Idiopathic Fecal Incontinence Research Articles

Rectosigmoid Junction

Physioanatomical aspects of the rectosigmoid junction are scarcely treated in the literature. We studied the anatomy and physiology of the rectosigmoid junction in a series of publications aiming at elucidating its function in the light of its anatomical structure. The sigmoid colon is a storage organ, and the rectum, apart from being a conduit, proved to be a storage organ, too. A sigmoidorectal junction reflex was recognized which regulates stool passage from the sigmoid colon to the rectum. A physiologic rectosigmoid sphincter was postulated to exist at the rectosigmoid junction. We described the “hypertonic rectosigmoid junction syndrome”, a new clinicopathological entity causing chronic constipation in 8 patients who had rectosigmoid sphincter achalasia; improvement occurred with rectosigmoid junction myotomy. An electrorectogram was characterized in the canine model and in humans both transrectally and percutaneously. The results suggest that slow waves or pacesetter potentials and the action potentials start at the rectosigmoid junction. It was postulated that the rectosigmoid junction is the site of a “pacemaker” triggering the pacesetter potentials that pace the action potentials which initiate the rectal contractile activity. When the electrosigmoidogram was studied in relation to the electrorectogram, the pacesetter potentials and action potentials of the sigmoid colon were found to differ from those of the rectum, indicating that they are independent and are probably triggered by different pacemakers. An artificial pacemaker was tested in dogs and in humans. Upon electric pulsing of the pacemaker, the rectal pressure increased, rectal neck pressure decreased and the rectal balloon was expelled. In 26 patients with chronic idiopathic constipation, sponta-neous balloon expulsion was effected each time the artificial pacemaker was operated, and in 11 patients with idiopathic fecal incontinence, the pulsing of the internal anal sphincter succeeded in elevating the rectal neck pressure, thereby aborting the rectoanal inhibitory reflex and the desire to defecate. Thus, an artificial pacemaker could be effective in the treatment of idiopathic constipation and fecal incontinence.

Parameters of the rectoanal inhibitory reflex in patients with idiopathic fecal incontinence and chronic constipation

The rectoanal inhibitory reflex is a response of the internal anal sphincter to rectal distention, reflecting the functional nature of the anal sampling mechanism of rectal discrimination. The aim of this study was to assess the parameters of the rectoanal inhibitory reflex in healthy volunteers and incontinent and symptomatically constipated patients. The rectoanal inhibitory reflex was recorded in 42 patients using reproducible threshold volumes. Excitatory and inhibitory latencies, maximum excitatory and inhibitory pressures, amplitude, and slope of inhibition, slope and time of pressure recovery, and area under the inhibitory curve were estimated. Pudendal nerve terminal motor latency and endoanal magnetic resonance imaging were performed in all incontinent patients. Significant linear trends were found for most parameters at each sphincter level when analyzed. Recovery time and area under the inhibitory curve differed between the sphincter levels and patient groups, with the most rapid recovery occurring in the distal sphincter of incontinent patients (P < 0.001). These pressure findings were not accounted for by differences in excitation between patient groups. A coordinated response by the internal anal sphincter to rectal distention with recovery of anal pressure from the distal to the proximal sphincter is suggested. Continence may rely on the character of internal anal sphincter inhibition, and recovery and preoperative assessment of rectoanal inhibitory reflex parameters may be important for predicting functional result following low anastomosis.

Reliability of pudendal nerve terminal motor latency.

To evaluate reliability of Pudendal Nerve Terminal Motor Latency (PNTML). Forty healthy subjects, 24 women and 16 men, and eight female patients were included. Four patients had idiopathic faecal incontinence and 4 an anal sphincter rupture after child-birth. PNTML measurement was performed by two observers with the patient in left lateral and supine position. Examinations were repeated on another day to evaluate intraindividual reproducibility. Interobserver reproducibility was 92%-116% for PNTML. Degree of agreement for PNTML between left lateral and supine position was 86%-111%. Intra-individual reproducibility in the supine and left lateral positions was 89%-109% and 88%-113% respectively. Normal values for mean PNTML were higher in women compared with men, 1.91 msec (2 SD, 0.52 msec) and 1.74 msec (2 SD, 0.33 msec) respectively, t = 2.44, 37 DF, P < 0.01. Reliability of PNTML in terms of interobserver and intraindividual reproducibility was high. Women had higher normal values for PNTML than men.

