__Pelvic_Floor_Re_education__Principles_and_Practice__Second_Edition

1.3. The Effects ofPregnancy and Childbirth on thePelvic Floor 41 Urinary Incontinence After Childbirth Wilson et al. examined maternal risk factors for postpartum urinary incontinence and found up to 22% of women complain of urinary incon- obesity to be associated with the development of tinence after delivery.'<\" :\" De novo stress urinary incontinence three months after childbirth.\" incontinence has been reported in 4-19% of Three studies, including a randomized controlled women who gave birth vaginally,\":\" Women who trial, observed that antepartum pelvic floor exer- had prep regnancy ur inary incontinence were cises significantly reduced the prevalence of more likely to complain of dail y incontinence 6 postpartum incontinence. P'\" :\" One study failed weeks and 6 months postpartum.\" Long-term to predict postpartum urinary and fecal inconti- persistence is high; 5 years postpartum, the risk nence with markers of collagen weakness like of urinary incontinence was 92% in women who striae, varicose veins, hemorrhoids, and joint developed symptoms during pregnancy or puer- hyperrnobility,\" perium (Fig. 1.3.2).In women who had remission of incontinence 3 months postpartum, 42% had Anal Sphincter Laceration and recurrence 5 years later.\" Compared with women who delivered by cesarean section, urinary incon- Anal Incontinence tinence is significantly more common after vaginal delivery.F'\":\" Clinically visible anal sphincter tears occur in up to 7% of vaginal deliveries. v\" :\" Studies using Obstetric and Maternal Risk Factors for endoanal ultrasound revealed that there are also Urinary Incontinence occult sphincter defects in 33% of primiparous and 4% of multiparous women after vaginal The literature on the contribution of obstetrical delivery.\" :\" The long-term impact of these occult factors to the development of urinary inconti- sphincter defects is not known. nence is inconsistent. In some studies, the dura- tion of the second stage of labor\" and birth The contraction pressure of the anal sphincter weight\" were associated with a higher incidence decreases significantly after vaginal deliverr7.47.52 of stress incontinence. Other authors did not find and does not return to antenatal strength,\" :\" significant correlation between stress inconti- even after 5 years. \" Anal sphincter pressures at nence, second stage of labor,\":\" or birth weight. rest are reduced after vaginal delivery, but not However, obstetric risk factors, which show a sta- after cesarean section.51.53.54 Resting pressures tistical significant correlation with the inconti- tend to recover 5 weeks to 6 months postpar- nence incidence immediately after delivery, tum,53.54whereas squeeze pressures increase, but might disappear three months later.\" The large might not reach antenatal values, 53particularly if Norwegian Epidemiology of Incontinence in the the anal sphincter was damaged. 54 Anal sphinc- County of Nord-Trendelag (EPINCONT) study ter ruptures can cause decreased contraction asked women more than 30-years-old about pressures compared with spontaneous deliveries incontinence symptoms after their first vaginal without perineal tears .51 The decrement of the delivery. The data were linked with a meticulous resting pressure was significantly greater in birth register. The study confirmed known risk women with a sonographically demon strated factors like age, body mass index, and parity, but internal sphincter defect, and squeeze pressures also demonstrated that birth weight >4,000 g, were lower in women with an external sphincter breech, and instrumental deliver y and epidural defect. \" are obstetric factors that seem to lose their influ- ence on incontinence (if they had any in the first Anal canal sensation assessed by mucosal elec- place), and that the ageing and weight gaining trosensitivity might be impa ired immediately processes take over.\" Forceps deliver y has also after vaginal delivery but seems to recover six been identified to increase the risk of postpartum months postpartum.54 In contrast, two studies urinary incontinence by 50% compared with with 232 women did not observe any changes in vaginal birth.\" anal sensation after vaginal deliver y\":\" After vaginal delivery, 0.04% to 5% of women develop anal incontinence symptoms.18.55.56 This

42 K. Baessler and B. SchUssler prevalence rises to levels of 17% to 57% after anal baby's head vigorously along an undesirable line . sphincter rupture, despite primary repair.48,51,54,57 The vacuum would be lost if not guided in an Even nine to twelve months after vaginal deliv- optimal direction. ery, incontinence of flatus was also more common in women with anal sphincter rupture.58 Most of Subsequent deliveries increase the incidence of these anal symptoms are transient, but might sphincter defects and anal incontinence.t':\" Pro- persist long term.59 Fecal incontinence symp- longed pudendal nerve terminal latency, instru- toms correlated with decreased anal pressures mental delivery, and higher maternal age\" were and sphincter defects imaged by endoanal also associated with an increased risk of post- ultrasound.l':\" partum alteration of fecal continence. Obstetric and Maternal Risk Factors for Although the immediate anal incontinence Anal Incontinence rate is significantly higher after sphincter lacera- tions, it seems that ageing is probably another Several obstetric risk factors for the development important factor in deteriorating pelvic floor of sphincter lacerations have been identified. It function. In a retrospective-matched control is the first vaginal delivery that causes most of study approximately 30 years postpartum, 29 the damage and results more frequently in anal women with anal sphincter disruption were com- sphincter tears.48,50,60 The occipitoposterior pre- pared with 89 women with episiotomy and 33 sentation,\" a higher birth weight,47,48,5o,6o,61 pro- longed second stage of labor,\":\" and maternal women delivered by cesarean section.\"The prev- age of more than 35 years\" were also associated with an increased sphincter laceration rate. An alence of flatus and fecal incontinence did not unchangeable feature - a subpubic arch angle differ significantly in the 3 groups (episiotomy of less than 90 degrees - was associated with group 31%, sphincter rupture group 42.7%, cesar- prolonged labor and the development of anal ean section group 36.4%). The prevalence of fecal incontinence.\" incontinence also did not differ significantly between episiotomy group (18%) and sphincter Sphincter lacerations occur more frequently rupture group (6.9%), but women who were deliv- with forceps-assisted deliveries than with vacuum ered by cesarean section did not develop fecal extraction.47,57,6o,61 Only sonographically visible incontinence.\" Although this study did not occult sphincter defects were also more common include clinical or sonographical examination to after forceps delivery. 51 Fecal incontinence symp- correlate findings and symptoms, the results toms correlate with sphincter defects and are display that successful management of childbirth seen in 38% of women delivered by forceps, in is not the ultimate end of care. Further direction 12% of women delivered by vacuum, and in 4% might be necessary to maintain an initially good of spontaneous deliveries, with a significant dif- outcome. ference between forceps -assisted and spontane- ous delivery.51 In general, the risk of developing Only one protective factor has been described; fecal incontinence is increased after operative Klein et al. showed that a strong exercise profile vaginal delivery\" but more so after use of (e.g. jogging or cycling 3 or more times per week) forceps.\" A systematic review estimated that one was associated with fewer third- and fourth- anal sphincter tear is avoided for every 18 women degree tears.\" who had a vacuum delivery instead of forceps .\" In up to 91% of women who sustained a third- Intrapartum Interventions: Impact on Pelvic degree tear, endoanal sonography showed resi- Floor Anatomy and Function dual sphincter defects indicating an inadequate primary sphincter repair.47,49,64 Routine Mediolateral and Midline Episiotomy Are Obsolete The higher risk of pelvic floor damage when using forceps in contrast to vacuum extraction Woolley67,68 reviewed the literature on the bene- might be explained by the ability to pull the fits and risks of episiotomies from 1980 to 1994. Woolley concluded that a mediolateral or midline episiotomy does not prevent damage to the anal

