OC-070 Assessment of rectal compliance and sensory function following temporary sacral nerve stimulation

Abstract

<h3>Introduction</h3> Sacral Nerve Stimulation (SNS) is an increasingly used minimally invasive treatment option in anorectal functional disorders. However, little is understood about its mechanism of action and studies report inconsistent anorectal physiological changes with stimulation. The study aim was to examine the effect of SNS on rectal compliance and rectal sensory function. <h3>Methods</h3> Nineteen consecutive patients (all female, median age 49 (30–74)) undergoing temporary SNS for faecal incontinence (FI) were studied prospectively. The clinical response was assessed using bowel diaries and Wexner scores. Anal manometry, rectal compliance and volume and pressure thresholds to rectal distension (barostat) were measured pre- and post- stimulation. <h3>Results</h3> Aetiology of FI was obstetric (9 patients, 47%), post-surgical (2, 10.5%), atrophic (2, 10.5%), scleroderma, subarachnoid haemorrhage and “idiopathic” (6, 32%). Endo-anal Ultrasound showed normal intact sphincters in 11 (58%), sphincter atrophy in 3 (16%) and sphincter defects in 5 (26%). Thirteen patients (68%) had favourable response to the stimulation, with Wexner scores reducing from 14.1±3.4 to 6.5±4.8 (p=0.0002). The presence of sonographic sphincter abnormalities did not influence the clinical response (p=0.806). Anal manometry: Anal pressures increased with stimulation: mean resting pressure increasing from 45±25 to 55±31 cm H₂O (p=0.095) and mean squeeze pressure from 62±47 to 88±61 cm H₂O (p=0.019). Compliance: Rectal compliance did not change with stimulation (pre: 12.9±3.9 ml/mm Hg, post: 12.5±3.9 ml/mm Hg, p=0.727). Sensory function: There was a trend towards reduction of the volume threshold for First Sensation (pre: 83±39 ml, post: 64±30 ml, p=0.062) and increase in the Maximum Tolerated Pressure (pre: 21.7±5.7 mm Hg, post: 25.0±8.0 mm Hg, p=0.036). <h3>Conclusion</h3> Short-term SNS is not associated with altered rectal compliance, but there are changes in thresholds to rectal distension. Taken together with the observation that outcome is not related to sphincter integrity, this supports the hypothesis of an afferent-mediated mechanism of action. The observed increase in anal pressures is most likely reflex-mediated and further assessment at more central levels of the brain-gut axis is indicated.