Rectal Hypersensitivity Worsens Stool Frequency, Urgency, and Lifestyle in Patients With Urge Fecal Incontinence

PURPOSE Rectal sensory mechanisms are important in the maintenance of fecal continence. Approximately 50 percent of patients with urge incontinence have lowered rectal sensory threshold volumes (rectal hypersensitivity) on balloon distention. Rectal hypersensitivity may underlie the heightened perception of rectal filling; however, its impact on fecal urgency and incontinence is unknown. This study was designed to investigate the impact of rectal hypersensitivity in patients with urge fecal incontinence.METHODS Prospective and retrospective audit review of all patients (n = 258) with an intact native rectum referred to a tertiary colorectal surgical center for physiologic investigation of urge fecal incontinence during a 7.5-year period. Patients with urge fecal incontinence who had undergone pelvic radiotherapy (n = 9) or rectal prolapse (n = 6) were excluded.RESULTS A total of 108 of 243 patients (44 percent) were found to have rectal hypersensitivity. The incidence of anal sphincter dysfunction was equal (90 percent) among those with or without rectal hypersensitivity. Patients with urge fecal incontinence and rectal hypersensitivity had increased stool frequency (P < 0.0001), reported greater use of pads (P = 0.003), and lifestyle restrictions (P = 0.0007) compared with those with normal rectal sensation, but had similar frequencies of incontinent episodes.CONCLUSIONS Urge fecal incontinence relates primarily to external anal sphincter dysfunction, but in patients with urge fecal incontinence, rectal hypersensitivity exacerbates fecal urgency, and this should be considered in the management and surgical decision in patients who present with fecal incontinence.Christopher L. H. Chan, F.R.C.S., is supported by a MRC Clinical Training Fellowship.     

Relationship between symptoms and disordered continence mechanisms in women with idiopathic faecal incontinence

BACKGROUND AND AIMS: Anal sphincter weakness and rectal sensory disturbances contribute to faecal incontinence (FI). Our aims were to investigate the relationship between symptoms, risk factors, and disordered anorectal and pelvic floor functions in FI. METHODS: In 52 women with "idiopathic" FI and 21 age matched asymptomatic women, we assessed symptoms by standardised questionnaire, anal pressures by manometry, anal sphincter appearance by endoanal ultrasound and magnetic resonance imaging (MRI), pelvic floor motion by dynamic MRI, and rectal compliance and sensation by a barostat. RESULTS: The prevalence of anal sphincter injury (by imaging), reduced anal resting pressure (35% of FI), and reduced squeeze pressures (73% of FI) was higher in FI compared with controls. Puborectalis atrophy (by MRI) was associated (p<0.05) with FI and with impaired anorectal motion during pelvic floor contraction. Volume and pressure thresholds for the desire to defecate were lower, indicating rectal hypersensitivity, in FI. The rectal volume at maximum tolerated pressure (that is, rectal capacity) was reduced in 25% of FI; this volume was associated with the symptom of urge FI (p<0.01) and rectal hypersensitivity (p = 0.02). A combination of predictors (age, body mass index, symptoms, obstetric history, and anal sphincter appearance) explained a substantial proportion of the interindividual variation in anal squeeze pressure (45%) and rectal capacity (35%). CONCLUSIONS: Idiopathic FI in women is a multifactorial disorder resulting from one or more of the following: a disordered pelvic barrier (anal sphincters and puborectalis), or rectal capacity or sensation.     

Abnormal visceral autonomic innervation in neurogenic faecal incontinence.

