Laparoscopic hiatal hernia repair in patients with poor esophageal motility or paraesophageal herniation.

Laparoscopic repair for gastroesophageal reflux disease is now an accepted therapy. However, controversy exists with regard to the choice of operation between complete 360-degree Nissen fundoplication versus partial 270-degree Toupe fundoplication. In addition there is some controversy with regard to the proper choice of operation in patients with poor esophageal motility. Another class of hiatal hernia patients are those patients with paraesophageal herniation. Questions regarding the approach to these patients include whether or not to use a reflux procedure at the time of repair and the role of mesh in repair of these large hernias. This retrospective study was undertaken to compare the results of laparoscopic Nissen fundoplication and Toupe fundoplication in patients with both normal and abnormal esophageal motility. In addition the subset of patients with paraesophageal herniation was studied in an effort to ascertain the best surgical approach in these patients. In this study a retrospective analysis was performed on 188 consecutive patients during the period 1995 to 2001. All patients who presented with hiatal hernia surgical problems during this period were included. Endoscopy was performed in all patients with esophageal reflux. Manometry was performed in all patients except those presenting as emergency incarcerations. pH probe testing was performed in those patients in whom it was deemed necessary to establish the diagnosis. Upper gastrointestinal radiographs were used to define anatomy in paraesophageal hernia patients when possible. All patients with esophageal reflux were first treated with a trial of medical therapy. Patients with esophageal reflux and normal esophageal motility underwent 360-degree Nissen fundoplication. Those patients with poor esophageal motility (less than 65 mm of mercury) underwent laparoscopic 270-degree Toupe fundoplication. Patients presenting with paraesophageal herniation underwent laparoscopic repair. When possible esophageal manometry was performed on these patients preoperatively and if normal peristalsis was documented a Nissen fundoplication was performed. If poor esophageal motility was documented before surgery a Toupe fundoplication was performed. Mesh reinforcement of the diaphragmatic hiatus was used if necessary to complete a repair without tension. Patients were followed both by their primary gastroenterologist and their surgeon. Follow-up studies including endoscopy, pH probe, and upper gastrointestinal series were used as necessary in the postoperative period to document any problems as they occurred. Of the 188 patients in the study 141 patients underwent Nissen fundoplication, 21 patients underwent Nissen fundoplication and repair of paraesophageal hernia, 15 underwent Toupe fundoplication, seven underwent Toupe and paraesophageal hernia repair, and four paraesophageal hernia repair alone. One hundred eighty-three patients underwent a laparoscopic operation. Five patients of the 188 underwent an initial open operation-two of these patients because of the size of their paraesophageal hernia. Three of these patients had reoperations of remote operations done years before at other institutions. Twenty-two patients with poor esophageal motility (11.7 %) were included in the study. Fifteen patients required Toupe fundoplication whereas seven patients required Toupe fundoplication and repair of paraesophageal hernias. Mesh repair of paraesophageal hernias was accomplished in ten patients. Patients undergoing Toupe fundoplication had a 13 per cent dysphagia rate less than 4 weeks postoperatively and a 0% dysphagia rate greater than four weeks postoperatively. Patients undergoing Nissen fundoplication had a 16 per cent dysphagia rate less than 4 weeks postoperatively, 2 per cent dysphagia rate greater than 4 weeks postoperatively and no dysphagia at 6 weeks postoperatively. Recurrent symptomatic reflux occurred in 1.4 per cent of Nissen fundoplications and 6.7 per cent of Toupe fundoplications. Of Nissen and paraesophageal repairs 14.2 per cent had reflux and 14.3 per cent of Toupe and paraesophageal repairs had recurrent symptomatic reflux. Overall, complication rate was low. Use of mesh to repair large paraesophageal hernias resulted in a recurrence rate of 0 per cent. There was no instance of infection or bowel fistulization related to the use of mesh. We conclude that laparoscopic Nissen fundoplication in patients with normal esophageal motility is associated with a low rate of dysphagia and a low rate of recurrent reflux. Toupe fundoplication when used in reflux patients with poor esophageal motility is associated with a low rate of dysphagia and an acceptable rate of recurrent reflux. Laparoscop

Gastric mucosal high-energy phosphate metabolism. Influence of ethanol and PGE2.