1.3. The Effects ofPregnancy and Childbirth on thePelvic Floor 43 sphincter and its sequelae . Episiotomy does not one severe tear. This number rises to 106 episiot- protect the newborn from intracranial hemor- omies among multiparas.\" On review of the lit- rhage or intrapartum asphyxia. Episiotomy does, erature, it seems that the mediolateral episiotomy however, prevent anterior lacerations. Midline rate in primiparas can be lowered to 20% and episiotomy carries a significant risk of extension 30%without an increase in anal sphincter damage into the anal sphincter. Episiotomy increases (Fig. 1.3.4),10,71,75 maternal blood loss. In the first week after vaginal delivery, perineal pain is more common after epi- Perineal pain, disturbed wound healing, and siotomy than after a spontaneous perineal lacera- dyspareunia are more common in women deliv- tion . However, these differences disappear by 1 ered by med iolateral than by midline episiotomy month postpartum.F'\" These conclusions are or with spontaneous perineal tear.\" :\" Women still valid; routine and selective midline episioto- belonging to the group with restricted use of epi- mies were associated with higher incidences of siotomy and women with an intact perineum sphincter lacerations'S\" and a reduction in started sexual intercourse earlier.\" the use of midline episiotomies resulted in an increase in the rate of intact perineum.\" Reduced Prospective randomized controlled trials and midline, as well as mediolateral episiotomy rates, retrospective studies have failed to demonstrate resulted in an increase in anterior and vaginal a protective effect of the mediolateral or midline lacerations.61,69-71 episiotomy on stress urinary incontinence after vaginal delivery.I7,70,71There was no difference in Most studies show that mediolateral episioto- stress urinary and anal incontinence rates or mies do not prevent sphincter ruptures.f':\" and a pelvic organ prolapse between women with or systematic and a Cochrane review of randomized without mediolateral episiotomy.\" Viktrup et al. controlled trials comparing restrictive versus found a higher rate of stress incontinence when a routine use of episiotomy concluded that the mediolateral episiotom y was performed.\" The restrictive episiotomy policies are beneficial in incidence of stress urinary incontinence did not terms of posterior vaginal trauma and pain.\" differ after episiotomies compared with sponta- Three retrospective case-control studies reported neous per ineal tears . a protective effect of the mediolateral episiotomy for the occurrence of severe sphincter lacera- Episiotomy did not influence PNTML38,39or the tions.5o,60,74 However, one of these studies calcu- urethral closure pressure.\" It did not result in lated that among primiparas, 48 episiotomies increased or decreased pelvic floor denervation.' would have to have been performed to prevent The ability to hold vaginal cones was more reduced after vaginal delivery when an episiot- omy was performed.\" FIGURE 1.3.4. Different rates ofmediolat- % eral episiotomies in nulliparous women 100 -,~..-. - - - - - - - - - - - - - - - - - - - - with corresponding third- and fourth- degree sphincter tears. It seems obvious 90 +--~-------------------­ thatepisiotomy rates can be restricted to 80 + - - - -, . , - - - - - - - - - - - - - - - - - - - - - - at least 20-30% without an increase in severe sphincter lacerations.s8,71,87-91 70 +-----\"\"\"\"'~III 60 +-------~~------------­ 50 + - - - - - - - - - -'-- . : = - - - - - - - - - - - - 40 .+-----------~-- ...- - - - - - - - - 30 + - - - - - - - - - - - - - - -.....-.....- - - - - - 20 +--------:=-::-----:-,------------:-------,----------,---------:::-:--,--------.......- - - - Thircllfourth degree tear rate (%) 1~ Ds;:~~;;=:~~::;~~;;:~:~=:;;:::;~~

