The anocavernosal erectile dysfunction syndrome II Anal ssure and erectile dysfunction

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1 (2000) 12, 279±283 ß 2000 Macmillan Publishers Ltd All rights reserved /00 $ The anocavernosal erectile dysfunction syndrome II Anal ssure and erectile dysfunction A Sha k 1 * and O El-Sibai 2 1 Department of Surgery and Experimental Research, Cairo University, Cairo; and 2 Department of Surgery, Menou a University, Egypt A previous study has demonstrated that the bulbocavernosus muscle (BCM) is a part of the external anal sphincter (EAS) [Sha k, Arch Androl, 1999]. It aids erection by compressing the penile bulb and the dorsal penile vein, and acts as a `suction ± ejection' pump in the ejaculatory process. Being a part of the EAS, the BCM is assumed to be involved in the different EAS pathologies. A recent study showed that erectile (ED) and ejaculatory dysfunction in 16 men with fecal incontinence (Fl) after an anal stula operation was cured after sphincteroplasty [Sha k, in press]. This article investigates the erectile and ejaculatory status in patients with anal ssure. The study comprised 32 men with acute anal ssure (mean age s.d. years), 21 with chronic anal ssure (mean age s.d. years), and 10 healthy volunteers (mean age s.d. years). Erectile dysfunction occurred in all men with an acute ssure and in 16 of the chronic ssure patients; erection had been normal before ssure occurrence. The volunteers had normal erection. The anal pain radiated to the penis and was exaggerated on erection and penile thrusting. Erectile dysfunction investigations showed normal results. The electromyographic (EMG) activity of the external and internal (IAS) anal sphincters and the BCM as well as anal, penile bulb and cavernosal pressures were recorded. The acute ssures were treated conservatively and chronic ones by internal anal sphincterotomy. The patients were followed for mean periods of s.d. months. The bulbocavernosus re ex as well as EMG activity of EAS and BCM were normal, while the resting EMG activity of the IAS was increased. The anal pressure in the acute and chronic anal ssure was increased (P < 0.01, P < 0.05, respectively), while the bulbar and cavernosal pressures showed no signi cant changes. Fissure treatment effected cure of the ssure and the ED in 30=32 of the acute and in 19=21 of the chronic cases. Erectile dysfunction persisted in the four patients in whom the ssures did not heal. In conclusion, a relationship is suggested to exist between anal ssure and ED. The ED occurred in the presence of anal ssure and was normalized with ssure cure. The BCM and anal pain seem to play a role in the etiology of ED associated with anal ssure. International Journal of Impotence Research (2000) 12, 279±283. Keywords: external anal sphincter; erectile dysfunction; incontinence; bulbocavernosus muscle; erectile dysfunction; external anal sphincter Introduction A previous study has demonstrated that the bulbocavernosus muscle (BCM) is a part of the external anal sphincter (EAS). 1 It aids erection by compressing the penile bulb and dorsal penile vein, 1±5 and in ejaculation by acting as a `suction ± ejection' pump for the seminal uid after it reaches the posterior urethra. 1 Being an extension of the EAS, the BCM is assumed to be involved in the different EAS pathologies. A recent study 6 on 16 men with erectile and ejaculatory dysfunction following fecal *Correspondence: A Sha k, 2 Talaat Harb Street, Cairo, Egypt. Received 16 January 2000; accepted 18 September 2000 incontinence (FI) after an anal stula operation, has shown diminished EMG activity of both the EAS and BCM, as well as reduced anal and bulbar pressures at rest, on voluntary squeeze and on electrostimulation of the EAS. Sphincteroplasty 6 rendered the patients continent and restored erectile function and ejaculation to normal. It was postulated that the diminished BCM EMG activity was due to EAS injury and that failure of BCM contraction to elevate the cavernosal pressure above systolic blood pressure would induce ED. 6 Ejaculation did not occur in jets, but in a seeping ow pattern probably caused by the loss of rhythmic contractions of the BCM. Based on the results of this study, it is suggested that anorectal disorders might affect the erectile function. This article investigates the erectile and ejaculatory status in patients with anal ssure.