Changes of denervation in the anal sphincter striated and smooth muscle in patients with neurogenic faecal incontinence are well established. This study aimed to determine if there is also a more proximal visceral autonomic abnormality. Thirty women with purely neurogenic faecal incontinence (prolonged pudendal nerve latencies and an intact sphincter ring) and 12 patients with neuropathic changes together with an anatomical disruption were studied. Two control groups consisted of 18 healthy volunteer women and 17 women with normal innervation but an anatomically disrupted sphincter. Rectal sensation was assessed using balloon distension and electrical mucosal stimulation, and anal sensation by electrical stimulation. Rectal compliance was studied to determine whether sensory changes were primary or caused by altered rectal wall viscoelastic properties. Anal canal pressure changes in response to both rectal distension and rectal electrical stimulation were measured to assess the intrinsic innervation of the internal anal sphincter. Patients with neurogenic incontinence alone had impaired rectal sensation to distension (53.1 v 31.5 ml, p < 0.05, neurogenic v controls) and to electrical stimulation (24.4 v 14.8 mA, p < 0.005). Patients with neurogenic incontinence and sphincter disruption also showed impaired sensation compared with healthy controls (55.8 ml v 31.5 ml, p < 0.05 and 22.9 mA v 14.8 mA, p < 0.05). Patients with only a disrupted sphincter had normal visceral sensation to both types of testing. Both rectal compliance and the response of the internal anal sphincter to rectal distension and electrical stimulation were normal in all patient groups. This study suggests that there is a visceral sensory abnormality in patients with neurogenic incontinence which is not caused by altered rectal compliance. As evaluated in this study the intrinsic innervation of the internal anal sphincter is not affected in this process.     

Relation between rectal sensation and anal function in normal subjects and patients with faecal incontinence.

The relation between sensory perception of rapid balloon distension of the rectum and the motor responses of the rectum and external and internal anal sphincters in 27 normal subjects and 16 patients with faecal incontinence who had impaired rectal sensation but normal sphincter pressures was studied. In both patients and normal subjects, the onset and duration of rectal sensation correlated closely with the external anal sphincter electrical activity (r = 0.8, p less than 0.0001) and with rectal contraction (r = 0.51, p less than 0.001), but not with internal sphincter relaxation. All normal subjects perceived a rectal sensation within one second of rapid inflation of a rectal balloon with volumes of 20 ml or less air. Six patients did not perceive any rectal sensation until 60 ml had been introduced, while in the remaining nine patients the sensation was delayed by at least two seconds. Internal sphincter relaxation occurred before the sensation was perceived in three of 27 normal subjects and 11 of 16 patients (p less than 0.001), and could be associated with anal leakage, which stopped as soon as sensation was perceived. The lowest rectal volumes required to induce anal relaxation, to cause sustained relaxation, or to elicit sensations of a desire to defecate or pain were similar in patients and normal subjects. In conclusion, these results show the close association between rectal sensation and external anal sphincter contraction, and show that faecal incontinence may occur as a result of delayed or absent external anal sphincter contraction when the internal anal sphincter is relaxed.     

Rectal compliance, capacity, and rectoanal sensation in fecal incontinence

OBJECTIVE: Assessments of the pathophysiology of fecal incontinence are skewed toward anal sphincter function; however, rectal compliance, rectoanal sensation and capacity may also be relevant. The aim of this study was to evaluate the usual and some novel diagnostic approaches in fecal incontinence. METHODS: In 22 unselected patients with fecal incontinence (21 F, 33-75 yr), we quantified: 1) symptoms, anorectal manometry, and anal ultrasound; 2) anal perception of temperature and light touch; 3) rectal sensitivity and compliance to distension; and 4) rectal reservoir function. Control values were obtained from two groups of 11 (seven F, 32-53 yr), and 32 (18 F, 19-44 yr) volunteers. RESULTS: Patients had urge (14), passive (four), or combined (four) fecal incontinence; symptoms were mild in three, moderate in nine, and severe in 10 patients. Most had low sphincteric pressures and ultrasonic abnormalities. Temperature perception was impaired (p < 0.05) in incontinent patients, to a greater extent in the proximal anal canal and in patients with passive, as opposed to urge, incontinence. Intraluminal pressures for sensations of rectal distension were lower in incontinent patients (p = 0.02). Artificial stools elicited sensations of rectal filling at lower volumes than did a barostat bag, and in patients with urge, as opposed to passive, incontinence. In patients and controls, the sensation of urgency was associated (r2 = 0.2, p < 0.01) with rectal compliance. CONCLUSIONS: We confirm that temperature sensation is impaired, and perception of rectal distension is not always reduced in fecal incontinence. Artificial stool tended to induce sensations at lower volumes than did balloon inflation. Altered sensory mechanisms may contribute to the pathophysiology of fecal incontinence.     

