Results of neurophysiologic evaluation in fecal incontinence

PURPOSE: Several methods of neurophysiologic assessment exist in the investigation of patients with fecal incontinence. However, the clinical significance of the information gained is uncertain. The aim of this prospective study was to evaluate the results of pudendal nerve terminal motor latency and fiber density in relation to clinical variables and manometric measurements. METHODS: Seventy-two patients with fecal incontinence (63 women; mean age, 62; range, 24–81 years) responded to a bowel questionnaire and underwent anorectal manovolumetry, anal ultrasonography, defecography, and electromyography, including pudendal nerve terminal motor latency and fiber density. RESULTS: Pudendal neuropathy (pudendal nerve terminal motor latency >2.5 ms) was found in 46 percent and increased fiber density (>1.7) in 82 percent. Pudendal neuropathy and increased fiber density were most common in patients with rectal prolapse or intra-anal intussusception. No difference was seen concerning anal resting and incremental pressures, rectal compliance, rectal sensibility or severity of incontinence in patients with unilateral, bilateral, or marked (>4 ms) pudendal neuropathyvs. patients with normal pudendal nerve terminal motor latency. In contrast, patients with increased fiber density had lower incremental pressures (P<0.05) and stated decreased rectal sensibility (P<0.05) compared with those with normal fiber density. These differences were most pronounced in patients with neurogenic or idiopathic incontinence. CONCLUSIONS: Pudendal neuropathy and increased fiber density are common in patients with fecal incontinence. Fiber density but not pudendal nerve terminal motor latency was correlated with clinical and manometric variables. The severity of nerve injury correlated with anal motor and sensory function in patients with neurogenic or idiopathic incontinence. The routine use of pudendal nerve terminal motor latency in the assessment of patients with fecal incontinence can be questioned.Read at The American Society of Colon and Rectal Surgeons' 100th Anniversary and Tripartite Meeting, Washington, D.C., May 1 to 6, 1999.     

Sacral Nerve Stimulation for Fecal Incontinence: External Anal Sphincter Defect <Emphasis Type="Italic">vs</Emphasis>. Intact Anal Sphincter

Purpose  This prospective study was designed to assess the effectiveness of sacral nerve stimulation for fecal incontinence in patients with external anal sphincter defect and to evaluate its efficacy regarding presence and size of sphincter defect. Methods  Fifty-three consecutive patients who underwent sacral nerve stimulation for fecal incontinence were divided into two groups: external anal sphincter defect group (n = 21) vs. intact sphincter group (n = 32). Follow-up was performed at 3, 6, and 12 months with anorectal physiology, Wexner’s score, bowel diary, and quality of life questionnaires. Results  The external anal sphincter defect group (defect <90°:defect 90°–120° = 11:10) and intact sphincter group were comparable with regard to age (mean, 63 vs. 63.6) and sex. Incidence of internal anal sphincter defect and pudendal neuropathy was similar. All 53 patients benefited from sacral nerve stimulation. Weekly incontinent episodes decreased from 13.8 to 5 (P < 0.0001) for patients with external anal sphincter defects and from 6.7 to 2 (P = 0.001) for patients with intact sphincter at 12-month follow-up. Quality of life scores improved in both groups (P < 0.0125). There was no significant difference in improvement in functional outcomes after sacral nerve stimulation between patients with or without external anal sphincter defects. Clinical benefit of sacral nerve stimulation was similar among patients with external anal sphincter defects, irrespective of its size. Presence of pudendal neuropathy did not affect outcome of neurostimulation. Conclusions  Sacral nerve stimulation for fecal incontinence is as effective in patients with external anal sphincter defects as those with intact sphincter and the result is similar for defect size up to 120° of circumference. ^†Deceased.     

