more aggressive clones, indirectly contributing to the aggressiveness of the tumor. Here, the main problem is the late diagnosis of pancreatic cancer, which gives cancer cells enough time for malignant evolution. Therefore, applying antifibrotic therapy at a late stage can be counterproductive. It may increase delivery of chemotherapy, but also lead to the escape of cancer cells.