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Changes in anorectal sensation have been reported in patients with fecal incontinence, and there is limited evidence that sacral nerve stimulation can restore normal sensation.The aims of the present study were to investigate changes in the transmission of sensory anorectal stimuli in a rodent model of fecal incontinence and to study the effects of sacral nerve stimulation on defecation behavior.An established model of fecal incontinence was utilized for this study.Pudendal nerve stretch and compression were used in 16 adult female Wistar rats and were monitored for 3 weeks: 6 rats received sacral nerve stimulation for 1 week by using an implantable neurostimulator and 10 rats had nonfunctioning "dummy" devices inserted. Five additional rats were sham operated. Anorectal cortical evoked potentials were used as a surrogate marker for anorectal sensory function.The primary outcomes measured were fecal incontinence index, evoked potential amplitude, and latency.Fifty percent of rats showed behavioral signs of fecal incontinence measured by the Fecal Incontinence Index (0.20), calculated by using the pellet distribution outside the cage's latrine area. Anorectal evoked potential amplitude was reduced in rats with a Fecal Incontinence Index0.20 (p = 0.019). The amplitude of forepaw evoked potentials recorded as a control was not different between groups. Chronic sacral nerve stimulation using the fully implantable device and custom rodent lead was safe and stable during this chronic prospective study. Incontinent rats (n = 3) that received sacral nerve stimulation showed an improvement of Fecal Incontinence Index and an increase of evoked potential amplitude to anorectal stimulation compared with the dummy implant controls (n = 5).The main limitation is the small number of animals that received sacral nerve stimulation.Chronic sacral nerve stimulation is feasible in rats when miniature telemetric devices are used. Behavioral signs of fecal incontinence were positively correlated with the latency of anorectal evoked potentials. See Video Abstract at http://links.lww.com/DCR/B712.RELACIÓN ENTRE LA ACTIVACIÓN CORTICAL EN RESPUESTA A LOS ESTÍMULOS ANORRECTALES Y EL COMPORTAMIENTO DE CONTINENCIA EN RATAS QUE SE COMPORTAN LIBREMENTE ANTES Y DESPUÉS DE LA APLICACIÓN DE ESTIMULACIÓN DEL NERVIO SACRO.Se han informado cambios en la sensación anorrectal en pacientes con incontinencia fecal y hay evidencia limitada de que la estimulación del nervio sacro puede restaurar la sensación normal.Los objetivos del presente estudio fueron investigar los cambios en la transmisión de estímulos anorrectales sensoriales en un modelo de roedor de incontinencia fecal y estudiar los efectos de la estimulación del nervio sacro en la conducta de defecación.Un modelo establecido de incontinencia fecal.Se utilizó estiramiento y compresión del nervio pudendo en 16 ratas Wistar hembras adultas y se les realizó un seguimiento durante 3 semanas: seis ratas recibieron estimulación del nervio sacro durante 1 semana utilizando un neuroestimulador implantable y diez ratas tuvieron insertados dispositivos "ficticios" no funcionantes. Se operaron simuladamente cinco ratas adicionales. Los potenciales evocados corticales anorrectales se utilizaron como marcador subrogado de la función sensorial anorrectal.Índice de incontinencia fecal, amplitud de potenciales evocados y latencia.El cincuenta por ciento de las ratas mostró signos de comportamiento de incontinencia fecal medidos por el Índice de incontinencia fecal (0.20), calculado utilizando la distribución de heces fuera del área de la letrina de la jaula. La amplitud del potencial evocado anorrectal se redujo en ratas con un índice de incontinencia fecal0.20 (p = 0.019). La amplitud de los potenciales evocados de la pata delantera registrados como control no fue diferente entre los grupos. La estimulación crónica del nervio sacro utilizando un dispositivo totalmente implantable y un cable de roedor personalizado fue segura y estable durante este estudio prospectivo crónico. Las ratas con incontinencia (N = 3) que recibieron estimulación del nervio sacro mostraron una mejora del índice de incontinencia fecal y un aumento de la amplitud del potencial evocado a la estimulación anorrectal en comparación con los controles de implante ficticio (N = 5).La principal limitación es el pequeño número de animales que recibieron estimulación del nervio sacro.La estimulación crónica del nervio sacro es factible en ratas cuando se utilizan dispositivos telemétricos en miniatura. Los signos conductuales de incontinencia fecal se correlacionaron positivamente con la latencia de los potenciales evocados anorrectales. Consulte Video Resumen en http://links.lww.com/DCR/B712. (Traducción-Dr. Jorge Silva Velazco).