2 280 Materials and methods Subjects A concentric electromyographic needle electrode (type 13L49, Disa, Copenhagen, Denmark) measuring 25 mm in length and 0.65 mm in diameter was introduced into the EAS, a second one into the IAS and a third one into the BCM, using a previously reported technique. 1 The study comprised 32 men with acute anal ssure (mean age s.d. years, range 32 ± 41), 21 with chronic anal ssure (mean age s.d. years, range 34 ± 44), and 10 healthy volunteers (mean age s.d. years, range 33 ± 42), who acted as controls. The subjects gave informed consent before entering the study which was also approved by the Faculty Review Board and Ethics Committee. All of the 32 subjects with acute anal ssure, in addition to anal pain complained of ED which started after the onset of the ssure; before that time, they had normal erection. During the sexual act, penile tumescence occurred, but full or rigid erection was rarely achieved and successful vaginal penetration was occasional. The anal pain was experienced at defecation and was radiating to the penis. The anal and penile pain was exaggerated on erection and penile thrusting, and during ejaculation. During the latter process, which occurred in jets, the patients suffered severe anal and penile pain. Of the 21 patients with chronic anal ssure, 16 had ED; tumescence, erection and vaginal penetration were achieved but the patients could not maintain rigid erection. Erection, penile thrusting and ejaculation were associated with mild anal and penile pain. In the acute stage of the chronic anal ssure, all of the 21 patients had ED; vaginal penetration could be achieved only occasionally and was associated with anal and penile pain. The patients had had normal erection before the occurrence of the anal ssure. The 10 healthy volunteers had normal erection and no history of ED in the past or at the time of entering the study. Physical examination with neurological assessment of all the subjects was normal. The results of laboratory work including blood count and hepatic and renal function tests as well as ECG were unremarkable. Methods The bulbocavernosus re ex, 7 the EMG activity of the external (EAS) and internal (IAS) anal sphincters and the BCM as well as the anal, penile bulb and cavernosal pressures were recorded. EMG studies Manometric studies The anal pressure was measured by means of a saline-perfused 10F catheter with two lateral 2 mm side ports and a closed distal end. The catheter was placed into the anal canal 1.5 ± 2 cm away from the anal ori ce and was infused with saline at 37 Cata rate of 2 ml=min. It was connected to a strain gauge pressure transducer (Statham 230B, Oxnard, CA, USA). The pressures in the penile bulb and the corpus cavernosum were measured by means of a 23-gauge needle inserted into either of them and connected to a Statham strain gauge pressure transducer. Erectile dysfunction investigations The endocrine pro le of the studied subjects was normal. Routine erectile function tests 8±11 as well as nocturnal penile tumescence and the penobrachial pressure index test showed normal results. Doppler examination of the penile arteries and cavernosometry were also normal. Treatment of anal ssure Acute anal ssure was treated by conservative measures including sitz baths, stool softeners, bulking agents and a high- bre diet. Chronic anal ssures were treated by lateral internal sphincterotomy. 12 Follow-up The patients were followed for a mean period of s.d. months (range 10 ± 21). They were questioned every month regarding anal and penile pain during sexual intercourse as well as the capability of vaginal penetration and maintenance of rigid erection during penile thrusting. To ensure reproducibility of the results, the aforementioned measurements and recordings were repeated at least twice in the individual subject, and the mean value was calculated. The results were analyzed statistically using the Student's t-test. Differences assumed signi cance at P < 0.05 and values were given as the mean standard deviation (s.d.).