Effects of short term sacral nerve stimulation on anal and rectal function in patients with anal incontinence

BACKGROUND: Some patients with faecal incontinence are not amenable to simple surgical sphincter repair, due to sphincter weakness in the absence of a structural defect. AIMS: To evaluate the efficacy and possible mode of action of short term stimulation of sacral nerves in patients with faecal incontinence and a structurally intact external anal sphincter. PATIENTS: Twelve patients with faecal incontinence for solid or liquid stool at least once per week. METHODS: A stimulating electrode was placed (percutaneously in 10 patients, operatively in two) into the S3 or S4 foramen. The electrode was left in situ for a minimum of one week with chronic stimulation. RESULTS: Evaluable results were obtained in nine patients, with early electrode displacement in the other three. Incontinence ceased in seven of nine patients and improved notably in one; one patient with previous imperforate anus and sacral agenesis had no symptomatic response. Stimulation seemed to enhance maximum squeeze pressure but did not alter resting pressure. The rectum became less sensitive to distension with no change in rectal compliance. Ambulatory studies showed a possible reduction in rectal contractile activity and diminished episodes of spontaneous anal relaxation. CONCLUSIONS: Short term sacral nerve stimulation notably decreases episodes of faecal incontinence. The effect may be mediated via facilitation of striated sphincter muscle function, and via neuromodulation of sacral reflexes which regulate rectal sensitivity and contractility, and anal motility.     

Effects of acute hyperglycaemia on anorectal motor and sensory function in diabetes mellitus.

AIMS: To determine the effects of acute hyperglycaemia on anorectal motor and sensory function in patients with diabetes mellitus. METHODS: In eight patients with Type 1, and 10 patients with Type 2 diabetes anorectal motility and sensation were evaluated on separate days while the blood glucose concentration was stabilized at either 5 mmol/l or 12 mmol/l using a glucose clamp technique. Eight healthy subjects were studied under euglycaemic conditions. Anorectal motor and sensory function was evaluated using a sleeve/sidehole catheter, incorporating a barostat bag. RESULTS: In diabetic subjects hyperglycaemia was associated with reductions in maximal (P<0.05) and plateau (P<0.05) anal squeeze pressures and the rectal pressure/volume relationship (compliance) during barostat distension (P<0.01). Hyperglycaemia had no effect on the perception of rectal distension. Apart from a reduction in rectal compliance (P<0.01) and a trend (P=0.06) for an increased number of spontaneous anal sphincter relaxations, there were no differences between the patients studied during euglycaemia when compared with healthy subjects. CONCLUSIONS: In patients with diabetes, acute hyperglycaemia inhibits external anal sphincter function and decreases rectal compliance, potentially increasing the risk of faecal incontinence.     

Utility of a combined test of anorectal manometry, electromyography, and sensation in determining the mechanism of ''idiopathic'' faecal incontinence.

Combined tests of anorectal manometry, sphincter electromyography and rectal sensation were carried out in 302 patients with faecal incontinence (235 women, 67 men). The results obtained were compared with 65 normal subjects (35 women, 30 men). A mechanism for incontinence was identified in all and the majority of patients had more than one abnormality. Two hundred and seventy eight patients (92%) had a weak external anal sphincter, 185 of these (67%, mostly women) also showed abnormal perineal descent, and 14 women showed clinical evidence of sphincter damage as a result of obstetric trauma. Ten per cent of patients with impaired external anal sphincter contraction showed associated evidence of spinal disease (impaired rectal sensation plus attenuated or enhanced reflex external anal sphincter activity). Unlike the other groups, the 'spinal' group contained equal numbers of men and women. Ninety seven patients (32%) had evidence of a weak internal anal sphincter. The external sphincter was also very weak and 92% of these patients also had perineal descent. Eighty two patients (27%) showed an unstable internal sphincter, characterised by prolonged 'spontaneous' anal relaxation under resting conditions and an abnormal reduction in anal pressure after conscious contraction of the sphincter or an increase in intraabdominal pressure. One hundred and forty two patients (47%) had a hypersensitive rectum associated with enhanced anorectal responses to rectal distension. All these patients had an abnormally weak external sphincter, suggesting that the hypersensitive or 'irritable' rectum should not be regarded as a cause of faecal incontinence unless accompanied by external sphincter weakness. Twenty four patients (8%) showed a normal basal and squeeze pressures and impaired rectal sensation; six showed giant rectal contractions during rectal distension. The results show that idiopathic faecal incontinence is not caused by a single abnormality, and it is suggested that combined anorectal manometry, electromyography, and sensory testing is a useful technique to identify the causes of faecal incontinence and provide a basis for appropriate treatment.     