Prevalence of pudendal neuropathy in fecal incontinence

PURPOSE: A prospective study was made of the prevalence and associations of pudendal neuropathy in 96 patients with fecal incontinence (72 females and 24 males). METHODS: Clinical exploration, perineal level measurement, anorectal manometry, and electrophysiologic evaluations (pudendal nerve terminal motor latency (PNTML) and external sphincter fiber density (FD)) were performed. RESULTS: 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 straining 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 63 (58.7 percent) patients with sphincter injury vs.in 31 of 33 (93.9 percent) patients with idiopathic fecal incontinence (P < 0.01). CONCLUSIONS: 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.Read at the meeting of The American Society of Colon and Rectal Surgeons, Orlando, Florida, May 8 to 13, 1994.     

Anal endosonography: Relationship with anal manometry and neurophysiologic tests

Thirty-seven patients were referred for evaluation of anal function; their clinical diagnoses were traumatic fecal incontinence (13), idiopathic (pudendal neuropathy) fecal incontinence (7), fecal soiling (9), and other (8). In all patients, anal endosonography (sphincter defects and internal sphincter thickness [IST]) and anal manometry (maximal basal pressure [MBP] and maximal squeeze pressure [MSP]) were performed. In 18 patients, neurophysiologic tests (EMG-maximal contraction pattern [MCP], single-fiber EMG [fiber density; FD], and pudendal nerve terminal motor latency [PNTML]) were also performed. Endosonography demonstrated in seven patients both an internal and external sphincter defect (Group 1), in seven patients an internal sphincter defect and in one patient an external sphincter defect (Group 2), and in 22 patients no sphincter defect (Group 3). There was a significant difference among these three groups for MBP and MCP, the lowest being in Group 1. Between the patients with traumatic fecal incontinence and idiopathic fecal incontinence, no differences in IST, MBP, MSP, MCP, FD, and PNTML were found. In two patients with a suspected obstetric trauma, there was an unexpected additional severe pudendal neuropathy. In one patient with a suspected obstetric trauma, no damage of the anal sphincters could be demonstrated. In one patient with suspected idiopathic fecal incontinence, there was an additional, unsuspected defect of the internal sphincter. There was concordance between endosonography and EMG in the mapping of the external sphincter. Clinical diagnoses can be misleading in differentiating between traumatic and idiopathic fecal incontinence; anal endosonography provides unsuspected and additional information about the sphincters; PNTML can reveal unsuspected neuropathy in traumatic fecal incontinence. Therefore, the combination of endosonography and PNTML is promising in selecting patients for surgery.     

Long-term results of electromyographic biofeedback training for fecal incontinence

PURPOSE: The aim of this study was to examine the long-term results of electromyographic biofeedback training in fecal incontinence. METHODS: Thirty-seven patients (1 male) received a customised program of 2 to 11 (median, 3) biofeedback training sessions with an anal plug electromyometer. Nine patients had persistent incontinence after anal sphincter repair, a further 8 patients had postsurgical or partial obstetric damage of the sphincter but no sphincter repair, 9 patients had neurogenic sphincter damage, and 11 patients were classified as having idiopathic fecal incontinence. Duration of voluntary sphincter contraction was measured by anal electromyography (endurance score) before and after treatment. A postal questionnaire was used to investigate the following variables: 1) subjective rating on a four-grade Likert-scale of the overall result of the biofeedback training; 2) incontinence score (maximum score is 18, and 0 indicates no incontinence); and 3) rating of bowel dissatisfaction using a visual analog scale (0 to 10). RESULTS: Twenty-two patients (60 percent) rated the result as very good (n=8) or good (n=14) immediately after the treatment period. Median endurance score improved from 1 to 2 minutes (P<0.0001). Median incontinence score improved from 11 to 7, and bowel dissatisfaction rating improved from 5 to 2.8 (bothP<0.0001). After a median follow-up of 44 (range, 12–59) months, 15 patients (41 percent) still rated the overall result as very good (n=3) or good (n=12). The incontinence score did not change during follow-up. Median bowel dissatisfaction rating deteriorated from 2.8 to 4.2 but remained better than before treatment. Poor early subjective rating and the need for more than three biofeedback sessions were predictive of worsening during follow-up. CONCLUSION: We think it is encouraging that in this study biofeedback treatment for fecal incontinence with an intra-anal plug electrode resulted in a long-term success rate in nearly one-half of the patients.     