3 Results 281 The study was completed in all subjects with no adverse effects during or after performance of the tests. The bulbocavernosus re ex was normal in the patients with acute and chronic ssure. EMG ndings The EMG activity of the EAS and BCM at rest and on electrostimulation using square wave stimuli of 1 ms duration and separated by 1 ms, was normal in the acute and chronic ssure patients (Figures 1 and 2). The IAS showed an increased resting EMG activity compared with normal controls; the increased EMG activity was more manifest in the acute than in the chronic anal ssure (Figure 3). Figure 2 EMG activity of (a) external anal sphincter and (b) bulbocavernosus muscle upon electrostimulation. Both muscles showed similar activity. S ˆ stimulation. Manometric ndings The anal, bulbar and cavernosal pressures of patients and normal controls at rest are shown in Figure 4 and Table 1. There was a signi cant increase of the anal pressure in both the acute and Figure 1 Resting EMG activity of (a) external anal sphincter, and (b) bulbocavernosus muscle. Both muscles showed similar activity. Figure 3 Resting EMG activity of the internal anal sphincter (a) Normal volunteer, (b) patient with acute anal ssure and (c) patient with chronic anal ssure. Figure 4 Pressure tracing of the anal, bulbar and cavernosal pressures. (a) normal subject, (b) patient with acute anal ssure, and (c) patient with chronic anal ssure.

4 282 Table 1 Anal, bulbar and cavernosal pressures of the acute and chronic ssure patients and of healthy controls* Pressure (cmh 2 O) Anal Bulbar Cavernosal Mean Range Mean Range Mean Range Healthy controls ± ± ± 12 Acute ssure x 94 ± { 9 ± { 9±11 Chronic ssure { 84 ± { 8 ± { 8±11 *Values are given as the mean s.d. {P > 0.05; {P < 0.05; P < P-values of the ssure patients were compared with those of the healthy volunteers. chronic ssure patients (P < 0.01, P < 0.05, respectively), while the bulbar and cavernosal pressures exhibited no signi cant changes (P > 0.05, P > 0.05, respectively) when compared with the normal controls. Treatment results Table 2 shows the results obtained with the treatment of the acute and chronic and ssure. Conservative treatment was successful in 27=32 patients with acute anal ssure. The remaining ve patients were operated upon by lateral internal sphincterotomy. Erectile function normalized in 30=32 patients 3 ± 5 weeks (mean ) after ssure cure, but persisted in the remaining two patients. These two patients belonged to the group of ve with acute ssure who had resisted the conservative treatment and were subjected to lateral internal sphincterotomy. Lateral internal sphincterotomy also failed to cure two patients in the group with chronic anal ssure (Table 2). The erectile function of these two patients did not improve. The remaining 19 patients of this group regained their normal erectile function. All patients who were cured of their ssure no longer have anal or penile pain during the sexual act and can maintain rigid erection. Discussion In the current study ED was encountered in all patients with acute anal ssure and in 76.1% of those with chronic anal ssure. However, all the Table 2 Results of treatment of acute and chronic anal ssure Fissure cure Erectile function No Conservative Surgical Normal Dysfunction Acute Chronic 21 Ð chronic ssure patients had ED in the acute stage. The patients of both groups had had normal erection before the ssure occurred. The erectile function tests were normal; nocturnal penile tumescence was normal due probably to absence of anal pain during REM sleep. After ssure cure, normal erection was achieved in 93.8% of the acute ssure patients and in 90.5% of the chronic anal ssure patients. The ED did not improve in the patients in whom the ssure persisted after treatment. The occurrence of ED in patients with anal ssure and its normalization after ssure cure suggest a causal relationship which requires discussion. A concept of the genesis of ED in anal ssure Anal ssure is associated with IAS spasm which was demonstrated in the current study by the increased IAS EMG activity and elevated anal pressure. The IAS is innervated by the autonomic pelvic plexus. 13 The nerve endings, lying exposed in the ssure appear to be irritated; this leads to pelvic plexus stimulation which is suggested to activate the cavernous nerve. The latter supplies the corpora cavernosa and might be responsible for inducing the penile pain at rest and during erection. It may be argued though, that cavernous nerve stimulation initiates erection. 