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.
Dis Colon Rectum. 2013 Nov;56(11):1273-81. doi: 10.1097/DCR.0b013e3182a42d16.
None of the current theories on fecal incontinence can explain fecal continence adequately.
This study aims to evaluate the mechanism controlling fecal continence.
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.
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.
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.
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).
目前关于大便失禁的理论都不能充分解释大便失禁的原因。
本研究旨在评估控制大便失禁的机制。
对 17 例健康志愿者进行直肠测压、直肠感觉容积和肛门直肠电感觉检查,在实施浅表局部肛门麻醉前后各进行 1 次,6 例志愿者实施椎管内麻醉前后各进行 1 次;对 1 例局部肛门麻醉注射前后、3 例胸 3 至腰 3 脊髓损伤患者也进行了相同的检查。
浅表局部肛门麻醉后,肛门电感觉下降,但基础肛门压力不变。缩榨压下降,直肠感觉容积不变。局部麻醉降低了在直肠逐渐充盈过程中记录到的远段肛门内压。在局部肛门麻醉注射后,同样如此,尽管更明显。椎管内麻醉后,肛门内对电刺激不敏感,但基础和缩榨压明显下降,球囊保持试验中的肛门内压增加完全消失。在脊髓损伤患者中,虽然可以自主收缩肛门外括约肌,但外括约肌不能随意收缩,球囊保持试验中肛门内压可超过 300mmHg。
这是部分实验性测量。在后续研究中,需要研究在日常临床实践中发现的模型的相关性。
我们的结果支持以下假说:由外括约肌收缩介导的大便失禁成分取决于不需要大脑参与的肛门外括约肌节制反射。该反射的传入受体可能是位于远段肛门内黏膜或黏膜下层的接触受体。因此,肛门外括约肌节制反射功能丧失将导致大便失禁(参见视频,补充数字内容 1,http://links.lww.com/DCR/A116)。