Electrophysiologic and manometric assessment of failed postanal repair for anorectal incontinence

The reason for failure to improve fecal incontinence after postanal repair in idiopathic (neurogenic) anorectal incontinence is unknown. The authors have studied 20 patients whose anorectal continence was not improved after Parks' postanal repair. Anorectal manometry, single fiber EMG of the external anal sphincter muscle, and measurements of the pudendal nerve terminal motor latency were studied before and nine months after postanal repair. All 20 patients had evidence of reinnervation within the external anal sphincter muscle before operation; 17 had a raised pudendal nerve terminal motor latency and all 20 had low resting voluntary contraction anal canal pressures. No significant differences were found between the resting, voluntary contraction anal canal pressures and single fiber EMG fiber density values before or after postanal repair. However, a significant increase in the pudendal nerve terminal motor latency was found after postanal repair (P<0.001) using a student's pairedt test. These results suggest that, in patients who are not rendered continent by postanal repair, a continuing neuropathic process takes place. Read at the joint meeting of the American Society of Colon and Rectal Surgeons with the Section of Colo-Proctology of the Royal Society of Medicine and the Section of Colonic and Rectal Surgery of the Royal Australasian College of Surgeons, New Orleans, Louisiana, May 6–11, 1984.     

Biofeedback training in patients with fecal incontinence

PURPOSE: This study was undertaken to assess the functional results of biofeedback training in patients with fecal incontinence in relation to clinical presentation and anorectal manometry results. METHODS: Twenty-six consecutive patients with fecal incontinence were treated with biofeedback training using anorectal manometry pressure for visual feedback. Ten patients had passive incontinence only, six patients had urge incontinence, and ten patients had combined passive and urge incontinence. RESULTS: Patients with urge incontinence had a lower maximum voluntary contraction pressure (92 ± 12 mmHg) and lower maximum tolerable volume (78 ± 13 ml) than patients with passive incontinence (140 ± 43 mmHg and 166 ± 73 ml). Twenty-two patients completed the treatment, five patients (23 percent) showed excellent improvement, nine patients (41 percent) had good results, and eight (36 percent) patients showed no improvement. At follow-up on average of 21 months after therapy, 41 percent of our patients reported continued improvement. The maximum tolerable volume was higher in those with excellent (140.4 ± 6.8 ml) or good (156.3 ± 6.64 ml) results of therapy than it was in those with poor results (88.5 ± 2.5 ml). Greater asymmetry of the anal sphincter also correlated to poor results. CONCLUSION: Biofeedback therapy improved continence immediately after training and at follow-up after 21 months, but the initial results were better. The urge fecal incontinence seems to be related to function of the external anal sphincter and to the maximum tolerable volume. Low maximum tolerable volume and anal sphincter asymmetry were associated with a poor outcome of therapy     

Biofeedback training is useful in fecal incontinence but disappointing in constipation

BACKGROUND: Successful biofeedback therapy has been reported in the treatment of fecal incontinence and constipation. It is uncertain which groups of incontinent patients benefit from biofeedback, and our impression has been that biofeedback is more successful for incontinence than for constipation. PURPOSE: This study was designed to review the results of biofeedback therapy at the Lahey Clinic. METHODS: Biofeedback was performed using an eightchannel, water-perfused manometry system. Patients saw anal canal pressures as a color bar graph on a computer screen. Assessment after biofeedback was by manometry and by telephone interview with an independent researcher. RESULTS: Fifteen patients (13 women and 2 men) with incontinence underwent a mean of three (range, 1–7) biofeedback sessions. The cause was obstetric (four patients), postsurgical (five patients), and idiopathic (six patients). Complete resolution of symptoms was reported in four patients, considerable improvement in four patients, and some improvement in three patients. Manometry showed a mean increase of 15.3 (range, ?3–30) mmHg in resting pressure and 35.7 (range, 13–57) mmHg in squeezing pressure after biofeedback. A successful outcome could not be predicted on the basis of cause, severity of incontinence, or initial manometry. Twelve patients (10 women and 2 men) with constipation underwent a mean of three (range, 1–14) biofeedback sessions. Each had manometric evidence of paradoxic nonrelaxing external sphincter or puborectalis muscle confirmed by defography or electromyography. All patients could be taught to relax their sphincter in response to bearing down. Despite this, only one patient reported resolution of symptoms, three patients had reduced straining, and three patients had some gain in insight. CONCLUSIONS: Biofeedback helped 73 percent of patients with fecal incontinence, and its use should be considered regardless of the cause or severity of incontinence or of results on initial manometry. In contrast, biofeedback directed at correcting paradoxic external sphincter contraction has been disappointing.     