44 K. Baessler and B. Schiissler Upright or Lateral Position for Birth, Perineal In summary, cesarean section is likely to avoid immediate direct trauma to the pelvic floor, as Massage, and Continuity ofCare well as early functional impairment, but long- term protection is not necessarily given. The ben- In several studies, supine or lithotomy position efits of short-term prevention of pelvic floor for childbirth had a negative effect on the dysfunction have to be weighed against the risk perineum.f':\" The adoption of upright pos itions of cesarean section as an operation, as well as the might protect the perineum56,79,8o and tend to psychosocial impacts. reduce forceps-assisted deliveries.\" Perineal massage during the weeks before delivery was The Woman's Contribution to Reduce Loss of shown to reduce the risk of sutured perineal Pelvic Floor Function trauma.\" Perineal massage and gentle stretching during contractions in the second stage of labor Antepartum pelvic floor exercises led to a decline resulted in fewer third-degree tears, but bladder of postpartum stress urinary incontinence'v\" and bowel function did not differ in a random- and an increase in vaginal pressures during vol- ized controlled trial of 1,340 women .\" Adoption untary pelvic floor contraction.\" Obese women of upright birth positions, warm compresses to have a higher risk of urinary incontinence during the perineum, flexion, and counter pressure to pregnancy and postpartum'S\" and several epide- the baby's head may be protective for both use of miological studies have highlighted that obesity episiotomy and occurrence of sphincter lacera- is associated with deteriorating pelvic floor func- tions.\" Continuity of care by midwives during tion. Whether the physiological increase in weight pregnancy, childbirth, and puerperium seems to during pregnancy contributes to incontinence, be beneficial with regard to antenatal hospital for instance, cannot be determined. The odds for admission, analgesia during childbirth, rates of anal sphincter trauma are decreased in women episiotomies, and the woman's satisfaction.\" who regularly pa rticipate in sporting activities like jogging.\" Cesarean Section: Only Partially Protective Immediate postpartum, as well as long-term, Conclusions: Can Vaginal Delivery Be studies have demonstrated that cesarean section might reduce, but not totally prevent, urinary Made Safer for the Pelvic Floor? and anal incontinence. Although cesarean section might prevent direct anal sphincter trauma, both It is evident that pregnancy and childbirth can elective and emergency cesarean section do not result in pelvic floor dysfunction. In everyday necessarily prevent the development of anal life, many precautions against potential damage incontinence.\" :\" Pelvic organ prolapse seemed and injury are taken, but so far no predictive considerably lower after cesarean section. factor for immediate postpartum pelvic floor However, in a rare prospective study before and dysfunction has been established. Even cesarean 6 weeks after childbirth, Sze et al. described stage section does not completely eliminate the risk of II prolapse (rCS standardization) in 32% of 41 pelvic floor dysfunction. Why should women women who had spontaneous vaginal deliveries undergo cesarean section when it does not prevent and in 35% of 26 women after cesarean section pelvic floor symptoms in the long term? Women during active labor. \" have much control over some risk factors. They should stay fit and healthy with a good diet and Pregnancyitselfcaused no changes in PNTML,84 regular low-impact sport, avoid constipation and and although no changes in the motor unit poten- obesi ty, perform antenatal pelvic floor exercises, tials were found after elect ive cesarean section, and consider having babies before the age of 35. they were increased after emergency cesarean sections, when labor had already progressed.' Can vaginal delivery be made safer if midwives Anal sphincter pressures at rest were reduced and obstetricians utilize the available data to after vaginal delivery, but not after cesarean minimize trauma and subsequent pelvic floor section.51,53,54 The same applies to anal canal dysfunction: no midline episiotomies, restrictive sensation.54

1.3. The Effects ofPregnancy and Childbirth on thePelvic Floor 45 use of mediolateral episiotomy for fetal indica- pelvic joint syndrome and developmental dyspla - tions, and vacuum rather than forceps delivery, sia of the hip. The Norwegian Association for continuous care during pregnancy and child- Women with Pelvic Girdle Relaxation (Land- birth, and lateral or upright birth position to foreningen for Kvinner Med Bekkenlosning- reduce instrumental deliveries? Prospective lon- splager). Acta Obstet Gynecol Scand. 1997;76: gitudinal interventional studies are warranted to 760-764. answer these questions . 13. Calguneri M, Bird HA, Wright V. Changes in joint laxity occurring during pregnancy. Ann Rheum References Dis. 1982;41:126-128. 14. Landon CR, Crofts CE, Smith ARB, et al. Mecha- 1. Samuels son E, Victor A, Svardsudd K. Determi- nical properties of fascia during pregnancy: a nants of urinary incontinence in a population possible factor in the development of stress incon- of young and middle-aged women. Acta Obstet tinence of urine. Contemp Rev Obstet Gynaecol. Gynecol Scand. 2000;79:208-215. 1990;2:40-46. 15. Lien KC, Mooney B, DeLancey JO, et al. Levator 2. Uustal Fornell E, Wingren G, Kjolhede P. Factors ani muscle stretch induced by simulated vaginal associated with pelvic floor dysfunction with birth. Obstet Gynecol. 2004;103:31-40. emphasis on urinary and fecal incontinence and 16. Noblett KL, Jensen JK, Ostergard DR. The rela- genital prolapse: an epidemiological study. Acta tionship of body mass index to intra-abdominal Obstet Gynecol Scand. 2004;83:383-389. pressure as measured by multichannel cystome- try. Int Urogynecol J Pelvic Floor Dysfunct. 3. Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemi- 1997;8:323-326 . ology of surgically managed pelvic organ prolapse 17. Viktrup L, Lose G, Rolff M, et al. The symptom of and urinary incontinence. Obstet Gynecol. 1997; stress incontinence caused by pregnancy or deliv- 89:501-506. ery in primiparas. Obstet Gynecol. 1992;79:945- 949. 4. MacLennan AH, Taylor AW, Wilson DH, et al. The 18. Chaliha C, Kalia V, Stanton SL, et al. Antenatal prevalence of pelvic floor disorders and their rela- prediction of postpartum urinary and fecal incon- tionship to gender, age, parity and mode of deliv- tinence . Obstet Gynecol. 1999;94:689-694. ery. BJOG. 2000;107:1460-1470. 19. King JK, Freeman RM. Is antenatal bladder neck mobility a risk factor for postpartum stress in- 5. Rortveit G, Daltveit AK, Hannestad YS, et al. continence? Br J Obstet Gynaecol. 1998;105:1300- Urinary incontinence after vaginal delivery or 1307. cesarean section. N Engl J Med. 2003;348:900- 20. Kristiansson P, Samuelsson E, von Schoultz B, 907. et al. Reproductive hormones and stress urinary incontinence in pregnancy. Acta Obstet Gynecol 6. Nygaard IE, Rao SS, Dawson JD. Anal inconti- Scand.2001;80:1125-1130. nence after anal sphincter disruption: a 30-year 21. Cutner A, Cardozo LD, Benness C], Assessment of retrospective cohort study. Obstet Gynecol. 1997; urinary symptoms in early pregnancy. Br J Obstet 89:896-901. Gynaecol. 1991;98:1283-1286. 22. van Rooyen AJ. Pregnancy and the lower urinary 7. Allen RE, Hosker GL, Smith AR, et al. Pelvic floor tract. I. A study of histological changes in the damage and childbirth: a neurophysiological lower urinary tract during pregnancy. S Afr Med study. B J Obstet Gynaecol. 1990;97:770-779. J. 1969;43:749-753. 23. O'Boyle AL, Woodman PJ, O'Boyle JD, et al. Pelvic 8. Grodstein F, Fretts R, Lifford K, et al. Association organ support in nulliparous pregnant and non- of age, race, and obstetric history with urinary pregnant women: a case control study. Am J Obstet symptoms among women in the Nurses ' Health Gynecol. 2002;187:99-102. Study. Am J Obstet Gynecol. 2003;189:428-434. 24. Sze EH, Sherard GB III, Dolezal JM. Pregnancy, labor, delivery, and pelvic organ prolapse. Obstet 9. Eason E, Labrecque M, Wells G, et al. Preventing Gynecol. 2002;100:981-986. perineal trauma during childbirth: a systematic 25. O'Boyle AL, O'Boyle JD, Ricks RE, et al. The review. Obstet Gynecol. 2000;95:464-471. natural history of pelvic organ support in preg- nancy. Int Urogynecol J Pelvic Floor Dysfunct. 10. Miodrag A, Castleden CM, Vallance TR. Sex hor- 2003;14:46-49. mones and the female urinary tract. Drugs. 1988;36:491-504. 11. Wahl LM, Blandau RJ, Page RC.Effect of hormones on collagen metabolism and collagenase activity in the pubic symphysis ligament of the guinea pig. Endocrinol. 1977;100:571-579. 12. MacLennan AH, MacLennan Sc. Symptom-giving pelvic girdle relaxation of pregnancy, postnatal

