MECHANISM OF SPHINCTER IMPAIRMENT FOLLOWING LOW ANTERIOR RESECTION

It has been postulated that reduction in anal resting pressure following low anterior resection is due to intraoperative injury to the internal anal sphincter during transanal passage of the stapling device or damage to its nerve supply in the course of rectal mobilization. The aim of this study was to assess the relative importance of either mechanism. Fourteen dogs had a standard segment of colon and distal rectum excised. Colorectal reconstruction was performed using either a low stapled EEA(R) (U.S. Surgical Corporation, Norwalk, CT) colorectal anastomosis (n = 7) or a handsewn anastomosis (n = 7). Anorectal manometry was performed preoperatively and again on the 10th postoperative day. Resting anal pressure was significantly reduced after EEA(R) anastomosis (mean +/- SEM: before, 49 +/- 3 mm Hg; after, 20 +/- 4 mm Hg; P < 0.001) and handsewn anastomosis (mean +/- SEM: before, 46 +/- 4 mm Hg; after, 35 +/- 4 mm Hg; P < 0.01). Postoperative resting pressures were also significantly reduced (P < 0.05) following EEA(R) anastomosis when compared with the handsewn group. This study suggests that damage to the innervation of the internal anal sphincter during rectal mobilization and further direct injury to the sphincter during transanal instrumentation both contribute to the fall in anal resting pressure observed following low anterior resection.