Electrophysiologic Studies and Clinical Findings in Females With Combined Fecal and Urinary Incontinence: A Prospective Study

Purpose Several clinical, urodynamic, and manometric findings suggest neurologic damage as a contributing factor in the development of combined fecal and urinary incontinence. In this study, we wanted to test the hypothesis of pudendal nerve neuropathy being a more frequent lesion in patients with double incontinence compared with patients with isolated fecal incontinence. Patients Ninety-three females with combined fecal and urinary incontinence and 36 females with isolated fecal incontinence were investigated. All patients underwent anal manometry, endoanal ultrasound, electromyography, and pudendal nerve terminal motor latency. Results No statistically significant differences were found in the age, history of vaginal delivery, and chronic straining between both groups. However, the rate of postmenopausal females was higher in the combined fecal and urinary incontinence group (85 vs. 67 percent; P = 0.02). Menopause was an independent risk factor of having double incontinence (odds ratio, 1.4; P = 0.02). Concentric needle electromyography of the external anal sphincter revealed increased duration of the motor unit potentials in 43 and 53 percent of patients with combined fecal and urinary incontinence and isolated fecal incontinence, respectively (P = 0.28). An increased number of polyphasic motor unit potentials was detected in 52 and 58 percent (P = 0.6). There was no statistically significant difference in the prevalence of bilateral (20 vs. 27 percent) or unilateral (23 vs. 14 percent) prolonged mean pudendal nerve terminal motor latency between both groups (P = 0.3). Conclusions Pudendal neuropathy is not a distinct characteristic of patients with double incontinence. The prevalence of pudendal neuropathy in these patients is similar to that observed in patients with isolated fecal incontinence. Others factors should be investigated to explain the common association of both types of incontinence. Presented at the meeting of The American Society of Colon and Rectal Surgeons, Philadelphia, Pennsylvania, April 30 to May 5, 2005, and the International Symposium Neurogastroenterology and Motility, Toulouse, France, July 3 to 6, 2005. Reprints are not available.     

Treatment of fecal incontinence

Opinion statement Fecal incontinence is a symptom of many disorders that can affect the nerves and muscles controlling defecation; it is not just due to exceptionally voluminous diarrhea. Underlying problems should be identified and treated, because that may improve incontinence. If treatment of the underlying problem does not correct incontinence, several approaches can be employed successfully. General approaches include stimulation of defecation at intervals to empty the rectum under supervised conditions; treatment of diarrhea, if present; addressing coexisting psychologic problems, such as depression; use of continence aids, such as adult diapers; and perineal skin care to prevent skin breakdown. Drug therapy includes use of constipating drugs, such as loperamide or diphenoxylate, that can impede the gastrocolic reflex, thereby limiting rectal filling and the likelihood of incontinence. Biofeedback training is useful in patients with some ability to sense rectal distention and to contract the external anal sphincter; instrumental learning using manometric or electromyographic biofeedback can be used to reinforce the rectoanal contractile response to rectal distention. Improvement in continence has been noted in up to 70% of suitable candidates with a single biofeedback training session. Patients with external anal sphincter disruption due to childbirth injury or other trauma may benefit from direct external anal sphincter repair (sphincteroplasty). In others, tightening up the anal canal by encirclement with nonabsorbable mesh (Thiersch procedure), perianal injection of fat, collagen, or synthetic gel, or radiofrequency electrical energy (Stretta procedure) may provide some palliation. Creation of a new sphincter mechanism by muscle transposition and encirclement of the anal canal is another approach that has been improved by use of electrical stimulators to keep the neosphincter contracted. Artificial anal sphincters patterned after artificial urinary sphincters have met with some success, but local infection remains problematic. When all else fails, fecal diversion (ileostomy, colostomy) can be effective in rehabilitating patients.     