46 K. Baessler and B. SchUssler 26. Rizk DE, Thomas 1. Relationship between the 40a. Dolan LM, Hosker GL, Mallett VT, Allen RE, length of the perineum and position of the anus Smith AR. Stress incontinence and pelvic floor and vaginal delivery in primigravidae. Int Urogy- neurophysiology 15 years after the first delivery. necol J Pelvic Floor Dysfunct. 2000:11:79-83. BJOG.2003;110:1107-1114. 27. Wijma J, Weis Potters AE, de Wolf BT, et al. Ana- 41. Iosif S, Ulmsten U. Comparative urodynamic tomical and functional changes in the lower urinary studies of continent and stress incontinent women tract during pregnancy. BJOG. 2001;108:726-732. in pregnancy and in the puerperium. Am J Obstet 28. Wijma J, Potters AE, de Wolf BT, Tinga DJ, Aar- Gynecol. 1981;140:645-650 . noudse JG. Anatomical and functional changes in 42. Farrell SA, Allen VM, Baskett TF. Parturition the lower urinary tract following spontaneous and urinary incontinence in primiparas. Obstet vaginal delivery. BJOG. 2003;110:658-663. Gynecol. 2001;97:350-356. 29. Meyer S, Bachelard 0, De Grandi P. Do bladder 43. Viktrup L, Lose G. The risk of stress incontinence neck mobility and urethral sphincter function 5 years after first delivery. Am J Obstet Gynecol differ during pregnancy compared with during 2001;185:82-87. the non-pregnant state? Int Urogynecol J Pelvic 44. Wilson PD, Herbison RM, Herbison GP. Obstetric Floor Dysfunct. 1998;9:397-404. practice and the prevalence of urinary inconti- 30. Iosif S, Ingemarsson I, Ulmsten U. Urodynamic nence three months after delivery. Br J Obstet studies in normal pregnancy and in puerperium. Gynaecol. 1996;103:154-161. Am J Obstet Gynecol, 1980;137:696-700. 45. Rortveit G, Daltveit AK, Hannestad YS, et al. 31. van Geelen JM, Lemmens WA, Eskes TK, et al. The Vaginal delivery parameters and urinary inconti- urethral pressure profile in pregnancy and after nence: the Norwegian EPINCONT study. Am J delivery in healthy nulliparous women. Am J Obstet Gynecoi. 2003;189:1268-1274. Obstet Gynecoi. 1982;144:636-649. 46. Reilly ET, Freeman RM, Waterfield MR, et al. Pre- 32. Sultan AH, Kamm MA, Hudson CN. Pudendal vention of postpartum stress incontinence in pri- nerve damage during labour: prospective study migravidae with increased bladder neck mobility: before and after childbirth. Br J Obstet Gynaecol, a randomised controlled trial of antenatal pelvic 1994;101:22-28. floor exercises. BJOG. 2002;109:68-76. 33. Rockner G, Ionasson A, Olund A. The effect of 47. Sultan AH, Kamm MA, Hudson CN, et al. Third mediolateral episiotomy at delivery on pelvic floor degree obstetric anal sphincter tears : risk factors muscle strength evaluated with vaginal cones. and outcome of primary repair. BMJ. 1994;308: Acta Obstet Gynecol Scand. 1991;70:51-54. 887-891. 34. Peschers UM, Schaer GN, DeLancey JO, et al. 48. Wood J, Amos L, Rieger N. Third degree anal Levator ani function before and after childbirth. sphincter tears: risk factors and outcome . Aust N Br JObstet Gynaecol. 1997;104:1004-1008. Z J Obstet Gynaecoi. 1998;38:414-417. 35. Peschers U, Schaer G, Anthuber C, et al. Changes 49. Fitzpatrick M, Fynes M, Cassidy M, et al. Prospec- in vesical neck mobility following vaginal deliv- tive study of the influence of parity and operative ery. Obstet Gynecol, 1996;88:1001-1006. technique on the outcome of primary anal sphinc- 36. Meyer S, Schreyer A, De Grandi P,et al. The effects ter repair following obstetrical injury. Eur J Obstet of birth on urinary continence mechanisms and Gynecol Reprod BioI. 2000;89:159-163. other pelvic-floor characteristics. Obstet Gynecoi. 50. lander C, Lyrenas S. Third and fourth degree 1998;92:613-618. perineal tears . Predictor factors in a referral 37. Snooks SJ, Swash M, Mathers SE, et al. Effect of hospital. Acta Obstet Gynecol Scand. 2001;80: vaginal delivery on the pelvic floor: a 5-year 229-234. follow-up. B J Surg. 1990;77:1358-60. 51. Sultan AH, Kamm MA, Hudson CN, et al. Anal- 38. Snooks SJ,Swash M, Henry MM, et al. Risk factors sphincter disruption during vaginal delivery. N in childbirth causing damage to the pelvic floor Engl J Med. 1993;329:1905-1911. innervation. Int J Colorectal Dis. 1986;1:20-24. 52. Chaliha C, Sultan AH, Bland JM, et al. Anal func- 39. Snooks SJ, Setchell M, Swash M, et al. Injury to tion : effect of pregnancy and delivery. Am J Obstet innervation of pelvic floor sphincter musculature Gynecoi. 2001;185:427-432. in childbirth. Lancet. 1984;2:546-550. 53. Small KA, Wynne JM. Evaluating the pelvic floor 40. Tetzschner T, Sorensen M, Rasmussen 00, et ai. in obstetric patients. Aust N Z J Obstet Gynaecoi. Pudendal nerve damage increases the risk of fecal 1990;30:41-44. incontinence in women with anal sphincter 54. Comes H, Bartolo DC, Stirrat GM. Changes in rupture after childbirth. Acta Obstet Gynecol anal canal sensation after childbirth. Br J Surg. Scand. 1995:74:434-440. 1991;78:74-77.