Fecal incontinence is a common disorder, but its pathophysiology is not completely understood.The aim of this review is to present animal models that have a place in the study of fecal incontinence.A literature review following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines performed in August 2016 revealed 50 articles of interest. Search terms included fecal/faecal incontinence and animal model or specific species.Articles not describing an animal model, in vitro studies, veterinary literature, reviews, and non-English articles were excluded.The articles described models in rats (n = 31), dogs (n = 8), rabbits (n = 7), and pigs (n = 4).Different fecal incontinence etiologies were modeled, including anal sphincter lesions (33 articles) ranging from a single anal sphincter cut to destruction of 50% of the anal sphincter by sharp dissection, electrocautery, or diathermy. Neuropathic fecal incontinence (12 articles) was achieved by complete or incomplete pudendal, pelvic, or inferior rectal nerve damage. Mixed fecal incontinence (5 articles) was modeled either by the inflation of pelvic balloons or an array of several lesions including nervous and muscular damage. Anal fistulas (2 articles), anal sphincter resection (3 articles), and diabetic neuropathy (2 articles) were studied to a lesser extent.Bias may have arisen from the authors' own work on fecal incontinence and the absence of blinding to the origins of articles.Validated animal models representing the main etiologies of fecal incontinence exist, but no animal model to date represents the whole pathophysiology of fecal incontinence. Therefore, the individual research questions still dictate the choice of model and species.

Obstetric injury to the pudendal nerve contributes significantly to fecal incontinence. The inferior rectal nerve, a terminal branch of the motor division of the pudendal nerve, innervates the external anal sphincter. Animal models have been developed to establish the scientific basis of sacral neuromodulation. The aims of this study were to determine the spinal location of inferior rectal nerve motoneurons projecting to the external anal sphincter and whether the inferior rectal nerve carries sensory fibers.Ten female virgin Wistar rats were used; 7 underwent bilateral inferior rectal nerve section and application of the neuronal tracer fluorogold. Five days later dorsal root ganglia L5 to S2 and the lumbosacral spinal cord were harvested and stained for activating transcription factor 3, a molecular marker of nerve injury. Three animals were used to confirm the specificity of activating transcription factor 3 nuclear labeling as a marker of axotomy.Fluorogold-labeled motoneurons were found exclusively at L6 in the dorsomedial sections of Onuf's nuclei (left and right), which contained 30 +/- 9 motoneurons with a median diameter of 28.3 microm (24.4-31.0) (25th-75th centiles). Double-labeled sensory neurons (fluorogold-labeled cytoplasm and activating transcription factor 3-labeled nuclei) were found in dorsal root ganglia L6 to S2 and were smaller in diameter (20.5 microm (17.8-26.7); median (25th-75th centiles)) than motoneurons (P.0,001).The external anal sphincter receives both motor and sensory innervation from the inferior rectal nerve. Activating transcription factor 3 nuclear staining may prove useful for quantifying the degree of nerve injury in animal models of fecal incontinence.

Childbirth is the most common cause of fecal incontinence and damage to the pudendal nerve is a major component of childbirth injury. This study was designed to develop an acute animal model of injury to the innervation of the external anal sphincter. Forty-eight female virgin wistar rats were studied. Two models of neuropathic injury were developed. Bilateral inferior rectal nerve crush (Group A) acted as a positive control. Prolonged intrapelvic retrouterine balloon inflation (Group B) simulated the pelvic compressive forces of labor. Quantitative analysis of external anal sphincter muscle function was performed by using electromyography, external anal sphincter specific force production, and stereologic calculation of external anal sphincter mass. Injury in both groups caused significant atrophy of the external anal sphincter (P = 0.002, ANOVA) and electromyographic evidence of reinnervation at one week. Specific force (mN force per mg mass) was not altered. External anal sphincter muscle mass recovered after four weeks in Group B. Balloon dilation within the boney pelvis results in denervation of the external anal sphincter and offers an experimental model of the effects of childbirth on the continence mechanism in humans.

