Abstract

The indications for sacral nerve stimulation are increasing, but the mechanism remains poorly understood. This study aimed to examine the effect of sacral nerve stimulation on rectal compliance and rectal sensory function. This was a prospective study. This study took place at a university teaching hospital. Twenty-three consecutive consenting patients (22 female; median age, 49 y) undergoing temporary sacral nerve stimulation for fecal incontinence were prospectively studied. Clinical response was assessed by the use of bowel diaries and Wexner scores. Anal manometry, rectal compliance, volume and pressure thresholds to rectal distension (barostat), and rectal Doppler mucosal blood flow were measured before and at the end of stimulation. Sixteen patients (70%) had a favorable clinical response. Median anal squeeze pressures increased with stimulation from 40 (range, 6-156) cmH2O to 64 (range, 16-243) cmH2O. Median rectal compliance did not significantly change with stimulation (prestimulation: 11.5 (range, 7.9-21.8) mL/mmHg, poststimulation: 12.4 (range, 6.2-22) mL/mmHg, P = .941). Rectal wall pressures associated with urge (baseline: 15.4 (range, 11-26.7) mmHg, poststimulation: 19 (range, 11.1-42.7) mmHg, P = .054) and maximal tolerated thresholds (baseline: 21.6 (8.5-31.9) mmHg, poststimulation: 27.1 (14.3-43.3) mmHg, P = .023) significantly increased after stimulation. Rectal Doppler mucosal blood flow did not significantly change with stimulation (baseline: 125.8 (69.9-346.8), poststimulation: 112.4 (50.2-404.1), P = .735). Changes in anal resting pressure and rectal wall pressures with stimulation were evident only in responders; however, changes in anal squeeze pressures were evident in both responders and nonresponders. The study reports results following short-term stimulation in a small but homogenous group of patients. A larger long-term study will follow. Temporary sacral nerve stimulation does not change rectal compliance, but is associated with significant changes to the pressure thresholds of rectal distension. This, together with the observation that outcome is not related to sphincter integrity, supports the hypothesis of an afferent-mediated mechanism of action.

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