1.3. The Effects ofPregnancy and Childbirth on thePelvic Floor 47 55. MacArthur C, Bick DE, Keighley MR. Faecal delivery? A natural experiment. Am J Obstet incontinence after childbirth. Br J Obstet Gynae- Gynecol 1996;175:897-901. col. 1997;104:46-50 . 70. Sleep J, Grant A, Garcia J, et al. West Berkshire perineal management trial. Br Med J (Clin Res Ed) 56. Zetterstrom JP, Lopez A, Anzen B, et al. Anal 1984;289:587-90. incontinence after vaginal delivery: a prospective 71. Sleep J, Grant A. West Berkshire perineal manage- study in pr imiparous women . Br J Obstet Gynae- ment trial: three year follow up. Br Med J (Clin Res col. 1999;106:324-330. Ed). 1987;295:749-751. 72. Reynolds JL. Reducing the frequency of episioto- 57. Abramo witz L, Sobhan i I, Ganansia R, et al. Are mies through a cont inuous quality improvement sph incter defects the cause of anal incont inence program. CMAJ. 1995;153:275-282. afte r vaginal deliver y? Results of a pro spective 73. Carroli G, Belizan J. Episiotomy for vaginal birth. study. Dis Colon Rectum. 2000;43:590-596 . Cochran e Database Syst Rev. 2000;Cd000081. 74. Anthony S, Buitendijk SE, Zondervan KT, et al. 58. Zetterstrom J, Lopez A, Anzen B, et al. Anal Episiotomies and the occurrence of severe peri- sph incter tears at vaginal delivery: risk factors neal lacerations. Br J Obstet Gynaecol. 1994;101: and clin ical outcome of primary repa ir. Obstet 1064-1067. Gynecol. 1999;94:21-28. 75. Henriksen TB, Bek KM, Hedegaard M, et al. Methods and consequences of changes in use of 59. Haadem K, Gudmundsson S. Can women with episiotomy. BMJ. 1994;309:1255-1258. intrapartum rupture of anal sphincter still suffer 76. Abraham S, Child A, Ferry J, et al. Recovery after after-effects two decades later? Acta Obstet childbirth: a preliminary prospective study. Med Gynecol Scand . 1997;76:601-603. J Aust. 1990;152:9-12. 77. Sartore A, De Seta F, Maso G, et al. The effects of 60. Poen AC, Felt Bersma RJ, Dekker GA, et al. Third mediolateral episiotomy on pelvic floor function degree obstetric perineal tears: risk factors and after vaginal delivery. Obstet Gynecol. 2004;103: the preventive role of mediolateral episiotomy. Br 669-673. J Obstet Gynaecol. 1997;104:563-566. 78. Gardo si J, Sylvester S, B Lynch C. Alternative posi - tions in the second stage of labour: a randomized 61. Klein MC, Janssen PA,MacWilliam L, et al. Deter- controlled trial. Br J Obstet Gynaecol. 1989;96: minants of vaginal-perineal integrity and pelvic 1290-1296. floor functioning in childbirth. Am J Obstet 79. Bofill JA, Rust OA, Schorr SJ, et al. A randomized Gynecol. 1997;176:403-410. prospective trial of the obstetric forceps versus the M-cup vacuum extractor. Am J Obstet Gynecol. 62. Frudinger A, Halligan S, Spencer JA, et al. Influ- 1996;175:1325-1330. ence of the subpubic arch angle on anal sphincter 80. Gupta JK, Hofmeyr GJ. Position for women during trauma and anal incontinence following child- second stage of labour. Cochrane Database Syst birth. BJOG. 2002;109:1207-1212. Rev. 2004;Cd002006. 81. Stamp GE, Kruzins GS. A survey of midwives who 63. Fitzpatrick M, Behan M, O'Connell PR, et al. Ran- participated in a randomised trial of perineal domised clinical trial to assess anal sphincter massage in labour. Aust J Midwifery. 2001;14:15- function following forceps or vacuum assisted 21. vaginal delivery. BJOG. 2003;110:424-429. 82. Hodnett ED. Continuity of caregivers for care during pregnancy and childbirth. Cochrane Data- 64. Poen AC, Felt Bersma RJ, Strijers RL, et al. Third- base Syst Rev. 2000;Cd000062. degree obstetric perineal tear: long-term clinical 83. Lal M, H Mann C, Callender R, et al. Does cesa- and fun ctional results after primary repair. Br J rean delivery prevent anal incontinence? Obstet Surg. 1998;85:1433-1438. Gynecol. 2003;101:305-312. 84. Tetzschner T, Sorensen M, Jonsson L, et al. Deliv- 65. Faltin DL, Sangalli MR, Roche B, et al. Does a ery and pudendal ner ve function. Acta Obstet second delivery increase the risk of anal inconti- Gynecol Scand. 1997;76:324-331. nence? BJOG. 2001;108:684-688. 85. Henderson JS. Effects of a prenatal teaching program on postpartum regeneration of the 66. Oberwalder M, Connor J, Wexner SD.Meta-analy- pubococcygeal muscle. JOGN Nurs. 1983;12:403- sis to determine the incidence of obstetric anal 408. sphincter damage. Br J Surg. 2003;90:1333- 1337. 67. Woolley RJ. Benefits and risk s of episiotomy: a review of the English-language literature since 1980. Part II. Obstet Gyne col Surv. 1995;50:821- 835. 68. Woolley RJ. Benefits and risks of episiotomy: a review of the English-language literature since 1980. Part 1. Obstet Gynecol Surv 1995;50:806- 820. 69. Bansal RK, Tan WM, Ecker JL, et al. Is there a benefit to episiotomy at spontaneous vaginal