The study was designed to determine the effect of further vaginal delivery on anal sphincter function in women after apparently uncomplicated primiparous forceps delivery.Fifty-two secundigravid women whose first child was forceps-assisted were compared with a control group of 20 women who had undergone spontaneous first vaginal delivery. Both groups were studied antenatally and again at 12 weeks after second delivery using a standardized bowel function questionnaire, endoanal ultrasound, and anal manometry. The primary outcome was fecal incontinence score after second delivery.Before second delivery, 20 of 52 (39 percent) of the forceps group and 3 of 20 (15 percent) control subjects (P = 0.103) reported minor alteration in fecal incontinence. Endoanal ultrasound was more frequently abnormal (38/52 (73 percent) vs. 6/20 (30 percent); P = 0.002), and median anal canal squeeze (71 vs. 104 mmHg; P = 0.004) and resting pressures (43 vs. 58 mmHg; P = 0.004) were lower in the forceps group. There was no difference in continence score between first and second delivery for the forceps group (P = 0.19) group or control subjects (P = 0.18). However, 10 of 38 (26 percent) women with an abnormal endoanal ultrasound after first forceps delivery developed new or worsening symptoms after second delivery.One-quarter of women with occult anal sphincter injury after first forceps delivery experienced some minor alteration in fecal continence after the second delivery.

Splenic flexure mobilization is widely considered to be an essential component of anterior resection for rectal cancer. It was our hypothesis that selective splenic flexure mobilization would reduce operative times without increasing morbidity or affecting cure. A total of 100 consecutive patients with rectal cancer (mean 8 (range, 4–15) cm from anal verge) who underwent anterior resection for cure between 1996 and 2002 had splenic flexure mobilization only as required to achieve a tension-free anastomosis. Operative time, postoperative morbidity, pathologic findings, and recurrence rates were recorded. There were no clinicopathologic differences between those who had splenic flexure mobilization (n = 26) and those who did not (n = 74). Mean operative time in the splenic flexure mobilization group was longer, 167 (range, 130–200) minutes vs. 120 (range, 95–180) minutes in the nonmobilized group (P = 0.023). Mean length of specimen resected was longer in the splenic flexure mobilization group: 36 vs. 18 cm (P = 0.008). Anastomotic complications (4 percent), local recurrence (7 percent, median follow-up, 38 months), perioperative morbidity (32 percent) and mortality (2 percent), and survival did not differ between the two groups. Routine splenic flexure mobilization is not required for safe anterior resection in patients with rectal cancer. Avoiding splenic flexure mobilization results in shorter operative times and does not increase postoperative morbidity, anastomotic leakage, or local recurrence.

PURPOSE: Third-degree tears are generally managed by primary anal sphincter repair. Postoperatively, some physicians recommend laxative use, whereas others favor bowel confinement after anorectal reconstructive surgery. This randomized trial was designed to compare a laxative regimen with a constipating regimen in early postoperative management after primary obstetric anal sphincter repair. METHODS: A total of 105 females were randomized after primary repair of a third-degree tear to receive lactulose (laxative group) or codeine phosphate (constipated group) for three days postoperatively. Patients were reviewed at three days and at three months postpartum. Recorded outcome measures were symptomatic and functional outcome and early postoperative morbidity. RESULTS: Forty-nine patients were randomly assigned to the constipated group and 56 patients to the laxative group. The first postoperative bowel motion occurred at a median of four (mean, 4.5 (range, 1–9)) days in the constipated group and at two (mean, 2.5 (range, 1–7)) days in the laxative group (P < 0.001). Patients in the constipated group had a significantly more painful first evacuation compared with the laxative group (P < 0.001). The mean duration of hospital stay was 3.7 (range, 2–6) days in the constipated group and 3.05 days in the laxative group (range, 2–5; P = 0.001). Nine patients in the constipated group complained of troublesome postoperative constipation compared with three in the laxative group (P = 0.033). Continence scores, anal manometry, and endoanal ultrasound findings were similar in the two groups at three months postpartum. CONCLUSIONS: Patients in the laxative group had a significantly earlier and less painful bowel motion and earlier postnatal discharge. There was no difference in the symptomatic or functional outcome of repair between the two regimens.

