Colonic Pseudo-obstruction is a poorly understood syndrome. It was first described by Ogilvie in 1948 and is characterized by signs of large bowel obstruction with a non-mechanical etiology. The suggested cause of this pathophysiology is an imbalance in the autonomic nerve supply to the colon. The syndrome affects mainly old, bedridden patients, usually hospitalised for non-colonic causes. The actual incidence of this syndrome is unknown, mainly due to the fact that spontaneous recovery may occur. When massive abdominal distention is apparent, diagnosis and treatment are usually problematic and other causes of obstruction must be ruled out. It is usually managed by water soluble contrast administered orally or rectally, or by colonic decompression. In extreme cases surgical treatment is required with significant morbidity and mortality. Pharmacologic management with parasympathomimetic drugs has been suggested recently. We describe the successful treatment of a patient with neostigmine and review the current literature.

The first 1,000 laparoscopic cholecystectomies performed in our department were reviewed. There was no operative mortality; conversion to open cholecystectomy was necessary in 2%. In the last 600 cases the rate of conversion had decreased to 0.5%. There was common bile duct injury in 0.3%, with the injuries identified during primary surgery. This clinical experience is consistent with previous studies, which proved that laparoscopic cholecystectomy is safe and should replace open operation as the procedure of choice.

We investigated the effect of octreotide in the treatment of severe acute pancreatitis in a case-control study. Experimental and clinical studies on the effect of octreotide in the treatment of acute pancreatitis have shown controversial results. Since January 1992, we have been conducting a prospective randomized study on the effect of octreotide in severe acute pancreatitis, in three hospitals in Israel. The entering criteria included three or more of the Ranson prognostic signs and CT findings of severe pancreatitis. Patients were randomly assigned to conservative treatment either with or without octreotide (0.1 mg subcutaneously three times a day). The end points of the study included: complication rate (ARDS, sepsis, renal failure, pseudocyst, fistula, and abscess), length of hospital stay, and mortality. From January 1992 to December 1996, 60 patients entered the study. After evaluating the files, 10 patients were excluded due to failure to meet the entering criteria, incomplete data, or incorrect diagnosis. Of the remaining 50 patients, 25 were assigned to octreotide (treatment group) and 25 to conservative treatment only (control group). The two groups matched with regard to age, sex, etiology, and severity of the disease. The complication rate was lower in the treatment group with regard to sepsis (24% vs 76%, P = 0.0002) and ARDS (28% vs 56%, P = 0.04). The hospital stay was shorter in the treatment group (20.6 vs 33.1 days, P = 0.04). Two patients died in the treatment group and eight in the control group (P < 0.019). These results suggest that octreotide may have a beneficial effect in the treatment of severe acute pancreatitis.

OBJECTIVES: To evaluate a simple model that produces progressive dose dependent pancreatitis, by intraparenchymal injection of sodium taurocholate. DESIGN: Open laboratory study. SETTING: Teaching hospital, Israel. MATERIALS: Forty eight Wistar rats. INTERVENTIONS: Sodium taurocholate was injected, 0.3 ml/100 g body weight, in concentrations of 5% and 10% into the pancreatic parenchyma of 32 Wistar rats, resulting in two distinct groups of severity. In 16 sham controls, saline was injected into the pancreas in similar fashion. Blood samples were withdrawn before, and 6, 24, 48, and 72 hours after induction of pancreatitis. RESULTS: Six hours after taurocholate injection, there was a sharp increase in the plasma activities of amylase, lipase, and lactate dehydrogenase (LDH). After 24 hours plasma activities of amylase and lipase decreased to near normal values while LDH remained slightly increased for 48 hours and decreased only after 72 hours. At 6 hours after the injection, interleukin-6 (IL-6) concentrations had increased slightly in the 5% group and decreased to the baseline values at 24 hours. In the 10% group, the increase in IL-6 values was significantly greater than in the 5% group (p = 0.04), and correlated well with severity of pancreatitis as defined by histology (p = 0.01) and mortality (p = 0.037). Twenty four hours after injection of taurocholate, morphological changes comprising diffuse necrosis of the pancreas, fat necrosis, and intestinal dilatation secondary to paralytic ileus were severe. Histopathological examination of the pancreas showed good correlation with the clinical findings and with mortality. No morphological changes were detected when saline was injected into the pancreas (sham control), and only mild rises of IL-6, lipase, amylase, and LDH activities were seen at 6 hours after injection. The mortality, after 10 days, was 80% in the 10% taurocholate group, 30% in the 5% taurocholate group, and 0 in the sham control group (p < 0.05). CONCLUSION: The intraparenchymal injection of taurocholate is easy to perform and highly reproducible. The histopathological injury is dose-dependent, as is the mortality. We conclude that this model is valuable for the study of new treatments for pancreatitis.