Rectal tone and compliance affected in patients with fecal incontinence after fistulotomy

AIM: To investigate the anal sphincter and rectal factors that may be involved in fecal incontinence that develops following fistulotomy(FIAF).METHODS: Eleven patients with FIAF were compared with 11 patients with idiopathic fecal incontinence and with 11 asymptomatic healthy subjects(HS). All of the study participants underwent anorectal manometry and a barostat study(rectal sensitivity, tone, compliance and capacity). The mean time since surgery was 28 ± 26 mo. The postoperative continence score was 14 ± 2.5(95%CI: 12.4-15.5, St Mark's fecal incontinence grading system).RESULTS: Compared with the HS, the FIAF patients showed increased rectal tone(42.63 ± 27.69 vs 103.5 ± 51.13, P = 0.002) and less rectal compliance(4.95 ± 3.43 vs 11.77 ± 6.9, P = 0.009). No significant differences were found between the FIAF patients and the HS with respect to the rectal capacity; thresholds for the non-noxious stimuli of first sensation, gas sensation and urge-to-defecate sensation or the noxious stimulus of pain; anal resting pressure or squeeze pressure; or the frequency or percentage of relaxation of the rectoanal inhibitory reflex. No significant differences were found between the FIAF patients and the patients with idiopathic fecal incontinence.CONCLUSION: In patients with FIAF, normal motor anal sphincter function and rectal sensitivity are preserved, but rectal tone and compliance are impaired. The results suggest that FIAF is not due to alterations in rectal sensitivity and that the rectum is more involved than the anal sphincters in the genesis of FIAF.     

Impaired rectal sensation in idiopathic faecal incontinence

In 15 patients suffering from idiopathic faecal incontinence and in 15 matched controls, manometric studies of anorectal pressure and studies of the rectoanal reflex and rectal sensitivity were carried out. Patients with idiopathic faecal incontinence had normal resting pressure but reduced squeeze and stress pressures; the anal sphincter relaxed before a sensation of rectal distension occurred. The conclusion is that both reduced voluntary muscle contraction and impairment of rectal sensation are conducive to soiling in idiopathic faecal incontinence.     

Pelvic floor neuropathy: a comparative study of diabetes mellitus and idiopathic faecal incontinence.

Twenty one patients with diabetic peripheral neuropathy, 18 with idiopathic faecal incontinence and 11 normal controls were studied with techniques of mucosal electrosensitivity, rectal distension for the quantitative assessment of anorectal sensation, and manometric and electromyographic tests for the assessment of anorectal motor function. An asymptomatic sensorimotor deficit was found in the anal canal of patients with diabetic peripheral neuropathy. Mucosal electrosensitivity thresholds in the anal canal were significantly higher (p less than 0.01 v controls) and fibre density of the external anal sphincter significantly raised (p less than 0.0001 v controls). Anal manometry and pudendal nerve terminal motor latencies were similar to controls. In patients with idiopathic faecal incontinence the tests of sensory and motor function also showed a sensorimotor neuropathy; compared with controls, mucosal electrosensitivity thresholds were significantly higher (p less than 0.002), anal canal resting and maximum squeeze pressures were significantly lower (p less than 0.05 and p less than 0.002 respectively), and pudendal nerve terminal motor latencies and fibre density of the external anal sphincter were significantly raised (both p less than 0.05). Sensory thresholds to rectal distension were similar in all groups. Pelvic floor sensorimotor neuropathy in diabetic patients has several features in common with that of patients with idiopathic faecal incontinence but its functional significance remains uncertain.     