PURPOSE: Involvement of the urinary tract by colorectal cancer is sufficiently rare to be encountered by an individual surgeon on an infrequent basis. The aim of this review is to highlight technical and oncologic issues that should be considered when dealing with complex colorectal cancer that involves the urinary tract. METHODS: The relevant literature from 1975 to 2001 was identified using the MEDLINE database of the U.S. National Library of Medicine and reviewed. Because of the diversity of forms of presentation of urologic involvement, few randomized, controlled trials are available, with most evidence derived from retrospective studies. RESULTS: Three distinct clinical situations in which the urinary tract may be affected by colorectal cancer were identified: involvement by primary colorectal cancer, involvement by recurrent cancer, and unexpected intraoperative findings of urinary tract involvement. Management strategies to identify and treat locally advanced primary or recurrent colorectal cancer involving the urinary tract improve survival with acceptable morbidity and mortality. Careful preoperative assessment of all patients with colorectal cancer will reduce unexpected identification of urinary tract invasion at the time of surgery. In patients in whom cure is not possible, endourologic techniques combined with judicious surgical resection can provide high-quality palliation. Optimal care of many of these conditions is facilitated by specialist urologic advice. CONCLUSIONS: The wide spectrum of possible urinary tract involvement by colorectal cancer requires individual patient-specific and disease-specific consideration. The literature offers important guidelines that aid decision making and improve management of these challenging problems.

PURPOSE: Colonic mucosal metabolism of butyrate may be impaired in ulcerative colitis. In this study we sought to confirm this observation, to determine if a similar change occurs in Crohn's colitis, and to establish whether a panenteric disorder of butyrate metabolism exists in either condition. METHODS: With use of a microculture technique, mucosal metabolic fluxes of14[C]-labeled butyrate and14[C]-labeled glutamine were measured as14[C] carbon dioxide production in mucosal biopsy specimens from the colon and ileum in patients with ulcerative colitis, Crohn's colitis, and healthy bowel. Results were expressed as pmol/µg biopsy DNA/hour. RESULTS: In the colon the mucosal metabolic fluxes of both butyrate and glutamine are reduced in both ulcerative colitis and Crohn's colitis compared with healthy controls. These changes were most marked in the presence of moderate to severe mucosal inflammation, there being no significant difference in mucosal metabolic flux between mildly inflamed mucosa and healthy controls. In the ileum the mucosal metabolic fluxes of butyrate and glutamine did not differ between healthy controls and those with either ulcerative colitis or Crohn's colitis. CONCLUSIONS: Changes in colonic mucosal metabolism of butyrate and glutamine in inflammatory bowel disease occur as a consequence of the inflammatory process and are not peculiar to ulcerative colitis. Ileal mucosal metabolism is unchanged in ulcerative colitis and Crohn's colitis, indicating the absence of a panenteric abnormality of mucosal metabolism in these two conditions.

PURPOSE: Anal sphincter damage can occur during vaginal delivery and may lead to impairment of fecal continence. The aim of this study was to determine the influence of irritable bowel syndrome on symptoms of fecal incontinence following first vaginal delivery. METHODS: A prospective, observational study was performed before delivery, six weeks, and six months following delivery in primiparous women. A bowel function questionnaire was completed, and anal vector manometry, mucosal electrosensitivity, pudendal nerve terminal motor latency, and anal endosonography were performed. A total of 208 women were assessed before and after delivery, and 104 primigravid women were studied after delivery only. A total of 34 of 312 (11 percent) had an existing diagnosis of irritable bowel syndrome. RESULTS: The prevalence of abnormal manometry or endosonography was similar in women with and without irritable bowel syndrome. However, six weeks after delivery, women with irritable bowel syndrome had a higher incidence of defecatory urgency (64 percent) and loss of control of flatus (35 percent) compared with those without (urgency, 10 percent,P

A squamous cell carcinoma arose in a skin-grafted ileostomy stoma 26 years after proctocolectomy for Crohn's colitis. The patient presented with peristomal ulceration and pain of several months' duration. Attention is drawn to this late complication of ileostomy which requires wide local excision and relocation of the stoma.