Paul M A Broens1, Freddy M Penninckx, José Boix Ochoa. 1. 1 Department of Surgery, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands 2 Department of Abdominal Surgery, University Hospital Gasthuisberg, Catholic University of Leuven, Leuven, Belgium 3 Department of Pediatric Surgery, Hospital Infantil Valle d'Hebrón, Autonomous University, Barcelona, Spain.
Abstract
BACKGROUND: None of the current theories on fecal incontinence can explain fecal continence adequately. OBJECTIVE: This study aims to evaluate the mechanism controlling fecal continence. DESIGN: Anal electrosensitivity, anorectal pressures, and rectal pressure volumetry tests were performed in 17 controls before and after superficial local anal anesthesia and in 6 controls before and after spinal anesthesia. The same tests were performed in 1 patient before and after injected local anal anesthesia and in 3 patients with spinal cord lesions at levels Th3 to L3. RESULTS: After superficial local anal anesthesia, anal electrosensitivity decreased, but basal anal pressure remained unaltered. Squeeze pressure decreased and rectal filling sensation levels remained. Local anesthesia reduced anal pressure recorded in the distal anal canal during progressive rectal filling. This was also the case, albeit more explicit, after the local anal anesthetic was injected. After spinal anesthesia, the anal canal became insensitive to electric stimulation, but basal and squeeze pressure values decreased substantially, and the increase in anal pressure during the balloon-retaining test disappeared completely. In the patients with spinal cord lesions, the external sphincter could not be squeezed on command, but during the balloon-retaining test, the anal sphincter did squeeze autonomously at more than 300 mmHg. LIMITATIONS: These were partially experimental measurements. The relevance of the found model in the daily clinical practice will have to be studied in a following study. CONCLUSIONS: Our results support the hypothesis that the component of fecal continence mediated by contraction of the external sphincter depends on a anal external sphincter continence reflex without involving the brain. Presumably, the afferent receptors of this reflex are contact receptors located superficially in the mucosa or submucosa of the distal anal canal. A nonfunctioning anal external sphincter continence reflex would, therefore, result in fecal incontinence (see Video, Supplemental Digital Content 1, http://links.lww.com/DCR/A116).
BACKGROUND: None of the current theories on fecal incontinence can explain fecal continence adequately. OBJECTIVE: This study aims to evaluate the mechanism controlling fecal continence. DESIGN: Anal electrosensitivity, anorectal pressures, and rectal pressure volumetry tests were performed in 17 controls before and after superficial local anal anesthesia and in 6 controls before and after spinal anesthesia. The same tests were performed in 1 patient before and after injected local anal anesthesia and in 3 patients with spinal cord lesions at levels Th3 to L3. RESULTS: After superficial local anal anesthesia, anal electrosensitivity decreased, but basal anal pressure remained unaltered. Squeeze pressure decreased and rectal filling sensation levels remained. Local anesthesia reduced anal pressure recorded in the distal anal canal during progressive rectal filling. This was also the case, albeit more explicit, after the local anal anesthetic was injected. After spinal anesthesia, the anal canal became insensitive to electric stimulation, but basal and squeeze pressure values decreased substantially, and the increase in anal pressure during the balloon-retaining test disappeared completely. In the patients with spinal cord lesions, the external sphincter could not be squeezed on command, but during the balloon-retaining test, the anal sphincter did squeeze autonomously at more than 300 mmHg. LIMITATIONS: These were partially experimental measurements. The relevance of the found model in the daily clinical practice will have to be studied in a following study. CONCLUSIONS: Our results support the hypothesis that the component of fecal continence mediated by contraction of the external sphincter depends on a anal external sphincter continence reflex without involving the brain. Presumably, the afferent receptors of this reflex are contact receptors located superficially in the mucosa or submucosa of the distal anal canal. A nonfunctioning anal external sphincter continence reflex would, therefore, result in fecal incontinence (see Video, Supplemental Digital Content 1, http://links.lww.com/DCR/A116).
Authors: Paul T Heitmann; Paul F Vollebregt; Charles H Knowles; Peter J Lunniss; Phil G Dinning; S Mark Scott Journal: Nat Rev Gastroenterol Hepatol Date: 2021-08-09 Impact factor: 46.802
Authors: Ji-Hong Chen; Sean P Parsons; Mitra Shokrollahi; Andrew Wan; Alexander D Vincent; Yuhong Yuan; Maham Pervez; Wu Lan Chen; Mai Xue; Kailai K Zhang; Arshia Eshtiaghi; David Armstrong; Premsyl Bercik; Paul Moayyedi; Eric Greenwald; Elyanne M Ratcliffe; Jan D Huizinga Journal: Front Physiol Date: 2018-09-20 Impact factor: 4.566