Combined sensory and motor deficit in primary neuropathic faecal incontinence.

Eleven patients with idiopathic faecal incontinence (IFI) and nine normal controls were studied with techniques of mucosal electrosensitivity and rectal distention for the quantitative assessment of anal and rectal sensation and with manometric and electromyographic tests for the assessment of anorectal motor function. The tests of motor function showed pelvic floor motor neuropathy in the patients with IFI, compared with controls, anal canal resting and voluntary contraction pressures were significantly (p less than 0.05, p less than 0.002) lower, pudendal nerve terminal motor latency and external anal sphincter fibre density were significantly (p less than 0.05, p less than 0.05) raised. The results of mucosal electrosensitivity (MES) disclosed a sensory deficit in the anal canal in patients with IFI, compared with controls, MES threshold was significantly (p less than 0.002) higher. Sensory thresholds to rectal distension were similar in the two groups. This study shows that sensory deficit of the anal canal occurs in combination with the motor neuropathy of the anal canal musculature in primary neuropathic faecal incontinence.     

Temperature-controlled radiofrequency energy (SECCA) to the anal canal for the treatment of faecal incontinence offers moderate improvement

BACKGROUND AND AIM: Faecal incontinence is a devastating complaint. Even after conservative treatment, many patients still remain incontinent. Few patients have a sphincter defect suitable for repair. Other emerging surgical therapies like dynamic gracilis plasty, neuromodulation or artificial bowel sphincter, carry side effects and show only moderate improvement. Temperature-controlled radiofrequency energy (SECCA) has shown promising results in the USA. Local tightening seems to be the mode of action with possible increased rectal sensitivity. We investigated the effectiveness of radiofrequency and possible changes in the anal sphincter with 3D-ultrasound in patients with faecal incontinence. PATIENTS AND METHODS: Eleven women, mean age 61 years (49-73) with long-standing faecal incontinence were included. Patients with large sphincter defects and anal stenosis were excluded. The SECCA procedure was performed under conscious sedation and local anaesthesia. Oral antibiotics were given. In four quadrants on four or five levels (depending upon length of the anus) radiofrequency was delivered with multiple needle electrodes. Patients were evaluated at 0, 6 weeks, 3 and 6 months and 1 year. Three-dimensional anal ultrasound was performed at 0 (before and after the procedure), 6 weeks and 3 months. Anal manometry and rectal compliance measurement were performed at 0 and 3 months. RESULTS: At 3 months, six of 11 patients improved, which persisted during follow-up of 1 year. The Vaizey score changed from 18.8 to 15.0 (P=0.03) and in those improved from 18.3 to 11.5 (P=0.03). Anal manometry and rectal compliance showed no significant changes, there was a tendency to increased rectal sensitivity concerning urge and maximal tolerated volume (both P=0.3). Responders compared with nonresponders showed no difference in test results. Side effects were local haematoma (2), bleeding 3 days (1), pain persisting 1-3 weeks (4) and laxatives-related diarrhoea during 1-3 weeks (4). CONCLUSION: The SECCA procedure seems to be promising for patients with faecal incontinence with a persisting effect after 1 year. No significant changes in tests were found.     

Sacral nerve stimulation for treatment of fecal incontinence: a novel approach for intractable fecal incontinence