48 K. Baessler and B. Schussler 86. Hojberg KE, Salvig JD, Winslow NA, et al. Urinary imminent: the influence on the urethral pressure incontinence: prevalence and risk factors at 16 profile, anal manometric and other pelvic floor weeks of gestation. Br J Obstet Gynaecol. 1999;106: findings-follow-up study of a randomized con- 842-850 . trolled trial. Acta Obstet Gynecol Scand. 2005;84: 65-71. 87. Anonymous . Routine vs selective episiotomy: a ran - 90. Donnelly V, Fynes M, Campbell D, et al. Obstetric domised controlled trial. Argentine Episiotomy events leading to anal sphincter damage. Obstet Trial Collaborative Group. Lancet. 1993;342: Gynecol. 1998;92:955-961. 1517-1518. 91. Sheiner E, Levy A, Walfisch A, et al. Third degree perineal tears in a university medical center where 88. Harrison RF, Brennan M, North PM, et al. Is midline episiotomies are not performed. Arch routine episiotomy necessary? Br Med J (Clin Res Gynecol Obstet. 2005;271:307-310. Ed). 1984;288:1971-1975. 89. Dannecker C, Hillemanns P, Strauss A, et al. Episiotomy and perineal tears presumed to be

1.4 Muscle Function and Ageing Brenda Russell and Linda Brubaker Key Messages it comprises over a third of the body mass and uses adenosine triphosphate (ATP) for its con- Normal muscle physiology in relation to the tractile functions. Nearly 85% of body heat is pelvic floor is discussed to enable an understand- produced as the byproduct of muscle activity, ing of dysfunction of the pelvic floor, particularly making muscle a key player in thermal homeo - of the anal and urethral sphincters, as a conse- stasis . Extensive vascularization perfuses the quence of denervation, vaginal delivery, and tissue to provide oxygen and nutrients and ageing. Clinical, electrophysioiogical, and mag- remove waste. Muscle is also a major endocrine netic resonance imaging (MRI) assessments are organ with an important role in metabolic regu- reviewed, and the mechanisms of repair and lation . Disuse of muscle in quadriplegics, for rehabilitation are outlined. example, leads to type II diabetes . Introduction Gross Anatomical Aspects Several important pelvic functions rely on The gross organization of muscle tissue has the healthy, functioning muscles. The urinary stress familiar bundles of muscle fibers wrapped in continence system includes the striated pelvic connective tissue layers.' These fascial layers are floor muscles and urethral sphincter muscles, slippery so that the muscles slide over each other, with both striated and smooth elements. Support enabling independence in function. Fibers termi- of pelvic organs is also believed to rely on healthy nate firmly on bone or anchor on adjacent fascia muscle functions . This chapter will review clini- so that the force developed by the muscle can be cally relevant aspects of normal and abnormal transmitted to the surrounding structures. In muscle, mechanisms of injury and repair, tech- limb muscles, the ends of the fibers move toward niques for muscle assessment, and opportunities each other when force is produced, resulting in to alter muscle for prevention or treatment of shortening. In situations where both ends are pelvic floor disorders. fixed, no relative movement can occur. This results in isometric contraction for production of Overview ofNormal Skeletal Muscle tension without a change in length, thus, provid- ing support. Muscles are richly innervated so that contraction can be controlled physiologically to shorten and An individual skeletal muscle fiber is a long, provide tension when necessary. Muscle tissue is thin cell with many nuclei. This structure is the major consumer of energy in humans because formed by the fusion of many myoblasts as a fiber develops to make the multinucleated syncytia. There is no limit to the length of a fiber, and a single fiber can span from tendon to tendon in a 49

so B. Russell and L. Brubaker limb muscle, being over a meter long in a tall person. The diameter of a muscle fiber ranges from 10urn in the finger to over 1,000urn in a body builder's biceps. Structure and Function ofNormal Skeletal Muscle Muscle is highly anisotropic, yielding a very dif- FIGURE 1.4.2. Human skeletal muscle cut in cross section and ferent appearance in the longitudinal and trans- stained with a myofibrillar ATPase to show slow type Ifibers as verse planes of section. In the longitudinal dark and fast type II fibers aslight. Note the polygonal shape of orientation, with light microscopy we see that the thefibers and the mosaic mixture between thetypes. Scale bar, bulk of the muscle fiber is striated (Fig. 1.4.1).The 50 um, (Source: Brenda Russell, University ofIllinois at Chicago.) dark bands are called the A-bands, and the light bands are called the I-bands. In the middle of the microscopy' reveals details about the striations I-band it is also possible to see the thin, dark Z- and other organelles (Fig. 1.4.3). The striations line. The unit of contraction is the sarcomere, are composed of interdigitating thick and thin which is defined between two adjacent Z-lines. In filaments bundled into myofibrils. The thick cross-section, the fibers are circular or polygonal myofilaments in the A-band are composed mainly (Fig. 1.4.2). Ultrastructure seen with electron of myosin molecules and the thin myofilaments in the I-band are polymers of actin. The thin myofilaments are anchored at the Z-line and extend into the A-band. The H-zone is the paler central region of the A-band into which the thin filaments have not penetrated. There are numer- ous additional molecules in the sarcomere, whose functions are to modulate contraction, transmit force effectively, sense mechanical changes, FIGURE 1.4.1. Light micrograph ofskeletal muscle in longitudinal FIGURE 1.4.3. Low-power electron micrograph ofrabbit skeletal section. Whitevastus muscle oftheguinea pig. Light micrograph muscle in longitudinal section. (Source: Reprinted from Williams of plastic-embedded muscle cut in a O.S-cm-thick longitudinal PL. Grays Anatomy. 38th edition. 742. Copyright 1996 Churchill section. Fibers are striated with A-bands (dark) and l-bands Livingston, with permission from Elsevier.) (light). Note peripherally located nuclei (n) and connective tissue (CT). Scale bar 10 um, (Source: Reproduced with permission from Eisenberg, 1983.)

