[The role of local excision in the treatment of rectal tumors].
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Biomedical subjects
Publications and source records attributed to W Montorsi.
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In 1989 there were 151,000 new cases of colorectal carcinoma in the United States. Approximately 50% of these patients will be at risk of developing liver metastases together with other sites of recurrence. However, the liver will be the main site of relapse in only 14,000 patients with colorectal cancer. Approximately 25% of patients with colorectal carcinoma have technically resectable hepatic metastases at the time of operation for primary lesion, and an additional 8-25% will develop metachronous hepatic metastases after primary resection. Recent reported experiences with surgical treatment of metastatic colorectal cancer in the liver seem to indicate that hepatic resection has become more acceptable, safe and effective therapy, and offers today when technically possible, the best prospect of survival in a conspicuous number of patients. For these reasons, although a prospective randomized trial has not been done comparing resection with nonresection, resection seems to give the best hope for cure and actually is the treatment of choice for selected patients. In fact in these patients is reported a significant prolongation of survival compared with those patients with unresectable liver metastases treated only with adjuvant therapy in the form of chemotherapy or radiation therapy. Median survival of resected patients with hepatic metastases has been reported to range from 6-12 months, and for patients with single metastases is reported to range from 4.5-6.2 months to 11 and 21 months. The benefits of surgical therapy have been emphasized by different experience, with a 5-year overall survival rate ranging from 20-40%. In a recent multicenter survey a 33% 5-year survival rate was demonstrated in 859 patients resected for hepatic metastases.
This study was performed to see whether or not protection of the endothelial cells contributes to the antithrombotic effects of heparin. New Zealand albino rabbits were subjected to jugular vein stasis by single caudal ligation for 2 h. Three treatments were given: saline (control group), heparin (0.2 mg/kg) 5 or 45 min before ligature of the vein. Groups of 6-8 animals were killed at 0, 5, 15, 30 and 120 min. The following parameters were determined: (1) involution and damage of the endothelial cells by scanning and transmission electron microscopy; (2) incidence and weight of thrombi in the lumens of the veins after 2 h stasis, and (3) effects of heparin on APTT and anti-Xa activity. In the control group, stasis caused a considerable involution of the endothelial cells in the first 30 min, followed by fibrin deposition and thrombus generation. Heparin strongly reduced the damage to the endothelial cells, with very evident protection of the cell membranes, and prevented thrombus generation: there were significant decreases in both incidence and weight of thrombi. These effects of heparin were evident both shortly after (maximal anticoagulant effect) and long after (no anticoagulant effect) pretreatment. We think that, under the experimental conditions we used, heparin prevented venous thrombosis at least partially by protection of the endothelial cells, through unknown mechanisms.
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Transient hypomagnesiaemia was noted postoperatively, particularly on the 1st day in patients submitted to intestinal procedures. Slight hypocalcaemia was also observed; this was often related to a low plasma Mg value. A hormonal mechanism is presumed to be the cause of this stress-linked fall in blood magnesium.
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