Richard G Molloy

Rectoanal inhibitory reflex following low stapled anterior resection of the rectum

The rectoanal inhibitory reflex plays an important role in the normal mechanisms of anorectal continence. Anterior resection abolishes the reflex, but whether it recovers, particularly after inverted stapled anastomosis, is not clear. Anal manometry was performed on patients undergoing low anterior resection for carcinoma. Maximum anal resting pressure and the rectoanal inhibitory reflex were assessed preoperatively and up to two years postoperatively. The reflex was present in 43 of 46 patients (93 percent) preoperatively, in 8 of 45 patients (18 percent) on the 10th postoperative day, and in 6 of 29 patients (21 percent) between six months and one year following surgery. Twenty patients were studied more than two years postoperatively, and in 17 (85 percent) the reflex was demonstrated. In the majority of low anterior resection patients, the rectoanal inhibitory reflex is abolished by surgery, remains absent throughout the first year, and has recovered by the end of the second postoperative year. This may be important in the recovery of anorectal function in these patients.

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® (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® 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® 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.

Long-term immunotherapeutic intervention with pentoxifylline in a mouse model of thermal injury and infection.

Major thermal or traumatic injury often results in abnormalities of immune function, and these abnormalities contribute to the increased susceptibility to infection observed in these patients. Abnormalities of T-cell function, including decreased proliferation and secretion of cytokines are observed following major injury and, conversely, there is markedly increased monokine production. Thus, therapy of this syndrome might logically be aimed at modulating the immune system to upregulate T-cell function and downregulate monocyte hyperactivation. Pentoxifylline (PTX), a methylxanthine derivative, has been shown to be therapeutically effective in several animal models. The purpose of this study was to evaluate PTX and its effect on cytokine production in a mouse model of thermal injury and to study its effect on survival after septic challenge. The results show that PTX therapy after injury can restore T-cell production of IL-2 and downregulate the hyperactive macrophage secretion of proinflammatory cytokines. However, improvement in survival resulting from this therapy following thermal injury and septic challenge depends on timing of dosage.