PURPOSE: Many patients with fecal incontinence demonstrate a functional deficit of the internal anal sphincter or the external sphincter muscles without any apparent structural defects. Few patients are amenable to repair or substitution of the sphincter. However, sacral nerve stimulation appears to offer a valid treatment option for fecal incontinence. The objectives of this study were: to evaluate the efficacy of temporary stimulation of the sacral nerve roots (percutaneous nerve evaluation) in patients with functional fecal incontinence; to determine the mechanisms of possible improvement; and to evaluate if temporary stimulation could be reproduced and maintained by implanting a permanent neurostimulation system. METHODS: Twenty-three patients with fecal incontinence, 18 females and 5 males, median age of 54.9 years (range 28-71), underwent a percutaneous nerve evaluation test. Eleven patients (47.8 percent) also had urinary disorders: urge incontinence (4), stress incontinence (3), and retention (4). Associated disorders included perineal and rectal pain (1), spastic paraparesis (1), and syringomyelia (1). All patients underwent a preliminary evaluation using stationary anal manovolumetry, pudendal nerve terminal motor latency measurements, and anal ultrasound. A percutaneous electrode for the stimulation of the sacral nerve roots was positioned at the level of the third sacral foramen (S3) in 20 patients and S2 in 2 patients (1 patient missing). Stimulation parameters used were: pulse width 210 microsec, frequency 25 Hz, and average amplitude of 2.8 V (range 1-6). The electrode was left in place for a minimum of 7 days. Five patients were successively implanted with a permanent sacral electrode with a stimulation frequency of 16 to 18 Hz and amplitude of 1.1- 4.9 V. RESULTS: Seventeen of the 19 patients (89.4 percent) who completed the minimum percutaneous nerve evaluation period of 7 days (median 10.7 (range 7-30)), had a reduction of liquid or solid stool incontinence by more than 50 percent, and fourteen (73.6 percent) were completely continent for stool. The most important changes revealed by manovolumetry were an increase in resting pressure (P < 0.001) and voluntary contraction (P = 0.041), reduction of initial pressure for first sensation (P = 0.049) and urge to defecate (P = 0.002), and a reduction of the rectal volume for urge sensation (P = 0.006). The percutaneous nerve evaluation results were reproduced at a median follow-up of 19.2 months (range 5 to 37) in the 5 patients who received a permanent implant. CONCLUSIONS: Temporary stimulation of the sacral roots (percutaneous nerve evaluation) can be of help in those patients with fecal incontinence, and the results are reproduced with permanent implantation. The positive effect on continence seems to be derived from not only the direct efferent stimulation on the pelvic floor and the striated sphincter muscle, but also from modulating afferent stimulation of the autonomous neural system, inhibition of the rectal detrusor, activation of the internal anal sphincter, and modulation of sacral reflexes that regulate rectal sensitivity and motility.     

Clinical presentation of fecal incontinence and anorectal function: what is the relationship?

OBJECTIVES: Fecal incontinence is classified into various types: passive, urge, and combined. Its clinical presentation is thought to be related to the underlying physiological or anatomical abnormality. The aim of the present study was to evaluate the associations between the frequency of clinical symptoms and anatomic and functional characteristics of the anorectum of patients with severe fecal incontinence. METHODS: Associations were explored in a consecutive series of 162 patients (91% women, mean age 59 [SD +/- 12] yr) with a mean Vaizey incontinence score of 18 (SD +/- 3). RESULTS: Urge incontinence was reported as "daily" by 55%, "often" by 27%, and "sometimes" by 7% of all patients. No significant associations were observed between the frequency of urge incontinence and either manometric data, anal mucosal sensitivity testing, or defects of internal anal sphincter (IAS) or external anal sphincter (EAS). A significant relation was observed between the frequency of urge incontinence and maximal tolerable volume (P= 0.03) and atrophy of the EAS (P= 0.05). Passive incontinence was reported as "daily" by 14%, "often" by 30%, and "sometimes" by 14% of all patients. Resting and maximal squeeze pressure were both associated (P < 0.001) with the frequency of passive incontinence. No relationship could be detected between clinical presentation and rectal sensation, anal mucosal sensitivity, defects, or atrophy of IAS or EAS. CONCLUSION: Most patients reported combined incontinence (59%) and underlying pathophysiologic abnormalities were identified. The hypothesized associations between urge and passive incontinence and functional and anatomical impairment of the anorectum are less clear-cut than previously assumed. Patients presenting with fecal incontinence should undergo physiologic investigation.     

Anal incontinence in patients with Addison's disease: a gluco- and mineralocorticoid independent sphincter malfunction?]