Gluteus maximus augmentation for the treatment of fecal incontinence

Fecal incontinence is a devastating problem for schoolaged children and adults. Medical and biofeedback therapies are unsuccessful in most patients who have severely defective internal and external sphincters. Continued fecal incontinence frequently leads to social isolation and withdrawal. Gluteus maximus augmentation of the sphincter mechanism is one surgical method for treating fecal incontinence. The authors present their results with gluteus maximus augmentation of the anal sphincter and describe patient selection criteria. From 1992 through 1996, seven patients underwent gluteus maximus augmentation of the anal sphincter for fecal incontinence. Six of these patients were children 5 to 6 years of age who had major deficiencies of their anorectal sphincter demonstrated by manometry. One patient was a 56-year-old adult woman who had acquired idiopathic fecal incontinence. Four of the six children (67%) had imperforate anus and two had cloacal anomalies (33%). The augmentation was performed in three stages. A sigmoid-end colostomy with a Hartman's pouch was followed 1 month later by rotation of a portion of the gluteus maximus for anorectal sphincter augmentation. A colostomy take down was performed 2 to 4 months later. All patients underwent dilatation after sphincter augmentation and were taught muscle exercises for using their neosphincter during the period before colostomy take down. Four of six children and the adult are continent postoperatively (71%). Both patients who remain incontinent are unable to sense rectal distention clinically or on anal manometric analysis but have excellent voluntary sphincter tone. Fecal incontinence can be successfully treated with gluteus maximus augmentation in carefully selected patients. Patients unable to sense rectal distension are unlikely to benefit from this procedure. The presence of a rectal reservoir and a skin-lined anal canal also appear to be important in attaining fecal continence.

Clinical value of anorectal manometry index in neurogenic fecal incontinence.

The present communication is an endeavor to assess the value of a simple motility index to separate patients with neurogenic or idiopathic fecal incontinence from those patients with the secondary form of the disease. Study population consisted of 23 patients with idiopathic fecal incontinence and 13 patients with fecal incontinence secondary to surgical or obstetric trauma. They all had a standard anorectal manometric study after a 12-hour fast. A motility index was then prepared taking into consideration the peak sphincter pressure values, contractility endurance, and rectal sensory threshold. Despite differences in the mean peak squeeze pressure and sensory threshold between the two groups, there were significant overlaps for all parameters of standard anorectal manometry in both groups. However, patients with idiopathic incontinence had an index of smaller than 28, and the group with the secondary form of incontinence had indexes higher than 30. 1) None of the four parameters of a conventional anorectal manometry can accurately separate patients with neurogenic incontinence from those with secondary forms of the disorder. 2) The anorectal motility index presented here can accurately separate the two groups. 3) This index is superior to the standard anorectal manometry in evaluating patients with fecal incontinence.

Disturbed Anal Sphincter Function Following Vaginal Delivery

Wynne, J. M.; Myles, J. L.; Jones, I.; Sapsford, R.; Young, R. E.; Hattam, A.; Cantamessa, S. E. Author Information

The Electrically Stimulated Gracilis Neosphincter Incorporated as Part of Total Anorectal Reconstruction after Abdominoperineal Excision of the Rectum