Evaluation of the sacroanal motor pathway by magnetic and electric stimulation in patients with fecal incontinence

PURPOSE: The aim of this controlled study was to examine whether it was feasible to use magnetic stimulation as a new diagnostic tool to evaluate the motor function of the sacral roots and the pudendal nerves in patients with fecal incontinence. PATIENTS AND METHODS: Nineteen consecutive patients (17 females) with a median age of 67 (range, 36–78) years referred for fecal incontinence and 14 healthy volunteers (six females) with a median age of 42 (range, 23–69) years were examined. Latency times of the motor response of the external anal sphincter were measured after electric transrectal stimulation of the pudendal nerve and magnetic stimulation of the sacral roots. RESULTS: The success rates of pudendal nerve terminal motor latency and sacral root terminal motor latency measurements were 100 and 85 percent, respectively, in the control group and 94 and 81 percent, respectively, in the fecal incontinence group. Median left pudendal nerve terminal motor latency was 1.88 (range, 1.4–2.9) milliseconds in the control group and 2.3 (range, 1.8–4) milliseconds in the fecal incontinence group (P<0.006). Median right pudendal nerve terminal motor latency was 1.7 (range, 1.3–3.4) milliseconds in the control group and 2.5 (range, 1.7–6) milliseconds in the fecal incontinence group (P<0.003). Median left sacral root terminal motor latency was 3.3 (range, 2.1–6) milliseconds in the control group and 3.7 (range, 2.8–4.8) milliseconds in the fecal incontinence group (P<3 0.03). Median right sacral root terminal motor latency was 3 (range, 2.6–5.8) milliseconds in the control group and 3.9 (range, 2.5–7.2) milliseconds in the fecal incontinence group (P=0.15). CONCLUSIONS: Combined pudendal nerve terminal motor latency and sacral root terminal motor latency measurements may allow us to study both proximal and distal pudendal nerve motor function in patients with fecal incontinence. Values of sacral root terminal motor latency have to be interpreted cautiously because of the uncertainty about the exact site of magnetic stimulation and the limited magnetic field strength.     

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.     

Internal anal sphincter in neurogenic fecal incontinence

In neurogenic fecal incontinence there is denervation of the external anal sphincter and pelvic floor muscles but the role of the internal anal sphincter is incompletely understood. We have evaluated the internal anal sphincter in 6 patients with neurogenic incontinence undergoing postanal repair and in 7 control subjects. All the incontinent subjects, but none of the controls, had evidence of pudendal neuropathy. Surface electromyography studies of the internal anal sphincter showed absence of electrical activity in 4 of 6 incontinent subjects; in the remaining 2 subjects and in 6 of 7 controls normal slow waves were present. Internal sphincter muscle strips from control subjects showed normal in vitro responses to noradrenaline, isoprenaline, dimethyl-phenylpiperazinium, and electrical field stimulation; muscle strips from the incontinent patients showed complete insensitivity except in 2 patients in whom there was contraction to noradrenaline and relaxation to isoprenaline. Electron microscopy showed normal smooth muscle in 5 control subjects and minor changes in 1 subject; all the incontinent patients showed abnormalities in the smooth muscle cells of the internal anal sphincter. These findings indicate that in neurogenic fecal incontinence neurogenic weakness of the external anal sphincter and pelvic floor muscles is associated with damage to the internal anal sphincter.     