This study investigated potential alterations in gastric mucosal energy metabolism following exposure to the damaging agent 50% ethanol (50% EtOH) alone and after pretreatment with either 16,16-dimethyl (dmPGE2) or the mild irritant 25% ethanol (25% EtOH). Fasted rats (n = 12-26/group) were orally given 1 ml of normal saline (NS), dmPGE2 in a dose of 5 micrograms/kg, or 25% EtOH. Fifteen minutes later, they randomly received 1 ml of NS or 50% EtOH. After 5 min, rats were anesthetized and their stomachs rapidly excised, frozen in liquid nitrogen, and lyophyllized. Once dried, the surface area (in square millimeters) of mucosal lesions was quantitated. Mucosa was then scraped off the underlying muscularis. Tissue metabolites (ATP, ADP, AMP, lactate, pyruvate, glucose, and glucose-6-phosphate) were measured in deproteinized, neutralized samples by enzymatic methods. In conjunction with the development of mucosal lesions involving an average of 45 mm2, ATP was significantly (P < 0.05) lower and AMP significantly higher in 50% EtOH-treated animals (indicating dephosphorylation) when compared with NS controls. Although both 25% EtOH and dmPGE2 prevented these lesions, only 25% EtOH prevented the ATP and AMP alterations. Fifty percent EtOH also significantly increased the tissue content of glucose and lactate over control values while glucose-6-phosphate was significantly decreased. With both protective agents pyruvate levels were significantly reduced, while glucose and lactate levels were not affected. In contrast to dmPGE2, the mild irritant (25% EtOH) significantly increased glucose-6-phosphate levels over control.(ABSTRACT TRUNCATED AT 250 WORDS)

Protection against ethanol injury in the canine stomach: role of mucosal glutathione.

The present study determined the role that mucosal glutathione (GSH) levels play in mediating the protective effects of a prostaglandin and a mild irritant against alcohol-induced gastric injury. An in vivo canine chambered stomach preparation was used in which the exteriorized mucosa was partitioned into two equal halves, one serving as control. Animals (5-8/group) received a subcutaneous injection of either normal saline (NS) or the GSH depletor N-ethylmaleimide (NEM; 50 mg/kg) and then were assigned to one of a variety of groups based on the perfusate used to bathe the experimental side of the chamber; NS bathed the control mucosa. At completion of the studies, mucosa from each side of the chamber was assayed for total GSH (mumol/g wet wt) and evaluated for microscopic damage. Both 16,16-dimethyl prostaglandin E2 (PGE2) (1 microgram/ml) and the mild irritant 8% ethanol, when topically applied to the gastric epithelium, increased mucosal GSH levels by approximately 20% compared with control values, and elicited no deleterious effects to the mucosa. Treatment of animals with NEM prevented these GSH effects by PGE2 and 8% ethanol without damaging the mucosa. Application of 40% ethanol to the mucosa markedly reduced levels of GSH and caused significant injury to the mucosal surface, much of it extending to the level of the gastric glands. When mucosa was pretreated with PGE2 or 8% ethanol before 40% ethanol exposure, deep gastric gland injury was virtually abolished. In animals receiving NEM, the protective effects of these agents against injury by 40% ethanol were prevented. Perturbations in tissue levels of GSH under these various experimental conditions failed to correlate histologically with the status of gastric mucosal integrity.

Prostaglandin-induced gastric mucosal protection against stress injury. Absence of a relationship to tissue glutathione levels.

The effects of 16,16 dimethyl prostaglandin E2 (dmPGE2) on the gastric mucosa of rats subjected to 1, 2, and 24 hours of water immersion stress were examined histologically. Results indicated a time-related increase in the total percentage length of glandular mucosa injured in normal saline (NS) pretreated rats that was significantly attenuated by subcutaneous dmPGE2 pretreatment (5 micrograms/kg) after 1 hour (46.0 +/- 12.9 vs. 16.8 +/- 2.3; p less than 0.005), 2 hours (45.4 +/- 1.0 vs. 13.8 +/- 2.2; p less than 0.001), and 24 hours (93.1 +/- 2.6 vs. 65.1 +/- 7.0; p less than 0.005) of water immersion stress. Moreover, dmPGE2 essentially prevented the occurrence of deep, glandular injury that, in NS controls, involved approximately 13% and 26% of the mucosal surface after 2 and 24 hours of immersion stress, respectively. Additionally, tissue levels of glutathione (mumole/g weight of wet tissue) were measured to determine its role under such conditions. After 1 hour of stress, there were no differences in glutathione levels between NS or dmPGE2 pretreated animals and fasted controls. After 2 and 24 hours of stress, there were likewise no differences in glutathione levels between NS and dmPGE2 pretreated groups, although levels in both groups were significantly decreased from fasted controls by approximately 30% at 2 hours and 37-47% after 24 hours. These histologic and biochemical data indicate that dmPGE2 attenuates both the extent and depth of glandular mucosal injury and does so in a manner unrelated to alterations in glutathione levels in gastric epithelium.