The authors investigated the feasibility and effectiveness of combining electrically stimulated gracilis neoanal (ESGN) sphincter and a coloperineal anastomosis in selected patients after abdominoperineal excision of the rectum (APER). The ESGN is effective in the treatment of idiopathic fecal incontinence. Between March 1989 and September 1993, 12 patients (9 men, 3 women) with a median age of 59.25 years (range, 45-70) underwent the procedure. The underlying disease was adenocarcinoma in 10, anal malignant melanoma in 1, and a sweat gland tumor in the other. In all patients, a sphincter saving resection was contraindicated. The procedure was performed in stages. Stage 1 involved a conventional APER with the formation of a perineal stoma. Eleven patients underwent a vascular delay procedure. All patients were defunctioned. In stage 2, the gracilis was mobilized, transposed around the anal canal, and the electrodes and hardware needed for electrical stimulation were implanted. Once muscle conversion was complete, the defunctioning stoma was closed. Eight patients were closed successfully. In seven of the eight patients, complete physiologic measurements were taken. Median basal and maximum neosphincter pressures were 30 and 122 cm H2O, respectively, at the start of electrical stimulation and 22.5 and 76.2 cm H2O, respectively, after 1 year. Median functioning neosphincter pressure was 36 cm H2O at 1 year. All of the patients whose stomas were closed experienced episodes of incontinence to solid stool and wore pads for persistent fecal soiling. They all reported difficulty in evacuation. Despite imperfect continence, no patient wished to go back to life with a stoma. The incorporation of ESGN as part of total anorectal reconstruction is technically feasible. The majority of patients are satisfied with their function and pleased to avoid a permanent stoma.

Disturbed anal sphincter function following vaginal delivery.

Recently interest in idiopathic (neurogenic) faecal incontinence has swung from denervation of the external anal sphincter to the internal sphincter. To evaluate the effects of vaginal delivery on the internal sphincter. 1372 mothers were studied antenatally and 1202 were accepted into the study. Sphincter pressures were measured antenatally, in the early postnatal period, and six to 10 weeks later in selected patients. 755 of 1202 subjects assessed antenatally were primiparous women and 447 multiparous women. Some 320 previous spontaneous vaginal deliveries (SVD) (mean 59 mm Hg) and 67 previous forceps deliveries (mean 58 mm Hg) had lower resting pressures than 755 primiparous women (mean 66 mm Hg) (p < 0.01). A total of 493 subjects were reassessed postnatally. There were 372 SVDs, 47 vacuum extractions, 20 forceps, and 54 caesarean deliveries. All vaginal deliveries but not caesarean sections dropped their resting anal pressures from antenatal values (p < 0.001). Some 227 first SVDs had a much greater fall than 145 subsequent SVDs. In 162 subjects who had undergone their first vaginal delivery and who were followed up there was some recovery but the resting pressures were still lowered at six to 10 weeks post partum. The first vaginal delivery causes a permanent lowering of resting anal pressures. The possible reasons for this are discussed.

Distal rectoanal excitatory reflex: a reliable index of pudendal neuropathy?

Denervation of the extrinsic anal sphincter and pudendal neuropathy are confirmed by electrophysiologic or electromyographic testing, techniques that may not be available universally and require special equipment and training. A simple manometric test that is easy to perform and complements existing studies was performed to confirm pudendal neuropathy. Fourteen patients with excessive defecatory straining and 30 patients with idiopathic fecal incontinence were studied by electrophysiology and balloon reflex manometry. Pudendal nerve terminal motor latency (PNTML) and rectoanal excitatory reflex were evaluated for abnormalities. Results were compared with 20 controls who had no anorectal complaints and who had similar testing performed. In controls, PNTML was normal in all but one person. Rectoanal excitatory reflex could be elicited in all controls with either 20 or 40 ml of air. Four different types of balloon reflex responses were observed in patient groups: diminutive excitation, delayed excitation, excitation at high volume of distention only, and absent excitation. Ten patients with fecal incontinence had normal PNTML but abnormal distal excitatory reflex, 5 patients had abnormal PNTML but normal distal excitatory reflex, and 15 patients had both PNTML and excitatory reflex that were abnormal. In patients with excessive defecatory straining, results of both tests were abnormal in six patients, and eight patients had abnormal excitatory reflex but normal PNTML. Pudendal neuropathy may result in abnormalities of excitatory reflex morphology or other characteristics. Abnormal distal excitatory reflex may complement electrophysiologic findings or may serve as a suitable alternative to confirm pudendal neuropathy in centers where facilities for formal testing are not available.

