Esophagojejunostomy with the EEA stapler.

Esophagojejunostomy after total gastrectomy was attempted in 27 operations with the EEA stapling device (U.S. Surgical Corp., Norwalk, Conn.). After removal of the specimen the anastomosis is performed with an end-to-side technique with insertion of the cartridge and its central rod through the open jejunal end. The 28 mm wide cartridge was used in 24 anastomoses and the 25 mm wide cartridge was used in two. In one case the 25 mm cartridge tore the distal esophagus, and the anastomosis had to be sutured manually. The median operation time was 305 minutes (range, 205 to 560 minutes), and the time to perform the anastomosis was 20 minutes (range, 15 to 60 minutes). Anastomotic leakage occurred in three patients, two of whom were stapled with the 25 mm cartridge. All healed with conservative treatment. One patient developed a stricture at the anastomotic site due to recurrence of the tumor. There was one hospital death. Median hospital stay was 16 days (range, 8 to 71 days) and median survival time was 11 months. It is concluded that the EEA stapler allows the construction of a fast and reliable esophagojejunostomy with good functional results after total gastrectomy for gastric cancer.

Jejunal mucosal DNA content and maturation. Inverse relation to serum gastrin levels in suckling and weanling rats.

Although pentagastrin has a tropic action on intestinal mucosa in suckling rat pups, and at weaning a rise in gastrin levels coincides with maturation of the intestinal mucosa, direct correlations of serum gastrin levels and intestinal maturation have yet to be made. Ten-day-old rats were subjected either to antrectomy to produce a 43% decrease in serum gastrin levels or to fundectomy to produce a 319% increase over gastrin levels in rumenectomized or normal animals. These changes were not associated with tropic or adaptive changes in jejunal or colonic mucosa as determined by jejunal and colonic DNA content, jejunal sucrase activity, jejunal villous height, or crypt depths in jejunum and colon at the beginning (day 15), middle (day 21), or end (day 27) of the weaning period. To the contrary, an inverse relation was found between serum gastrin levels and both jejunal mucosal DNA content and sucrase activity as an index of maturation.

Recurrence after parietal cell vagotomy for peptic ulcer disease.

The value of parietal cell vagotomy as a safe surgical procedure in the treatment of chronic peptic ulcer disease has been seemingly limited by the high recurrence rate usually reported. In this 10 year experience of 405 consecutive parietal cell vagotomy operations, 57 patients with recurrent ulceration were evaluated to try to answer the questions of where and why recurrent ulceration appears and how to treat it. Patients with pyloric or prepyloric ulcer disease had recurrence of disease earlier than did patients with chronic duodenal ulcer disease. Consequently, pyloric or prepyloric ulcer patients had a higher recurrence rate in the early postoperative period than chronic duodenal ulcer patients, but this difference disappeared after the seventh postoperative year. Patients with recurrent chronic duodenal ulcer disease have high postoperative acid secretion levels, indicating incomplete vagotomy as a causative factor. Patients with recurrent pyloric or prepyloric ulcer disease have postoperative acid secretion similar to that of patients without recurrence, suggesting another etiologic factor. Thirty of 57 patients with recurrent ulcer had successful medical treatment. A conservative attitude towards recurrences is justified, particularly when symptoms are few and the postoperative acid secretion tests indicate complete or partial vagotomy. Surgical therapy consisting of truncal vagotomy and pyloroplasty in cases of incomplete vagotomy and antrectomy in cases of complete vagotomy should be reserved for patients with symptoms and a disease course that cannot be controlled by conservative treatment.

Parietal cell vagotomy in the surgical treatment of chronic duodenal, pyloric and prepyloric ulcer disease.

During the 1970s, parietal cell vagotomy (PCV) gradually became accepted as a suitable method in the surgical treatment of prepyloric, pyloric and duodenal ulcer disease. This study reports the data from a study of 405 consecutive patients with chronic ulcer disease treated with PCV. Mortality was low (0.5%) and there were few postoperative sequelae (periodic loose stools in 2% and mild dumping in 2%). Reduction in basal acid output was 75% and in pentagastrin stimulated acid secretion 50%. The ulcer recurrence rate was initially higher in pyloric-prepyloric (PU/PPU) than in duodenal ulcer disease but after the seventh postoperative year this difference was no longer statistically significant. The accumulated recurrence rate was 17.5%. Few side effects and a comparatively low recurrence rate makes PCV the method of choice in the surgical treatment of peptic ulcer disease.

Prophylactic oophorectomy in colorectal carcinoma.