1.4. Muscle Function and Ageing Sl signal the need for adaptation, and regulate outer sarcolemal membrane with the release of assembly and disassembly in training or calcium from the inner membrane reticulum to disuse.':\" initiate contraction (Fig. 1.4.4). A series of small transverse tubules (T-tubules) open to the extra- Contraction occurs when the thick and thin cellular space at the sarcolema and envelop the filaments slide past each other, making a shorter myofibrils twice, each sarcomere at the ends of sarcomere with the I-band becoming smaller. the A-band. The T-tubules carry the action poten- Note that the filaments do not change in length. tial from the muscle surface to the interior of the The molecular motors driving this contraction fiber. The endoplasmic reticulum is a separate are the myosin cross-bridges, which cyclically inner membrane system, called the sarcoplasmic bind, rotate, and detach from the actin filaments reticulum, which surrounds the myofibrils over using energy provided by ATP hydrolysis. The the ir entire length and pumps, stores, and releases force generated throughout the fiber at the bil- calcium ions. The excitation spreads inwards lions of cross-bridges is transmitted by the intra- through the T-tubule triggers and releases cellular and extracellular cytoskeleton. Forces go calcium via the junction between the T-tubules longitudinally through the ends of the fiber and and sarcoplasmic reticulum. The pumps that laterally to the membrane at the Z-disc. return the calcium to the reti culum are located throughout the sarcoplasmic reticulum. Fat Muscle fibers have a very extensive membrane system that fun ction to link the excitation of the TRIAD ! ...ITOCHONDRIA \" FIGURE 1.4.4. Schematic three-dimensional diagram showing thesubcellular structure ofskeletal muscle. (Source: Reproduced from The Journal ofCell Biology 1974;60:732-754, by copyright permission ofthe Rockefeller University Press.)

52 B. Russell and L. Brubaker droplets and glycogen store energy, and rows of mitochondria lie in close proximity to the myofi- brils, ready to supply ATP for the contractile process . Normal Skeletal Muscle Adaptation Normal muscle is highly adaptive so that the FIGURE 1.4.5. Diagram showing innervation of a slow, type I molecular composition and size of the fibers can (dark) and fast, type II (light) fibers. When thenerve iscut (indi- be changed to match the needs of the person over cated by scissors in middle panel) the slow fibers atrophy. The time. Thus, training can easily increase the fiber denervated fibers are later reinnervated by sprigs from a surviv- strength by enlarging the fiber diameter, and ing motor neuron and convert thefibers from theiroriginal slow improve endurance by increasing blood flow, tothenew fast (dark) fibers resulting in agroup offibers with the mitochondrial content, and oxidative capacity. same fiber type and loss ofthe normal mosaic pattern. (Source: Conversely,disuse causes fiber atrophy and limits Adapted from figure provided by Brenda Russell, University of ability. In extreme situations, the speed of con- Illinois atChicago.) traction can be altered by exchange of the iso- forms of the contractile proteins.v' human, the fast-twitch muscle fibers are predom- inantly type IIX and IIA, but type IIB fibers Individual fibers can be evaluated by tech- with very low oxidative capacity are seldom niques such as histochemistry, biochemistry, found. Human fast fiber characteristics include molecular biology, morphology, or physiology. moderate to high concentrations of mitochon- Quantification by these methods has yielded dria, fast myosin ATPase, and variable glycogen enormous heterogeneity of function in the human content. muscles. Nonetheless , it has been useful to lump these functions and classify broad fiber types. Skeletal muscles perform complex motor func- The relative proportion of fiber types within a tions . Those muscles lying deep or close to the muscle varies from person to person and is partly bones provide posture and sustain tension over determined by genetics. However, this ratio can long periods of time and are predominantly slow- be modified with exercise and training. twitch. The most superficial muscles often have higher leverage over the joints and are recruited Muscle fibers that contract at a relatively slow to perform rapid voluntary movements, such as speed and can sustain activity over long periods throwing. These fibers in human are predomi- without loss of tension are called type I, slow- nantly fast-fatigable type IIX. However, most twitch, slow-oxidative, or slow fatigue-resistant muscles perform mixed functions and normally fibers. They generate energy via aerobic metabo- have different fiber types intermixed in a mosaic lism from both fat and carbohydrates. Slowfibers pattern (Fig. 1.4.5). have a high concentration of mitochondria, increased intracellular myoglobin to store and Within the Pelvic Floor transport oxygen, and a rich capillary bed. Myo- globin, mitochondria, and blood all contain red The pelvic floor and the sphincter muscles pigments, so these slow fatigue-resistant muscles contract constantly, except during voiding or are red. defecation. \" This requires strength and fatigue resistance, but not speed, so as expected, these A twitch with a rapid contractile rise time fibers have a high percentage of slow type 1 fibers. defines the second major group as fast fibers, The pelvic floor muscles act as a functional group which are also known as type II fibers. They have to keep the vagina, urethra, and anal canal closed myosin ATPase enzymes with a rate of shorten- while at rest. A pelvic muscle contraction assists ing 3 to 5 times that of slow muscle fibers. Fast with stabilization of the urethra and raises ure- type II fibers are further subdivided into types IIA, IIB, and IIX, according to their metabolism and fatigue-resistant properties. Small lab ani- mals and humans differ in these fast subtypes. In