3 However, it seems that the penile pain aborts the erectile effect of cavernous nerve stimulation, and this might explain the inability of the patient to maintain full or rigid erection during the sexual act. Another factor contributing to causing ED in anal ssure patients appears to be related to its effect on the two cavernosus muscles: BCM and ischiocavernosus. Although in these patients tumescence occurs, they fail to have rigid erection. The latter is produced by contraction of the two cavernosus muscles. 14 Previous studies have demonstrated that during erection the BCM, being an extension of the EAS, contracts simultaneously with the EAS. 1 Contraction of the EAS in presence of a ssure, presumably leads to severe anal pain due to its squeezing effect on the underlying ssure in the

5 anal canal. It is believed that this anal pain aborts the EAS contraction and consequently BCM contraction with a resulting failure of the patient to achieve rigid penile erection. It may be assumed that anal and penile pain inhibit ischiocavernosus muscle contraction. A further route that might be considered in the pathogenesis of ED in the ssure patients are the chemicals that are secreted in association with pain. Pain may stimulate the release of epinephrine and norepinephrine which lead to vasocontraction and ED. Erectile function may also be affected by some of the chemicals that are secreted at the site of the ssure, such as cytokines, proteolytic enzymes, etc. 15 However, we believe that the cause of ED in ssure patients is multifactorial and not necessarily due to a single factor. Ejaculation in the ssure patients was normal though painful. Semen emission in jets indicates the rhythmic activity of the BCM. The penile and anal pain during ejaculation is suggested to be caused by BCM contraction and the associated EAS contractions. The disappearance of pain after ssure cure advocates a possible relationship. In conclusion, a relationship is suggested to exist between ED and anal ssure. Erectile dysfunction occurred in the presence of anal ssure and normalized with its cure. The cause of ED appears to be multifactorial. Anal and penile pain, the BCM, as well as the release of chemicals seem to play a role in the genesis of ED associated with anal ssure. Acknowledgements Margot Yehia and Waltraut Reichelt assisted in the preparation of this manuscript. References 1 Sha k A. The physioanatomic entirety of the external anal sphincter with the bulbocavernosus muscle: a new concept. Arch Androl 1999; 42: 45 ± Sha k A. Response of the urethral and intra-corporeal pressure to cavernosus muscle stimulation. Role of the muscles in erection and ejaculation. Urology 1995; 46: 85 ± Sha k A. Extrapelvic cavernous nerve stimulation in erectile dysfunction. Human study. Andrologia 1996; 28: 151 ± Shirai M, Ishii N. Hemodynamics of erection in man. Arch Androl 1981; 6: 27 ± Andersson KE, Wagner G. Physiology of penile erection. Physiol Rev 1995; 75: 191 ± Sha k A. The injured external anal sphincter in erectile dysfunction. The ano-cavernosal erectile dysfunction syndrome. Andrologia (in press). 7 Siroky MB, Sax DS, Krane RJ. Sacral signal tracing: the electrophysiology of the bulbocavernosus re ex. J Urol 1979; 122: 661 ± Bain CL, Guay AT. Reproducibility in monitoring nocturnal penile tumescence and rigidity. J Urol 1992; 148: 811 ± Metz P, Bengtsson J. Penile blood pressure. Scand J Urol Nephrol 1981; 15: 161 ± Schwartz AN et al. Assessment of normal and abnormal erectile function: color Doppler ow sonography versus conventional techniques. Radiology 1991; 180: 105 ± Wespes E, Delcour C, Struyven J, Schulmann CG. Cavernometry-cavernography; its role in organic impotence. Eur Urol 1984; 10: 229 ± Corman ML. Anal ssure. In: Corman ML, (ed). Colon and Rectal Surgery, 4th edition, Lippincott-Raven: Philadelphia 1998, pp 206 ± Frenckner B, Ihre T. In uence of autonomic nerves on the internal anal sphincter. Gut 1976; 17: 306 ± Lue TF et al. Hemodynamics of erection in the monkey. J Urol 1983; 130: 1237 ± Guyton AC, Hall JE. Pain, headache and thermal sensations. In: Guyton AC, Hall JE, (eds). Human Physiology and Mechanisms of Disease. 6th edition. WB Saunders Co: Philadelphia, 1997, pp 392 ±

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