Anorectal motor function was evaluated in 15 female patients with Addison's disease and androgen deficiency and 15 age-matched healthy volunteers. Medical history revealed symptoms of faecal incontinence in 5 patients. The patients showed decreased maximum retention volumes (p less than 0.01) in the rectal saline infusion test. Lowered anal sphincter resting (p less than 0.01) and squeeze pressure (p less than 0.01) was demonstrated in patients with adrenocortical insufficiency. No differences between patients and controls were found in respect of perception volume, minimal distension volume for sphincter relaxation and rectal compliance by means of intrarectal balloon distension. Electromyography of the external anal sphincter was performed in 8 patients and showed no evidence for a neurogenic defect. Relevant morphological changes of the anorectum could be excluded endoscopically in 13 of the 15 patients. Therefore impaired anorectal muscular function is responsible for faecal incontinence in patients with Addison's disease and androgen deficiency. Further investigations will show, whether these findings are the consequence of lowered androgen production.     

Sacral nerve stimulation for treatment of fecal incontinence

PURPOSE: Many patients with fecal incontinence demonstrate a functional deficit of the internal anal sphincter or the external sphincter muscles without any apparent structural defects. Few patients are amenable to repair or substitution of the sphincter. However, sacral nerve stimulation appears to offer a valid treatment option for fecal incontinence. The objectives of this study were: to evaluate the efficacy of temporary stimulation of the sacral nerve roots (percutaneous nerve evaluation) in patients with functional fecal incontinence; to determine the mechanisms of possible improvement; and to evaluate if temporary stimulation could be reproduced and maintained by implanting a permanent neurostimulation system. METHODS: Twenty-three patients with fecal incontinence, 18 females and 5 males, median age of 54.9 years (range 28–71), underwent a percutaneous nerve evaluation test. Eleven patients (47.8 percent) also had urinary disorders: urge incontinence (4), stress incontinence (3), and retention (4). Associated disorders included perineal and rectal pain (1), spastic paraparesis (1), and syringomyelia (1). All patients underwent a preliminary evaluation using stationary anal manovolumetry, pudendal nerve terminal motor latency measurements, and anal ultrasound. A percutaneous electrode for the stimulation of the sacral nerve roots was positioned at the level of the third sacral foramen (S3) in 20 patients and S2 in 2 patients (1 patient missing). Stimulation parameters used were: pulse width 210µsec, frequency 25 Hz, and average amplitude of 2.8 V (range 1–6). The electrode was left in place for a minimum of 7 days. Five patients were successively implanted with a permanent sacral electrode with a stimulation frequency of 16 to 18 Hz and amplitude of 1.1–4.9 V. RESULTS: Seventeen of the 19 patients (89.4 percent) who completed the minimum percutaneous nerve evaluation period of 7 days (median 10.7 (range 7–30)), had a reduction of liquid or solid stool incontinence by more than 50 percent, and fourteen (73.6 percent) were completely continent for stool. The most important changes revealed by manovolumetry were an increase in resting pressure (P<0.001) and voluntary contraction (P=0.041), reduction of initial pressure for first sensation (P=0.049) and urge to defecate (P=0.002), and a reduction of the rectal volume for urge sensation (P=0.006). The percutaneous nerve evaluation results were reproduced at a median follow-up of 19.2 months (range 5 to 37) in the 5 patients who received a permanent implant. CONCLUSIONS: Temporary stimulation of the sacral roots (percutaneous nerve evaluation) can be of help in those patients with fecal incontinence, and the results are reproduced with permanent implantation. The positive effect on continence seems to be derived from not only the direct efferent stimulation on the pelvic floor and the striated sphincter muscle, but also from modulating afferent stimulation of the autonomous neural system, inhibition of the rectal detrusor, activation of the internal anal sphincter, and modulation of sacral reflexes that regulate rectal sensitivity and motility.     

