The recto-anal inhibitory reflex: Abnormal response in diabetics suggests an intrinsic neuroenteropathy†

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Abstract

As electrical stimulation of the rectum has been shown to result in reflex internal sphincter inhibition mediated by intrinsic nerves, we aimed to evaluate the integrity of these nerves in the rectum of diabetic patients. Anal canal pressure, recto-anal inhibitory reflex (RAIR) and continence were evaluated in 30 diabetic patients (male : female 13 : 17, median age 57 years, range 37-70) and these data were compared with similar data obtained from 22 age- and sex-matched healthy controls (male : female 9 : 13, median age 51 years, range 19-65 years). Median duration of diabetes was 8 years (range 3-30). Twelve (40%) of the 30 diabetics had impaired continence for gas (n = 12) and liquid faeces (n = 3). None of the controls had incontinence. Median maximum resting anal canal pressure (MRP) was: patients 30 mmHg (range 20-75 mmHg) versus controls 40 mmHg (range 20-105 mmHg, P=0.61). Median maximum squeeze pressure (MSP) was 65 mmHg (range 30-150 mmHg) in patients versus 84 mmHg (range 35-230 mmHg) in controls (P=0.59). Median threshold rectal mucosal electrosensation (RMES-T) was 27 mA (5-40 mA) in patients versus 13 mA (5-28 mA) in controls (P=0.03). Maximum tolerable rectal mucosal electrosensation was 40 mA (20-60) in patients versus 20 mA (10-30), in controls (P=0.042, all comparisons using the Wilcoxon rank test). Recto-anal inhibitory reflex was present in eight, abnormal in five (one incontinent) and absent in 17 (11 incontinent) diabetics, while it was present in 18 and abnormal in four controls (test of proportion, P = 0.031). Blood glucose in diabetics on the day of the procedure was 98 mg/dL (70-165 mg/dL). Rectal mucosal electrosensitivity and RAIR were impaired in significantly more patients with diabetes than controls, implying impairment of intrinsic neuronal function. The recto-anal inhibitory reflex was either impaired or absent in all diabetic patients with incontinence.

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