Etiology and management of fecal incontinence

Fecal incontinence is a challenging condition of diverse etiology and devastating psychosocial impact. Multiple mechanisms may be involved in its pathophysiology, such as altered stool consistency and delivery of contents to the rectum, abnormal rectal capacity or compliance, decreased anorectal sensation, and pelvic floor or anal sphincter dysfunction. A detailed clinical history and physical examination are essential. Anorectal manometry, pudendal nerve latency studies, and electromyography are part of the standard primary evaluation. The evaluation of idiopathic fecal incontinence may require tests such as cinedefecography, spinal latencies, and anal mucosal electrosensitivity. These tests permit both objective assessment and focused therapy. Appropriate treatment options include biofeedback and sphincteroplasty. Biofeedback has resulted in 90 percent reduction in episodes of incontinence in over 60 percent of patients. Overlapping anterior sphincteroplasty has been associated with good to excellent results in 70 to 90 percent of patients. The common denominator between the medical and surgical treatment groups is the necessity of pretreatment physiologic assessment. It is the results of these tests that permit optimal therapeutic assignment. For example, pudendal nerve terminal motor latencies (PNTML) are the most important predictor factor of functional outcome. However, even the most experienced examiner's digit cannot assess PNTML. In the absence of pudendal neuropathy, sphincteroplasty is an excellent option. If neuropathy exists, however, then postanal or total pelvic floor repair remain viable surgical options for the treatment of idiopathic fecal incontinence. In the absence of an adequate sphincter muscle, encirclement procedures using synthetic materials or muscle transfer techniques might be considered. Implantation of a stimulating electrode into the gracilis neosphincter and artificial sphincter implantation are other valid alternatives. The final therapeutic option is fecal diversion. This article reviews the current status of the etiology and incidence of incontinence as well as the evaluation and treatment of this disabling condition.     

Pudendal neuropathy in evacuatory disorders

PURPOSE: Aims of the present study were to assess frequency of pudendal neuropathy in patients with constipation and fecal incontinence, to determine its correlation with clinical variables, anal electromyographic assessment, and anal manometric pressures, and to determine usefulness of the pudendal nerve terminal motor latency assessment in evaluation of these evacuatory disorders. METHODS: From 1988 to 1993, 395 patients (constipated, 172; incontinent, 223) underwent pudendal nerve terminal motor latency, electromyography, and anal manometry. Pudendal neuropathy was defined as a pudendal nerve terminal motor latency greater than 2.2 ms. RESULTS: Patients were a mean age of 60.7 (range, 17–88) years. Overall incidence of pudendal neuropathy was 31.4 percent (constipated, 23.8 percent; incontinent, 37.2 percent; P<0.05). Incidence of pudendal neuropathy dramatically increased after 70 years of age in both groups (22 percent vs. 44 percent; P<0.05). Moreover, subjects with pudendal neuropathy were older than those without pudendal neuropathy (mean age, 67 vs. 57 years; P<0.05). The presence of pudendal neuropathy was associated with decreased motor unit potentials recruitment in patients with incontinence (P<0.01). Patients with and without pudendal neuropathy had a similar mean squeezing pressure in both groups. CONCLUSION: Pudendal neuropathy is an age-related phenomenon. Although pudendal neuropathy is associated with abnormal anal electromyographic findings in patients with incontinence, no association with anal manometric pressures was found. Pudendal nerve terminal motor latency assessment is a useful tool in the evaluation of patients with fecal incontinence, but its role in the assessment of constipated patients remains unknown.     

Postdelivery anal function in primiparous females

PURPOSE: A study was performed to evaluate the early morphologic and functional consequences of vaginal delivery on the anal sphincter in primiparous females. METHODS: Among a cohort of 197 primiparous females who agreed to participate in a clinical evaluation of fecal incontinence and in a transanal ultrasound examination 12 weeks after delivery, 52 also underwent anal manometry using a radial six-port catheter, of whom 10 were asymptomatic and had a normal sphincter at ultrasound and the remaining 42 had clinical signs of anal incontinence or ultrasonographic defects of the anal sphincter or both. Anal sphincter pressures and asymmetry index were analyzed at rest and during voluntary squeeze. Manometric and ultrasound results were compared, together with clinical symptoms. RESULTS: Fourteen patients with clinical signs of anal incontinence had lower resting and squeeze anal pressures than continent patients (P<0.05), but similar anal asymmetry indexes. Patients with incontinence and an anal defect had the lowest resting and squeeze anal pressures (P<0.05). Forceps assistance to delivery was not associated with a higher frequency of anal sphincter lesions. Resting and squeeze anal pressures were lower in the forceps group (P<0.005), but anal asymmetry indexes were similar. Finally, manometric results were identical in the presence or absence of anal sphincter endosonographic defects. CONCLUSIONS: Anal sphincter defects are frequent after the first vaginal delivery, but are not always associated with functional or clinical abnormalities. Resting and squeeze anal pressures were significantly decreased in patients with incontinence and an anal defect and after forceps-assisted deliveries. Anal asymmetry index was not found useful in this population of young primiparous females.Presented in part at the Journées Francophones de Pathologie Digestive, Paris, France, March 21 to 25, 1998.     

