Self-expandable metal stents as a new treatment option for perforated duodenal ulcer.

Primary stenting and drainage has been shown to be an effective and safe way to treat esophageal perforations and anastomotic leaks after gastric bypass surgery. We present a case series of eight patients with perforated duodenal ulcers treated with covered self-expandable metal stents (SEMS). The first two patients received their stents because of postoperative leakage after initial traditional surgical closure. The following six patients had SEMS placed as primary treatment due to co-morbidities or technical surgical difficulties. Endoscopy and stent treatment in these six patients was performed at a median of 3 days (range, 0 - 7 days) after initial symptoms. Six patients had percutaneous abdominal drainage. Early oral intake, 0 - 7 days after stent placement, was possible. All patients except one recovered without complications and were discharged 9 - 36 days after stent placement. This series indicates that primary treatment with SEMS and drainage might be an alternative to surgery in patients with perforated ulcer disease.

Endoscopic sutured closure of a gastric natural orifice transluminal endoscopic surgery access gastrotomy compared with open surgical closure in a porcine model. A randomized, multicenter controlled trial.

BACKGROUND AND STUDY AIMS: In natural orifice transluminal endoscopic surgery (NOTES) procedures it is essential to be able to perform secure closure of the access perforation. The aim of this study was to compare endoscopically sutured closure of a gastric access gastrotomy using the tissue apposition system (TAS), with closure via laparotomy in a randomized multicenter study. METHODS: A total of 32 pigs (18 - 42 kg) were used in this study. The gastric NOTES access was created using a needle knife and a 20-mm balloon. Following transgastric pelvic peritoneoscopy, the endoscope was withdrawn into the stomach. The animals were then randomized to endoscopic closure or laparotomy with surgical closure. Procedure time, recovery time, and weight gain were measured. At necropsy, adhesions, abscesses or peritonitis were recorded. RESULTS: Of the 32 pigs, 29 survived 14 days without complications. All endoscopic and all open surgical closures were secure at postmortem. On average two suture pairs were used for endoscopic closure. Surgical closure was quicker (12.5 vs. 20.1 minutes). Recovery time and postoperative weight gain were similar for both groups. Two pigs in the endoscopic group died: one of gastric dilatation, without leakage from the gastrotomy; another was euthanized due to rectal prolapse. In the laparotomy group one pig was euthanized after 7 days due to abdominal wound dehiscence. At necropsy there were significantly more intra-abdominal adhesions in the laparotomized group. CONCLUSION: This randomized controlled study of endoscopic and surgical closure of a gastrotomy made for transperitoneal access for NOTES procedures suggests that both techniques are comparable in technical closure rates, postoperative recovery, and prevention of peritonitis. There were fewer adhesions in the endoscopic group.

Transgastric peritoneoscopy and appendectomy: thoughts on our first experience in humans.

We present a series of three patients operated on by means of natural-orifice transgastric peritoneoscopy, including one appendectomy. A standard double-lumen gastroscope was used together with standard endoscopic tools. In all patients abdominal access through the gastric wall was smooth using a needle-knife/guide-wire/balloon technique. The whole abdominal cavity could be visualized and the appendix was found in two patients. In one patient the procedure was converted to laparoscopic appendectomy and in one to open surgery. In the third patient transgastric appendectomy was performed. The gastric access site was closed with the T-tag technique. Patients were allowed to drink and eat as soon as they woke up. Postoperatively patients were followed clinically and with standard laboratory tests daily until discharged. One patient (converted to open surgery) had a serious complication (pneumothorax). The transgastric approach to the abdominal cavity was shown to be feasible, but significant technical problems remain to be resolved.

Surgical outcome and cost-minimisation-analyses of laparoscopic and open hernia repair: a randomised prospective trial with one year follow up.

OBJECTIVE: To compare outcome and costs between laparoscopic and open hernia repair. DESIGN: Prospective randomised study. SETTING: One university and two district hospitals in Sweden. SUBJECTS: 200 men aged 25-75 years. MAIN OUTCOME MEASURES: Operating time, hospital stay, complications, and time to recovery. A cost-minimisation-analysis was used in which the total costs were calculated for a defined period of time for each option. RESULT: The one year follow-up rate was 98%. Mean (SD) operation times in the laparoscopic and open groups were 72 (30) and 62 (25) minutes, respectively (p = 0.009). Hospital stay and complication rates did not differ between the groups. Among employees the mean (SD) periods off work in the laparoscopic and open groups were 10 (8) and 23 (21) days, respectively (p = 0.0001). The mean direct costs of the laparoscopic operation were increased by SEK 4037 (US$ 483) but the savings in indirect costs resulting from earlier return to work were SEK 11392 (US$ 1364). CONCLUSIONS: Laparoscopic hernia repair gave the employed patients faster recovery and return to work, and was the most cost-effective strategy provided that both direct and indirect costs were included.

Effects of a novel 21-aminosteroid or methylprednisolone in experimental total intestinal ischemia.