Prevalence of pudendal neuropathy in fecal incontinence

A prospective study was made of the prevalence and associations of pudendal neuropathy in 96 patients with fecal incontinence (72 females and 24 males). Clinical exploration, perineal level measurement, anorectal manometry, and electrophysiologic evaluations (pudendal nerve terminal motor latency (PNTML) and external sphincter fiber density (FD)) were performed. Pudendal neuropathy (defined as PNTML > 2.2 ms or FD > 1.65) was found in 67 patients (69.8 percent) and was more common in females (75 percent) than in males (50 percent; P = 0.05). Pudendal neuropathy was also more frequent in patients with pathologic perineal descent (85 percent vs. 55 percent; P < 0.01) or exhibiting risk factors such as difficult labor or excessive defecatory straining (P < 0.01). Perineal level at staining correlated inversely with both PNTML and FD (P < 0.01). Manometric findings suggested greater external anal sphincter damage in patients with pudendal neuropathy than in those suffering fecal incontinence but no neuropathy (P < 0.05). Pressure caused by the striated anal sphincter was also inversely correlated to PNTML. Pudendal neuropathy was encountered in 37 of 33 (58.7 percent) patients with sphincter injury vs. in 31 of 33 (93.9 percent) patients with idiopathic fecal incontinence (P < 0.01). Pudendal neuropathy is an etiologic or associated factor often present in patients with fecal incontinence. In this sense, clinical, perineometric, and manometric findings correlate with pudendal neuropathy, though such explorations do not suffice to detect it.

Faecal incontinence 1994: which test and which treatment?

Faecal incontinence is a disabling condition caused by: (1) sphincter damage caused by childbirth, anorectal surgery, trauma, fistulae and abscesses; (2) pudendal neuropathy ("idiopathic faecal incontinence") caused by stretch injury by long-standing constipation or prolonged labor; (3) diminished rectal compliance in proctitis, low anterior resection or small pouches; (4) faecal impaction causing paradoxal diarrhoea; (5) neurological disease involving the pelvic floor and or the central nervous system; (6) diarrhoea. Often several factors play a role in a patient. A medical history and physical examination will generally provide a reasonable diagnosis. Anorectal function tests can show one or more abnormalities. Anal manometry can show low sphincter pressures; rectal compliance can show a small rectal volume; anal mucosal sensitivity measurement can show a high threshold and neurophysiological tests can demonstrate diminished muscle activity and a delayed pudendal nerve motor latency. Anal endosonography and defaecography have a direct clinical impact. Anal endosonography is a promising diagnostic tool demonstrating sphincter defects, even those not previously suspected. A sphincter defect demonstrated by anal endosonography provides a solid basis for a sphincter repair. Defaecography can reveal an intussusception, which is an indication for performing a rectopexy in the incontinent patient. A suggested work-up of the incontinent patient is given in a table. Besides the classic surgical treatments such as sphincter repair, rectopexy and post-anal repair new (surgical) options have been tried. The most promising new therapy seems the dynamic gracilis repair.

Pelvic floor neuromuscular function in middle aged and elderly women with idiopathic fecal incontinence

Pelvic floor neuromuscular function in middle aged and elderly women with idiopathic fecal incontinence

Langzeitergebnisse der posterioren Raffung nach Parks Eine elektromyographische, manometrische und radiologische studie bei 31 patienten

This study was carried out to document the long-term results of postanal repair for idiopathic faecal incontinence. Thirty-one patients (mean age 65.6 years) were followed up for 2-7.5 years (median 4.2 years). Continence was improved in 16 (52%) patients, only 2 (6%) of whom regained normal continence. No significant change in resting and pressure, maximum squeeze pressure, pelvic descent or anorectal angle was seen postoperatively. The electromyographical signs, e.g. duration and amplitude of action potentials, average amplitude, and integrals of the curves did not change significantly after the operation. The mean right pudendal nerve terminal motor latency (PNTML) increased from 2.38 ms before to 2.59 ms after surgery (P > 0.05). No significant change in the continence and defaecation index was seen postoperatively.

Evidence of electromechanical dissociation of the internal anal sphincter in idiopathic fecal incontinence.

