Laparoscopic treatment of intrasplenic pancreatic pseudocyst.

INTRODUCTION: Pseudocyst formation commonly follows pancreatitis, but erosion into the spleen is rare and potentially life threatening. We report a case of an intrasplenic pancreatic pseudocyst treated laparoscopically with distal pancreatectomy and splenectomy. METHODS: A 50 year old male with a history of chronic alcoholic pancreatitis, presented with abdominal pain for 3 months, worsening over the past several days. A CT scan showed a broad 9 cm subcapsular fluid collection suspicious for an intra-splenic pseudocyst. The patient underwent laparoscopic distal pancreatectomy and splenectomy. RESULTS: There were no intraoperative complications and the patient was discharged on day 8. The final pathology revealed a benign cystic lesion measuring 9 x 6 x 3 cm that was not communicating with the pancreatic duct, and 2 smaller pseudocysts in the pancreatic body and tail. A previous scan did not reveal any abnormalities in the spleen, and showed the other pancreatic pseudocysts. At 8 month follow up the patients was symptom free, with no new pseudocysts. CONCLUSIONS: Splenic parenchyma involvement is an unusual complication of pancreatic pseudocyst. The optimal treatment is controversial. Percutaneous drainage carries a high recurrence rate and risk of hemorrhage. Open surgery is effective, but associated with significant morbidity. Laparoscopy offers an effective method of treatment without the potential complication of a large abdominal incision.

Dietary calcium does not reduce experimental colorectal carcinogenesis after small bowel resection despite reducing cellular proliferation.

It has been proposed that colorectal carcinogenesis is accompanied by increased mucosal cell proliferation and that the converse may also apply. To examine this thesis, the crypt cell production rate (CCPR) was measured in eight groups of rats (n = 187) that had received 1,2 dimethylhydrazine, 70% small bowel resection, supplemental dietary calcium, or a combination of these. Analysis of variance showed the following: (1) the CCPR decreased between the ileum and distal colon; (2) the CCPR decreased between 16 and 32 weeks; (3) 1,2 dimethylhydrazine and small bowel resection increased the CCPR and calcium decreased the CCPR independently of one another; (4) the CCPR interacted with 1,2 dimethylhydrazine x small bowel resection, calcium x 1,2 dimethylhydrazine and interacted between the site of bowel and calcium, 1,2 dimethylhydrazine, small bowel resection, and 1,2 dimethylhydrazine x small bowel resection (p = 0.014 to p < 0.001). The tumour yield was reduced by calcium in 1,2 dimethylhydrazine treated animals (chi 2 = 14.1, df = 3, p < 0.01) but was unaffected by calcium in 1,2 dimethylhydrazine and small bowel resection treated animals despite significant differences in the CCPR. An increase of the CCPR both preceded and accompanied colorectal carcinogenesis but reduction of the CCPR was not invariably accompanied by reduced carcinogenes.

Inguinal herniotomy in young infants.

Ninety-two consecutive infants aged up to 12 months underwent primary inguinal herniotomy over a 5-year period. All were treated in a district hospital paediatric surgical unit according to recommendations of the British Association of Paediatric Surgeons. After a mean follow-up of 45.8 months, one patient had a failed repair and four (4 per cent) a hernia recurrence. One infant developed a wound infection. Infantile hernia can be managed safely and efficiently in a district hospital.

Reduction of mucosal crypt cell proliferation in patients with colorectal adenomatous polyps by dietary calcium supplementation.

The crypt cell production rate was measured in 14 patients with adenomatous colorectal polyps, 17 patients with colorectal cancer and 12 control subjects. The median (interquartile range) rate (cells per crypt per hour) was found to be significantly higher (P less than 0.001) in the polyp (2.45 (1.94-3.20)) and cancer (3.01 (2.35-3.68)) groups compared with controls (1.25 (0.70-1.85)). A double-blind cross-over study was performed in patients with adenomatous polyps consisting of 2 months' treatment, 2 weeks' washout, followed by 2 months' treatment with dietary calcium supplementation (1.25 g day-1) versus placebo. A significant reduction in the crypt cell production rate occurred with calcium treatment compared with the placebo (1.25 (0.6-2.25) versus 2.15 (1.58-3.08) cells per crypt per hour, P = 0.035). This study demonstrates a significant reduction in mucosal cell proliferation by dietary calcium supplementation in patients with adenomatous polyps. Such treatment may be worthy of further investigation in patients at high risk of developing colorectal polyps.

Influence of dietary calcium supplements on ileoanal pouch function and cytokinetics.

A double-blind cross-over study was undertaken in 16 patients after panproctocolectomy and ileoanal pouch reconstruction to compare supplementary calcium (1.5 g/day) with placebo over 2 months with a 2-week washout period. Stool frequency was recorded and the effects on pouch mucosal crypt cellular proliferation were determined using an in vitro stathmokinetic technique which measures the crypt cell production rate (CCPR) and an immunohistochemical method using the Ki67 monoclonal antibody for proliferating nuclei. The median (interquartile range) diurnal stool frequency was reduced by calcium (4 (3-5) per day) compared with values obtained before treatment (7 (5-10) per day, P less than 0.002) and with placebo (7 (6-9) per day, P = 0.002). Similarly, calcium reduced nocturnal stool frequency (1 (0-1) per night) compared with pretreatment and placebo (both 2 (1-3) per night, P less than 0.05) values. Calcium reduced the mean(s.e.m.) CCPR to 1.88(0.41) cells per crypt per hour compared with pretreatment (3.63(0.53), P = 0.01) and placebo (3.24(0.43), P = 0.002) values. Median (interquartile range) Ki67 activity was also reduced by calcium (13.2 (9.7-16.7) per cent), compared with values obtained before treatment (27.3 (14.3-30.2) per cent, P = 0.001) and with placebo (26.0 (17.2-32.0) per cent, P = 0.001). Stool frequency was significantly correlated with the CCPR (diurnal: r = 0.37; nocturnal: r = 0.31, both P less than 0.05). Nine patients used antidiarrhoeal medication while receiving placebo compared with four patients receiving calcium (P = 0.032). This study has shown that supplementary oral calcium significantly reduced stool frequency in patients with pouches, a reduction that was associated with reduced cell proliferation. The mechanisms for this effect are not known.

Prevention of peritoneal adhesions in rats with verapamil, hydrocortisone sodium succinate, and phosphatidylcholine.

OBJECTIVE: To assess the effectiveness of verapamil, hydrocortisone sodium succinate, and phosphatidylcholine in the prevention of experimental adhesions. DESIGN: Randomized trial. MATERIAL: 80 rats. INTERVENTIONS: Laparotomy and intraperitoneal irrigation with saline 40 degrees C, then verapamil hydrochloride 1 mg/kg intravenously 15 min before, during, and after irrigation; or hydrocortisone sodium succinate 50 mg/kg intravenously half an hour before irrigation; or phosphatidylcholine 5.5 mg/kg orally eight days before and seven days after irrigation plus 0.5 mg/ml in the irrigation fluid; or no further intervention. MAIN OUTCOME MEASURES: Development of adhesions two weeks after irrigation, and completeness of wound healing. RESULTS: Adhesions developed in 13 of 19 control animals; 7 of 20 that were given verapamil; 6 of 20 that were given hydrocortisone; and 3 of 20 given phosphatidylcholine. CONCLUSION: Adhesions that developed in rats after laparotomy and intraperitoneal irrigation with saline at 40 degrees C can be significantly reduced by phosphatidylcholine.