Efficacy of endoscopic ultrasound-guided celiac plexus block and celiac plexus neurolysis for managing abdominal pain associated with chronic pancreatitis and pancreatic cancer.

BACKGROUND/GOALS: Endoscopic ultrasound (EUS)-guided celiac plexus block (CPB) and celiac plexus neurolysis (CPN) have become important interventions in the management of pain due to chronic pancreatitis and pancreatic cancer. However, only a few well-structured studies have been performed to evaluate their efficacy. Given limited data, their use remains controversial. Herein, we evaluate the efficacy of EUS-guided CPB and CPN in alleviating chronic abdominal pain due to chronic pancreatitis and pancreatic cancer respectively. STUDY METHODS: Using Medline, Pubmed, and Embase databases from January 1966 through December 2007, a thorough search of the English literature for studies evaluating the efficacy of EUS-guided CPB and CPN for the management of chronic abdominal pain due to chronic pancreatitis and pancreatic cancer was conducted, along with a hand search of reference lists. Studies that involved less than 10 patients were excluded. Data on pain relief was extracted, pooled, and analyzed. RESULTS: A total of 9 studies were included in the final analysis. For chronic pancreatitis, 6 relevant studies were identified, comprising a total of 221 patients. EUS-guided CPB was effective in alleviating abdominal pain in 51.46% of patients. For pancreatic cancer, 5 relevant studies were identified with a total of 119 patients. EUS-guided CPN was effective in alleviating abdominal pain in 72.54% of patients. CONCLUSIONS: EUS-guided CPB was 51.46% effective in managing chronic abdominal pain in patients with chronic pancreatitis, but warrants improvement in patient selection and refinement of technique, whereas EUS-guided CPN was 72.54% effective in managing pain due to pancreatic cancer and is a reasonable option for patients with tolerance to narcotic analgesics.

[Forms of an in vivo polymerization product, n-butyl-2-cyanoacrylate, within the gastric wall].

The in vivo morphology of sclerosants, n-butyl-2-cyanoacrylate (Histoacryl; referred hereinafter to briefly as HA) polymer formed within the gastric wall was investigated in an animal experiment. The results indicate that HA polymer formed after local injection of HA into the stomach wall with deliberate avoidance of contact with blood got scattered in an arboroid pattern, suggesting thus that when HA is injected into the gastric mucosa at an extravascular site, the resulting polymer is likely to get scattered and miss the target site. Polymerization products that were formed after injection of HA alone were deep purple, dense, firm, rounded in shape and lesser in adverse histologic influence upon the walls of stomach. On the other hand, those formed by injection of HA with Lipiodol were large-sized, light brown and oval-shaped ones with more irregular margins and less distinct boundaries as compared to those seen after injection of HA alone. These results of the study led us to conclude that at the present time it would seem wise to limit the use of HA for this particular therapeutic purpose only to those cases of bleeding gastric varices.

[Distribution of ethanolamine oleate after injection in esophageal varices].

The purpose of this study is to know the systemic distribution of sclerosant injected into esophageal varices. Sclerotherapy for esophageal varices was performed for 14 times in 11 patients. The patients were divided into two groups according to the content of sclerosant. Seven patients received a total of 9 intravariceal injections (IVI) with 7 to 30ml of 5% ethanolamine oleate (EO) which contained meglumine diatrizoate (Angiographin) and four patients received a total of 5 IVI with 10 to 20ml of 4.5% EO which contained a 10% volume of 99mTcO-4 solution (EO-99mTc). Distribution of injected materials was observed by X-ray fluoroscopy in the former group and by a scintillation camera in the latter. In both methods most of the sclerosant disappeared from the injected site within five minutes leaving a trace in the varices. Then, the sclerosant was disseminated throughout the body via portal vein. When more than 20ml of sclerosant was injected, some flowed into the azygos vin through the periesophageal vin. After IVI the varices showed atrophic changes, though the sclerosant did not stay in the varices.