OBJECTIVE: To investigate whether tirilazad mesylate, a 21-aminosteroid, protects the small intestinal mucosa from injury following total warm or cold ischemia and reperfusion. DESIGN: Randomized vehicle-controlled experimental study. SETTING: A university department of surgery. ANIMALS: Wistar rats. The warm ischemia series preceded the cold ischemia series. Animals were randomized within each series. Microscopic evaluation was performed on coded tissue slides. INTERVENTIONS: Warm ischemia was induced by a hydrostatic pressure cuff inflated to 10 mm Hg above the systolic arterial pressure for 60 minutes. Cold ischemia was studied after small intestinal transplantation. The transplant was stored for 5 hours in University of Wisconsin solution at 8 degrees C. Ischemia was followed by 60 minutes of reperfusion. In both series, tirilazad mesylate (3 mg/kg) or methylprednisolone sodium succinate (30 mg/kg) was given. Controls were given tirilazad vehicle or saline solution. MAIN OUTCOME MEASURE: Microscopic grade of small intestinal mucosal injury. RESULTS: Mucosal injury was evident in all groups of animals that were subjected to warm or cold ischemia. Reperfusion following cold ischemia induced a significant reperfusion injury. Neither tirilazad nor methylprednisolone protected the small intestinal mucosa during ischemia or reperfusion. CONCLUSION: Mucosal injury following warm or cold intestinal ischemia and reperfusion is caused by factors other than or in addition to lipid peroxidation, which is preventable by use of a 21-aminosteroid.

Regeneration of small bowel mucosa after intestinal ischemia.

BACKGROUND AND METHODS: The objective of this study was to evaluate the histologic reconstitution of the small intestinal mucosa after a standardized ischemic injury and to determine if the early repair process takes place by cell renewal or migration of existing mucosal cells. Therefore, male Wistar rats, weighing 190 to 320 g, were subjected to total warm intestinal ischemia by means of a hydrostatic pressure clamp for 45 or 90 mins. These rats were compared to sham-operated controls. Intestinal biopsies were obtained just before reperfusion and at various times up to 48 hrs thereafter. Mucosal injury was evaluated microscopically by a blinded examiner. RESULTS: Variable mucosal reconstitution occurred within 3 hrs, after 45 mins of ischemia, whereas mucosal repair required up to 18 hrs after 90 mins of ischemia. In a second series of experiments, 45 or 90 mins of ischemia and 5 hrs of reperfusion were followed by the iv administration of radioactively labeled thymidine. Intestinal biopsies were taken 1 hr later and prepared for autoradiography. No increase in mucosal mitoses was observed. CONCLUSIONS: The mucosal reconstitution occurred rapidly after 45 mins and 90 mins of total warm intestinal ischemia and primarily through mucosal cell migration.

Cold ischemic and reperfusion injury in a model of small bowel transplantation in the rat.

Following 0, 5, or 18 h of cold ischemia in the University of Wisconsin or Sacks' solution syngenic small bowel transplantation was performed to the renal vessels. Mucosal injury during ischemia or at reperfusion was evaluated microscopically using a grading scale from 0 to 8. The series subjected to small bowel transplantation without cold ischemia showed superficial damage to the tips of the villi (median grade 2) with no further exacerbation at reperfusion and complete healing 24 h thereafter. Moderate villous injury (median grade 3) was demonstrated following 5 h of cold ischemia. This injury was exacerbated to grade 4 (p less than 0.05) following reperfusion but was almost completely healed 24 h later. Grade 4 tissue injury was seen following 18 h of cold ischemia without further exacerbation at reperfusion and no clear tendency to healing 24 h later.

The sequence of development of intestinal tissue injury after strangulation ischemia and reperfusion.

Tissue injury at reperfusion has been reported after partial ischemia. However, previous attempts to demonstrate a component of injury caused by reperfusion after total ischemia have failed. This study was performed to evaluate the hypothesis that in such situations the extent of the tissue injury caused by ischemia itself prevented detection of a reperfusion component. Rats were subjected to near-total intestinal ischemia by means of a hydrostatic pressure clamp that produced preferential venous occlusion (strangulation) for periods from 1 to 90 minutes. Tissue injury was evaluated microscopically by a blinded examiner. Ischemic periods of 20 minutes or less did not induce detectable tissue injury. Longer durations of ischemia caused villous injury: the longer the period of ischemia, the more extensive the tissue injury. However, there was no exacerbation of injury seen after reperfusion, regardless of the duration of ischemia. In a separate series of rats, total arterial occlusion was employed without concomitant venous congestion. Such isolation arterial occlusion of 40 to 60 minutes' duration was followed by a statistically significant exacerbation of tissue injury at reperfusion. Thus total intestinal ischemia may be followed by reperfusion injury if there is no concomitant congestion and if ischemic injury is not too extensive.

The influence of a histamine2-receptor antagonist on the healing of an experimentally induced gastric mucosal lesion.

The effect of an H2-receptor antagonist (ranitidine) on the healing of gastric mucosal lesions was studied. Mucosal lesions were induced by a standardized thermo-mechanical technique. The healing process was assessed by macro- and light microscopical examination. It was further evaluated by measurements of the tissue contents of hydroxyproline, a chemical compound reflecting collagen, and of DNA and RNA, reflecting cell frequency and protein synthesis respectively, in the gastric wall from both injured and wound-free areas. The healing process was more rapid in ranitidine-treated animals than in controls. After four weeks, however, the lesion in nine out of ten animals had healed in the ranitidine-treated group and seven of nine rats in the control group. At that time the amounts of hydroxyproline, DNA and RNA did not differ between the two groups. These findings may be taken as an indication that the tissue components of the healed lesions were similar in ranitidine-treated rats and in the saline controls, i.e. the different speeds of the healing process did not seem to influence the components of the scar tissue.