The relationship of pudendal nerve terminal motor latency to squeeze pressure in patients with idiopathic fecal incontinence

PURPOSE: With the advent of transanal ultrasonography it has been possible to identify those incontinent patients without sphincter defects. The majority of these patients are now thought to have neurogenic fecal incontinence secondary to pudendal neuropathy. They have been found to have reduced anal sphincter pressures and increased pudendal nerve terminal motor latencies. The aim of this study was to determine whether in those incontinent patients who do not have a sphincter defect, prolonged pudendal nerve terminal motor latency correlates with anal manometry, in particular maximum squeeze pressure. METHODS: Sixty-six incontinent patients were studied with transanal ultrasonography, anorectal manometry, and pudendal nerve terminal motor latency. Twenty-seven continent controls had anorectal manometry and pudendal nerve terminal motor latency measured. RESULTS: Maximum resting pressure and maximum squeeze pressure were significantly lower in the group of incontinent patients with bilateral prolonged pudendal nerve terminal motor latency (median maximum resting pressure = 26.5 mmHg; median maximum squeeze pressure = 60 mmHg) when compared with incontinent patients with normal bilateral pudendal nerve terminal motor latencies (median maximum resting pressure = 46 mmHg; median maximum squeeze pressure = 79 mmHg; maximum resting pressure P = 0.004; and maximum squeeze pressure P = 0.04). In incontinent patients with no sphincter defects no correlation between pudendal nerve terminal motor latency and maximum squeeze pressure was found (r = -0.109, P = 0.48) and maximum squeeze pressure did not correlate with bilateral or unilateral prolonged pudendal nerve terminal motor latency (r = -0.148, P = 0.56 and r = 0.355, P = 0.19 respectively). CONCLUSIONS: In patients with idiopathic fecal incontinence damage to the pelvic floor is more complex than damage to the pudendal nerve alone. Although increased pudendal nerve terminal motor latency may indicate that neuropathy is present, in patients with neuropathic fecal incontinence, pudendal nerve terminal motor latency does not correlate with maximum squeeze pressure. Normal pudendal nerve terminal motor latency does not exclude weakness of the pelvic floor.     

Prospective comparison of short- and long-term effects of pelvic floor exercise/biofeedback training in patients with fecal incontinence after surgery plus irradiation versus surgery alone for colorectal cancer: Clinical,functional and endoscopic/endosonographic findings