Rectal compliance as a routine measurement

PURPOSE: The clinical impact of rectal compliance and sensitivity measurement is not clear. The aim of this study was to measure the rectal compliance in different patient groups compared with controls and to establish the clinical effect of rectal compliance. METHODS: Anorectal function tests were performed in 974 consecutive patients (284 men). Normal values were obtained from 24 controls. Rectal compliance measurement was performed by filling a latex rectal balloon with water at a rate of 60 ml per minute. Volume and intraballoon pressure were measured. Volume and pressure at three sensitivity thresholds were recorded for analysis: first sensation, urge, and maximal toleration. At maximal toleration, the rectal compliance (volume/pressure) was calculated. Proctoscopy, anal manometry, anal mucosal sensitivity, and anal endosonography were also performed as part of our anorectal function tests. RESULTS: No effect of age or gender was observed in either controls or patients. Patients with fecal incontinence had a higher volume at first sensation and a higher pressure at maximal toleration (P=0.03), the presence of a sphincter defect or low or normal anal pressures made no difference. Patients with constipation had a larger volume at first sensation and urge (P<0.0001 andP<0.01). Patients with a rectocele had a larger volume at first sensation (P=0.004). Patients with rectal prolapse did not differ from controls; after rectopexy, rectal compliance decreased (P<0.0003). Patients with inflammatory bowel disease had a lower rectal compliance, most pronounced in active proctitis (P=0.003). Patients with ileoanal pouches also had a lower compliance (P<0.0001). In the 17 patients where a maximal toleration volume<60 ml was found, 11 had complaints of fecal incontinence, and 6 had a stoma. In 31 patients a maximal toleration volume between 60 and 100 ml was found; 12 patients had complaints of fecal incontinence, and 6 had a stoma. Proctitis or pouchitis was the main cause for a small compliance. All 29 patients who had a maximal toleration volume>500 ml had complaints of constipation. No correlation between rectal and anal mucosal sensitivity was found. CONCLUSION: Rectal compliance measurement with a latex balloon is easily feasible. In this series of 974 patients, some patient groups showed an abnormal rectal visceral sensitivity and compliance, but there was an overlap with controls. Rectal compliance measurement gave a good clinical impression about the contribution of the rectum to the anorectal problem. Patients with proctitis and pouchitis had the smallest rectal compliance. A maximal toleration volume<60 ml always led to fecal incontinence, and stomas should be considered for such patients. A maximal toleration volume>500 ml was only seen in constipated patients, and therapy should be given to prevent further damage to the pelvic floor. Values close to or within the normal range rule out the rectum as an important factor in the anorectal problem of the patient.Drs. Sloots and Poen were supported by a grant from Janssen-Cilag. Presented at the meeting of the Dutch Society of Gastroenterology, Veldhoven, the Netherlands, October 7 to 8, 1999.     

Anal function in geriatric patients with faecal incontinence.

The association of faecal incontinence with constipation and confusion in the elderly is well recognised but the anal function of faecally incontinent geriatric patients is poorly understood. Anal studies were therefore performed on 99 geriatric patients (49 with faecal incontinence, 19 continent patients with faecal impaction and 31 geriatric control patients with normal bowel habit) and 57 younger healthy control patients. An age related reduction in anal squeeze pressure but not resting pressure was identified. A reduction in anal resting pressure was detected in the faecally incontinent geriatric patients but squeeze pressure did not differ significantly from that found in the other geriatric patients. Anal sensation was impaired in the faecally incontinent patients. No difference was found between the groups as measured by pudendal nerve terminal motor latency. Gross neuropathy of the distal part of the pudendal nerve does not account for the observed external anal sphincter weakness in geriatric patients or for their faecal incontinence. Internal anal sphincter dysfunction is an important factor in faecal incontinence in the elderly.     

Progressive systemic sclerosis of the internal anal sphincter leading to passive faecal incontinence.

Two female patients aged 62 and 44 years with progressive systemic sclerosis and passive faecal incontinence are described. Both had the typical gut motility disorders of dysphagia, heartburn, and constipation. Anorectal physiology tests showed a low resting pressure in both and an absent rectoanal inhibitory reflex in one. In both patients anal endosonography showed a thin internal anal sphincter with changed reflectivity suggestive of fibrosis. In both patients anorectal sensation and pudendal nerve function were normal. Histological examination of the rectum in one patient showed collagenous replacement of the rectal muscularis propria with prominent atrophy of the musculature. This study suggests that the internal sphincter may be selectively affected by progressive systemic sclerosis, which may lead to passive faecal incontinence.