This study was designed to evaluate the relationship between internal sphincter electromyographic frequency and ambulatory anal pressures in order to clarify the pathophysiology of internal anal sphincter dysfunction in fecal incontinence. Seventy-two patients of median age 55 years (range, 24-75; 63 females) with neurogenic fecal incontinence and 33 normal subjects of median age 48.5 years (range, 25-74; 21 females) underwent fine-wire anal sphincter electromyography and anal manometry. The median internal anal sphincter electromyographic frequency was incontinent 0.25 Hz (0.2-0.34) and the control was 0.44 Hz (0.36-0.55; P < 0.03). Ambulatory resting pressures were incontinent median 54 cm of H2O (34-68 cm of H2O) and control 94 cm of H2O (72-102; P < 0.01). Internal sphincter electromyographic frequency correlated with anal resting pressures in both groups (P < 0.002). Internal sphincter electromyographic silence not attributable to electrode movement or the rectoanal inhibitory reflex, lasting 0.5 to 4 minutes occurred in all but two of the incontinent patients. The anal pressure during this period did not significantly change (P > 0.1). No recruitment of the external sphincter or puborectalis was noted during these episodes. Such electromechanical dissociation was not seen in the control group. The frequency of transient internal sphincter relaxation was 4 (ranges 2-6) per hour in controls and 8 (ranges, 6-12) per hour in incontinent patients (P < 0.01). Rectal pressures did not exceed midanal pressures in any of the controls but did in all of the incontinent patients on at least one occasion per hour in the incontinent group. Internal anal sphincter activity exhibits electromechanical dissociation and relaxes abnormally in incontinent patients.

History and examination in the assessment of patients with idiopathic fecal incontinence

This study was undertaken to identify those factors from the history and examination which might predict the pathophysiologic basis of idiopathic fecal incontinence. In a prospective study of 237 patients with idiopathic fecal incontinence (female to male, 7:1.7; mean age, 54.8 years; median history, 3 years), history, examination, and anorectal physiology studies findings have been analyzed using contingency table analysis. In patients with idiopathic fecal incontinence, anorectal physiology studies have shown that a low maximum basal pressure (< 45 cm H2O) is predominantly attributable to internal and sphincter weakness, and low maximum squeezing pressure (< 76 cm H2O) is indicative of voluntary sphincter deficiency. In this study, a low maximum basal pressure is correlated with leakage, gaping of the anus on traction of the anal verge, and decreased resting tone on digital examination (all P < 0.05). A low maximum squeezing pressure is correlated with incontinence en route to the lavatory, urgency, both stress and urge incontinence of urine, reduced voluntary contraction in the external anal sphincter and puborectalis on digital examination, and a reduced or absent anorectal angle (all P < 0.05). This study has shown that an informed history and digital examination can predict the manometric findings of specialist anorectal physiology studies.

Anal endosonography in healthy subjects and patients with idiopathic fecal incontinence

This study investigates the normal ultrasonographic morphology of pelvic floor striated muscle and evaluates whether there are differences between males and females and between healthy subjects and patients with idiopathic fecal incontinence. Manometric and ultrasonographic studies of the anal canal were performed in 30 healthy volunteers and in 26 patients with idiopathic fecal incontinence. Verification of ultrasonographic findings was obtained by studying anatomic preparations. Ultrasonography reliably identified the internal and external anal sphincter and frequently visualized neighboring structures. In addition, it detected muscular structures that have not clearly been described previously. However, differences in external sphincter function between males and females and between healthy subjects and incontinent patients were not reflected by alterations in muscle thickness. Endosonography of the anal canal clearly delineates muscular structures and may even visualize structures that have been previously incompletely defined. However, it remains to be shown that differences in certain muscular functions have a morphologic correlate that can be detected by endosonography.

Does electrical stimulation of the pelvic floor alter the proctographic parameters in faecal incontinence?

Objective: To evaluate the effects of electrical stimulation of the pelvic floor on proctographic parameters in patients with faecal incontinence. Design: Patients with faecal incontinence, resistant to medical or surgical management, were randomly selected for anorectal studies. Patients: The study included 24 patients suffering from idiopathic faecal incontinence with anal sphincter weakness and detectable pudendal neuropathy randomly selected for treatment with a pudendo-anal reflex electrical stimulator. Interventions: Manometric studies, electrophysiological tests and X-ray videoproctography were performed before and after chronic intermittent application of a pudendo-anal reflex electrical stimulator over 8 weeks. Main outcome measure: Improvement in the parameters relating to continence control

