Gangrenous cholecystitis: innovative laparoscopic techniques to facilitate subtotal fenestrating cholecystectomy when a critical view of safety cannot be achieved.

BACKGROUND: Gangrenous cholecystitis is associated with a higher conversion rate of conversion from laparoscopic to open than acute non-gangrenous cholecystitis. New strategies and techniques are needed to decrease conversion rates and improve outcomes. METHODS: In this article, we provide a richly detailed, illustrated description of a modified fundus-first technique that we have developed over the last 15 years and now use routinely with rare conversions. We also compared outcomes of laparoscopic (LC) and open (OC) approaches for pathologically confirmed gangrenous cholecystitis in 146 patients during 1995-2005, the first 10 years during which these two approaches were performed contemporaneously at our institution on comparable patients. RESULTS: Among the 142 patients that met the inclusion criteria, laparoscopic procedures were started in 112 (79%) of these patients, with successful completion in 72 resulting in an overall conversion rate of 36%. During the last 5 years, however, in cases where the described laparoscopic technique was used, no patient has required conversion. The laparoscopic LC group had shorter average ICU stay (p < 0.05) and overall length of stay (2 vs 6 days, p < 0.001). Intraoperative cholangiography was completed in 37 of 72 LC patients (52%) versus 6 of 30 OC (20%). In five of the LC patients, a filling defect was seen on the cholangiogram and laparoscopic transcystic common bile duct stones, thereby avoiding a second anesthetic and endoscopic procedure. CONCLUSIONS: In the setting of severe inflammation, a number of procedural modifications can be incorporated to allow the surgeon to approach dissection of the gangrenous gallbladder using a flexible operative plan designed to optimize safe completion of this challenging procedure, with the expected improvement in surgical outcomes.

Transient receptor potential ankyrin 1 mediates chronic pancreatitis pain in mice.

Chronic pancreatitis (CP) is a devastating disease characterized by persistent and uncontrolled abdominal pain. Our lack of understanding is partially due to the lack of experimental models that mimic the human disease and also to the lack of validated behavioral measures of visceral pain. The ligand-gated cation channel transient receptor potential ankyrin 1 (TRPA1) mediates inflammation and pain in early experimental pancreatitis. It is unknown if TRPA1 causes fibrosis and sustained pancreatic pain. We induced CP by injecting the chemical agent trinitrobenzene sulfonic acid (TNBS), which causes severe acute pancreatitis, into the pancreatic duct of C57BL/6 trpa1(+/+) and trpa1(-/-) mice. Chronic inflammatory changes and pain behaviors were assessed after 2-3 wk. TNBS injection caused marked pancreatic fibrosis with increased collagen-staining intensity, atrophy, fatty replacement, monocyte infiltration, and pancreatic stellate cell activation, and these changes were reflected by increased histological damage scores. TNBS-injected animals showed mechanical hypersensitivity during von Frey filament probing of the abdomen, decreased daily voluntary wheel-running activity, and increased immobility scores during open-field testing. Pancreatic TNBS also reduced the threshold to hindpaw withdrawal to von Frey filament probing, suggesting central sensitization. Inflammatory changes and pain indexes were significantly reduced in trpa1(-/-) mice. In conclusion, we have characterized in mice a model of CP that resembles the human condition, with marked histological changes and behavioral measures of pain. We have demonstrated, using novel and objective pain measurements, that TRPA1 mediates inflammation and visceral hypersensitivity in CP and could be a therapeutic target for the treatment of sustained inflammatory abdominal pain.