It is a well established fact that women with recurrent colorectal carcinoma have a high frequency of ovarian metastases. This study was undertaken to see if microscopic metastases could be found in serial sections of ovaries removed at the time of primary operation. Of 58 patients, 4 had microscopic metastases and an additional 2 patients had macroscopic metastases. This finding, plus the risk of the development of a primary ovarian carcinoma, favors prophylactic oophorectomy in women with colorectal carcinoma.

Dimethylhydrazine-induced colonic neoplasia: dissociation from endogenous gastrin levels.

The potential tropic effect of gastrin in promoting colonic carcinogenesis was tested in rats (n = 133) with 6- to 16-fold variations in endogenous gastrin resulting from antrectomy or fundectomy, followed by 12 injections of 1,2-dimethylhydrazine (10 mg/kg). The incidence and grade of differentiation of resulting tumors, as well as the thickness, content of nucleic acids, and specific activity of DNA in colonic mucosa, were similar in both high-gastrin and low-gastrin animals and were unchanged from data in unoperated control animals receiving only the carcinogen. Long-term changes in endogenous gastrin concentration are not followed by colonic mucosal tropic effects, and gastrin does not act as a cofactor in dimethylhydrazine-induced carcinogenesis at this dosage.

Ileal resection potentiates 1,2-dimethylhydrazine-induced colonic carcinogenesis.

The effect of colonic hyperplasia produced by resection of the distal third of the small bowel (DSBR) on the development of chemical carcinogenesis of the colon by dimethylhydrazine (DMH) was tested in rats. For the most part the amounts of RNA and DNA in the small bowel were the same with the combined treatments as with either one alone; quantities of nucleic acids tended to increase only in transverse and distal colon. After 37 weeks the number of neoplasms per rat was increased six-fold by combining DSBR with DMH. Neoplasms were spread throughout the colon after combined treatment as opposed to the ascending colong after DMH alone. Postresectional hyperplasia appears to increase the incidence and distribution of colon tumors.

Promotion of azoxymethane-induced colonic neoplasia by resection of the proximal small bowel.

Potential enhancement of intestinal neoplasia by compensatory mucosal hyperplasia was tested in rats subjected to 50% proximal small bowel resection (PSBR) 10 days after the last of 16 weekly injections of azoxymethane. Azoxymethane alone increased jejunal contents of RNA and DNA each by 26% at 17 to 18 weeks (p less than 0.01) before there was macroscopic evidence of neoplasia. Three months after PSBR alone, ileal hyperplasia was characterized by increased amounts of RNA (42 to 76%) and DNA (68 to 95%), taller villi, deeper crypts, and luminal dilation (p less than 0.05 to 0.001); however, the colon showed only patchy hyperplasia. When the combined effects of azoxymethane and PSBR were observed 26 to 30 weeks after the first injection, rats with PSBR had an increased number of colonic tumors per animal (2.9 versus 1.6 for controls; p less than 0.02). Despite the intense ileal hyperplasia produced by PSBR, ileal neoplasia did not occur. Enhanced colonic carcinogenesis followed sequential exposure of the mucosa to the carcinogen (azoxymethane) and to the promoting factor (PSBR).

Compensatory postresectional hyperplasia and starvation atrophy in small bowel: dissociation from endogenous gastrin levels.

Because exogenous gastrin has been implicated as a tropic hormone for mucosal cells of the intestinal tract and as a regulator of mucosal growth, we studied the effects on the gut of endogenous 23-fold variations of serum gastrin produced by various gastric operations. These were pyloroplasty, vagotomy and pyloroplasty, antrectomy, and fundectomy. After jejunal resection, RNA content, DNA content, incorporation of [3H]thymidine into DNA, crypt depth, and villus height in midgut and ileum were independent of gastrin levels. Loss of RNA and DNA during starvation was not prevented by high endogenous concentrations of serum gastrin, and DNA specific activity was not affected. Tropic effects distal to the duodenum produced by exogenous gastrin and pentagastrin may be results of supranormal levels.

Alien cancers of the duodenum.

Invasion of the duodenum by contiguous cancer or an isolated metastasis can manifest itself with the signs and symptoms of primary cancer of the duodenum. Fourteen patients were identified with this type of diagnostic confusion. All of their tumors were in the second or third portion of the duodenum. Although the median length of survival after excision of the tumor or palliative bypass operations in these patients was nine months, considerably longer survival times have also been described. Barium enema examinations and excretory urograms should be considered as diagnostic tests for any patient with a tumor of the duodenum to identify the contiguous carcinomas of the colon and kidney subject to long palliation.