Abnormalities of innervation of internal anal sphincter in fecal incontinence

Physiological and histological studies have shown that the internal and sphincter is abnormal in idiopathic fecal incontinence. We have recently demonstrated that the in vitro contractile response of the internal anal sphincter to the sympathetic neurotransmitter noradrenaline is decreased in incontinence. In this study we have further defined this reduced sensitivity and provided more information about the intrinsic innervation in both the normal and the incontinent sphincter muscle. Muscle strips from 12 incontinent patients undergoing post and repair and from 11 controls undergoing rectal excision for low rectal carcinoma were studied. Responses to noradrenaline were recorded initially alone and then in the presence of phentolamine, an alpha-adrenoceptor blocker. In the presence of phentolamine, noradrenaline caused relaxation: there was no significant difference in the relaxation-response curves and the EC50 was the same in the two groups. These results demonstrate that the previously documented reduced sensitivity to noradrenaline is due to an altered sensitivity of the alpha-adrenoceptors. Electrical field stimulation produced relaxations in all muscle strips, but only in the controls was the magnitude of the relaxation significantly increased in the presence of phentolamine. This indicates that there is an alpha-adrenergic excitatory component of the response to electrical field stimulation of the intramural nerves, which was present in tissues from control patients but which was absent in tissues from patients with idiopathic fecal incontinence.

Does perineal descent correlate with pudendal neuropathy?

A prospective study was undertaken to assess the potential correlation between increased perineal descent (IPD) and pudendal neuropathy (PN) in 213 consecutive patients. These 165 females and 48 males of a mean age of 62 (range, 18-87) years had constipation (n = 115), idiopathic fecal incontinence (n = 58), or chronic intractable rectal pain (n = 40). All 213 patients underwent cinedefecography (CD) and bilateral pudendal nerve terminal motor latency (PNTML) assessment. Perineal descent (PD) of more than the upper limit of normal of 3.0 cm during evacuation was considered increased. Pudendal neuropathy was diagnosed when PNTML exceeded the upper limit of normal of 2.2 milliseconds. Although 65 patients (31 percent) had PD, only 16 (25 percent) of these 65 patients had neuropathy. Moreover, PN was also found in 42 (28 percent) of 148 patients without IPD. Conversely, only 16 (28 percent) of the 58 patients who had PN also had IPD, and IPD was present in 49 (32 percent) of 155 patients without PN. The frequency of PN according to the degree of IPD was: 3.0 to 4.0 cm, 6 of 27 patients (22 percent); 4.1 to 5.0 cm, 4 of 15 (27 percent); 5.1 to 6.0 cm, 4 of 12 (25 percent); 6.1 to 7.0 cm, 2 of 8 (25 percent); and > 7.0 cm, 0 of 3 (0 percent). Linear regression analysis was undertaken to compare the relationships between measurements of PD at rest (R), push (P), and change (C = P-R) and values of PNTML. These values for all 213 patients were: R, r = 0.048; P, r = 0.031; and C, r = -0.050. The correlation coefficients were equally poor for all the individual subgroups analyzed, including the patient's sex or diagnosis. In summary, no correlation was found between PD and PNTML. The lack of a relationship was seen for the entire group as well as for those patients with either neuropathy or increased perineal descent. Therefore, the often espoused relationship between increased PD and PN was not supported by this prospective evaluation. Although increased PD and prolonged PNTML are frequently observed in patients with disordered defecation, they may represent independent findings.

Rectal sensory evoked potentials: an Assessment of their clinical value

To assess abnormalities of sensory conduction in anorectal disease we have evaluated peripheral sensory perception and somatosensory evoked potentials produced by rectal stimulation in control subjects and patients with either constipation or idiopathic faecal incontinence. Evoked potentials were also recorded after posterior tibial and dorsal genital nerve stimulation. Rectal sensation was also assessed using electrical stimulation. Reproducible evoked potential recordings after anorectal stimulation were possible in only a minority of subjects and when recorded showed intersubject and intrasubject variation. In the constipated group there was a significant difference in rectal electrical sensation (P < 0.05) from controls. We conclude that peripheral sensory testing demonstrates an abnormality in severe constipation. However, cerebral evoked potentials cannot be reliably recorded after rectal stimulation, and when recorded the latencies are of too broad a range to discriminate between health and disease. This probably relates to the difference between somatic and visceral pathways.