Objective. The influence of irradiation on the clinical severity of incontinence, sphincter function, morphologic features and short/long-term treatment effects of sphincter training therapy is still insufficiently understood in irradiated patients with fecal incontinence after surgery for colorectal cancer. These parameters were compared in irradiated and non-irradiated patients and followed prospectively with regard to short- and long-term training effects. Material and methods. Forty-one patients having been irradiated after surgery (50.0±5.0 Gy) and 54 non-irradiated patients with fecal incontinence participated in this prospective, non-randomized trial. Baseline evaluation included a semiquantitative severity assessment score of fecal incontinence (modified Cleveland Incontinence Score (MCIS)), rectal manometry and endoscopy. After 3 weeks (short term) of intensive in-hospital pelvic floor exercise combined with biofeedback training, a second evaluation was made. In addition, anal endosonography (EUS) was performed in cases of treatment failure. After one year (long term) a third evaluation was made clinically (MCIS score). Results. Irradiated patients presented with a significantly higher degree of fecal incontinence (lower MCIS) compared to non-irradiated patients: 7.4±2.2 versus 8.7±2.7 points (p<0.001). Rectosigmoidal inflammation was more frequent in irradiated than non-irradiated patients (26.9% versus 9.3%) (p<0.03). Sphincter pressure, sensation/pain threshold and the rectoanal inhibitory reflex were similar in both groups. A significant short-term training effect was observed in both groups following sphincter training therapy in terms of an increase in MCIS from 7.4±2.2 to 9.4±2.7 points in the irradiated group and from 8.7±2.7 to 11.4±2.5 points in the non-irradiated group (p<0.0001). After one year the scores were 8.2±3.8 and 10.7±4.4 points, respectively (p<0.0001). There was a significant correlation (p<0.001) between baseline MCIS and the short- and long-term MCIS. In patients with short-term treatment failure (16.6%) anal EUS revealed structural defects of the external sphincter in four patients. There was no association of sphincter diameter with sphincter pressure, sensation/pain threshold and short/long-term MCIS. Conclusions. The main result of this study is that irradiated patients show short- and long-term training effects comparable with those of non-irradiated patients despite the higher degree of incontinence at baseline. The correlation between the initial MCIS and short- and long-term treatment effects may be regarded as an important clinical predictor for treatment outcome. Functional and morphologic features are less suitable for this purpose.     

Use of vector volume manometry and endoanal magnetic resonance imaging in the adult female for assessment of anal sphincter dysfunction

PURPOSE: This study compared conventional water-perfused and vector volume anal manometry in female patients with neurogenic fecal incontinence and chronic anal fissure and in healthy female volunteers. We used endoanal magnetic resonance (MR) imaging to measure internal and external sphincter lengths and thicknesses and contrasted these with the manometric findings in the different anorectal conditions. METHODS: One hundred thirty-three female subjects were studied over an eight-month period, including 33 control volunteers, 83 patients with neurogenic fecal incontinence, and 17 patients with chronic anal fissure. Conventional manometry was contrasted with automated vector volume-derived parameters. Endoanal magnetic resonance images were obtained using a previously described internal coil with a 0.5 T Asset scanner measuring quadrantal internal sphincter thickness and averaged coronal internal and external sphincter lengths. RESULTS: There was a statistically significant relationship between parameters measured by conventional manometry and those variables derived from vector volume manometry at rest and squeeze. There was no difference in sectorial vector-derived pressures within any anorectal condition and no correlation between quadrantal internal sphincter thickness measurements and sectorial pressures at rest. Patients with chronic anal fissure and neurogenic fecal incontinence had constitutionally shorter superficial and subcutaneous external sphincters than healthy control subjects (P<0.001). CONCLUSIONS: There is no association between manometric findings and morphologic sphincter measurement; however, the shorter distal external sphincter in patients with fissure might render the lower anal canal relatively unsupported after internal sphincterotomy in the female patient.Poster presentation at the meeting of the Association of Coloproctology of Great Britain and Ireland, Jersey, United Kingdom, June 29 to July 1, 1998.     

Sphincter repair for fecal incontinence after obstetrical or iatrogenic injury

Forty patients with fecal incontinence underwent sphincter repair between 1975 and 1984. Divided sphincter musculature resulted from obstetrical injury in 23 and previous anorectal surgery in 17. Eighteen had undergone a previous attempt at repair. Fifteen patients experienced seepage of stool and 25 had gross incontinence. In nine patients, reconstruction of the external sphincter was by overlap of the muscle ends. Twenty-four others underwent accurate approximation of the external sphincter muscle and anterior plication of the levator muscles, and in seven the anal canal was made smaller by narrowing the anal orifice. Follow-up was an average of 67 months after operation (range, 2.4 to 166 months). Continence was objectively improved in 62 percent (P<.01) when performance criteria were analyzed by Wilcoxon signed-rank test, although 85 percent of the patients reported subjective improvement. Requirements for protective pads were reduced in 57 percent (P<.01) and fewer social limitations were experienced in 52 percent (P<.01). There was no significant correlation between outcome and type of operation. Read at the meeting of the American Society of Colon and Rectal Surgeons, Houston, Texas, May 11 to 15, 1986.