1.4. Muscle Function and Ageing 53 thral pressure.\" Changes in muscle function metabolism to sustain it, changes in those genes occur as a result of ageing and vaginal delivery. can also compromise cardiac and skeletal muscle function. These SNPSs are more common than In normal women, the urethral sphincter also one might imagine, but are often masked until a contracts continuously, except during voiding, second event, such as trauma or extreme exer- again, being best served by slow fatigue-resistant cise, or a pathological incident further stresses type I fibers.t'\" With cough, the intraurethral the muscle. pressure increases more and before the bladder pressure increases.\" It is believed that disrup- Neural tions in this urethral responsiveness may playa role in stress urinary incontinence.\" In limb A common reason for lack of muscle function is muscles, repetitive muscle contractions can cause pathology of innervation. This can be from any fatigue .\" Verelst et al. found no differences in the of the major neurological diseases, such as mul- time to fatigue between continent and stress tiple sclerosis, but it can also arise from trauma incontinent women.\" to the spinal cord or peripheral nerves. Recovery depends on regeneration and reprogramming of Mechanisms ofSkeletal the motor recruitment pathways. Muscle Weakness Cardiovascular Anything that affects production and trans- It is often forgotten that continuous oxygenation mission for useful mechanical work also limits is essential for endurance because of the constant muscle function. Normal skeletal muscle func- demand for fuel by muscle fibers. Thus, pati- tion obviously requires the motor machinery to ents with heart failure, pulmonary problems, or contract, but also depends on innervation to anemia will have secondary locomotor difficul- provide the correct patterns of motor unit recruit- ties with continuous exercise, although short ment, vascular flow to provide the oxygen, and bursts are feasible. Regional blood flow can be an intact connective tissue and skeleton for useful compromised by many factors, including trauma transmission of force. or diabetes, which secondarily affect peripheral nerves. Mechanical and Myopathic Damage Muscle Repair and Rehabilitation Extreme exercise, overstretch, or trauma can Cellular Mechanisms of Repair damage muscle tissue. IS In the pelvic floor region, vaginal delivery with ripping of the muscle at its Muscle has a great ability to repair itself, and insertion or in the center is a common traumatic complete recovery can be expected as long as the injury. Also, the birth process, with its extreme underlying nerve and vascular systems are func- demands on endurance and partial nerve or tional. Muscle fibers have a population of adult vascular damage, might be expected to reduce stem cells called satellite cells.\":\" One in about muscle performance that would be further exac- every 20 muscle nuclei are actually these dormant erbated by underlying genetic differences. satellite cells locally situated under the base- ment membrane, but not actually fused into the There have been great advances in genetic syncytium of the muscle fiber.\" Local injury understanding in muscle diseases in the past elicits an inflammatory response that is maximal decades. Many single nuclear polymorphisms at 3-5 days and which triggers these satellite (SNPSs) have been identified in myopathies cells to divide and to fuse with an adult fiber and reproduced in transgenic mouse models.\" in the immediate vicinity.\" Major damage results Although over half of these genetic changes have in the migration of satellite cells from surround- been found in contractile proteins, they also ing healthy fibers. Note that research on affect force transmission, such as dystophin in adult stem cells is currently very active and the muscular dystrophy. Given the importance of calcium handling to trigger contraction, and of

54 B.Russell andL.Brubaker proliferation, mobilization, targeting, and differ- Clinical Aspects ofRehabilitation entiation into skeletal muscle is being rapidly characterized.\" There is much hope that deeper The pelvic floor muscles may be a primary or understanding of these processes will permit secondary target of muscle rehabilitation. For improvement of repair in the future. most pelvic floor disorders, these muscles are a primary target, and are trained with progressive If a muscle tissue is strained to a breaking strengthening programs that eventually incorpo- point , satellite cells will fuse and bridge the gap rate real-life strategies for using muscles to reduce to reconnect healthy portions on the distal and urinary incontinent episodes. There is no con- proximal ends of the injury. The greatest amount sensus for the optimal technique, although a of muscle repair occurs at the ends of the fibers,\" wide variety of programs appear to be adequate although there is also repair in the central clinically. Long-term compliance remains a chal- regions. P'\" lenge.\" Pelvic muscle training may also be a sec- ondary target as part of trunk stabilization Denervation leads to loss of muscle control and programs.P:\" Interested readers are referred to muscle atrophy. However, the denervated motor these primary sources for further information. endplate regions are readily innervated by ingrowing dendrites from nearby healthy nerves . Research in this area is often challenging There is also potential for the formation of because pelvic muscle training is typically only entirely new motor endplates by incoming axons . a part of the overall nonsurgical intervention. The reinnervated muscle fiber will receive the Commonly, a myriad of low-risk, but potentially pattern of activity from the newly connected high-impact, behavioral techniques are recom- nerve and the fiber will change its type to meet mended simultaneously with muscle training. this new pattern. This sprouting of nerves can This is most logical from a clinical care stand- result in groups of neighboring fibers sharing point. However, to date, the most important identical innervation and, hence, leading to a aspect of this treatment \"package\" remains group of one kind of fiber rather than the usual unclear. mosaic seen in cross-section (Fig. 1.4.6). Clinical Assessment FIGURE 1.4.6. Human skeletal muscle ofa patient with a long- Clinical assessment of muscle function is impor- standing denervation disorder. The muscle is cut incross-section tant for planning treatment, as well as for pelvic and stained with a myofibrillar ATPase toshow slow type Ifibers floor research. There is no consensus on the asdark and fast type II fibers aslight. Note thatthenormal mosaic optimal method of muscle measurement for clin- pattern has been replaced by denervation and reinnervation. ical or research purposes. There are several methods for assessing pelvic muscle function, Scale bar100 urn. (Source: Brenda Russell, University ofIllinois at including vaginal palpation, vaginal pressure measurement, electromyography, and transanal Chicago.) palpation. Although imaging plays a role, it remains a research tool at this time and will not be reviewed in detail here. Digital assessment is often performed in a casual clinical manner and may be sufficient for gross assessment of muscle function and symmetry. Several scoring systems are available for further refinement of the digital assessment. All of these hands-on measures have undergone some degree of testing, but none of them qualify or are accepted as the gold standard for assessing pelvic muscle function. Vaginal palpation is the most commonly used method of assessing pelvic muscle function because it is simple to perform, requires no equip-

1.4. Muscle Function and Ageing ss ment, and costs little. Two methods for palpation EMG using surface patches.f:\" The Oxford have been described in the literature; the Oxford system and pressure perineometry in continent grading system\" and the Brink scale.\" women has not shown good correlation in the single small study reporting these results.\" The Oxford grading system applies a 6-point Vaginal dynamometers and perineometers categorical scale (0 = nil, 1 = flicker, 2 = weak, have been introduced in an effort to provide a 3 =medium, 4 =strong, and 5 =very strong) for more standardized assessment of pelvic floor muscle strength. Morin et al. reported their rating pelvic muscle strength. Determination of experience in 89 premenopausal women who pelvic muscle strength using the Brink scale is underwent a standardized assessment using the based on three muscle contraction variables; modified Oxford grading system and a dynamo- intensity of the \"squeeze\" generated by the muscle metric speculum.\" These investigators confirm contraction, vertical displacement of the exa- prior reports that digital grading often results in miners fingers as the muscles lateral to the clinical overlap.\" They reported that the correla- vagina contract, and duration of the muscle tion between the modified Oxford grading system contraction. and the dynamometric assessment was moderate to good . Bo and Finckenhagen reported the interrater reliability of the Oxford scale and compared Magnetic Resonance Imaging has been used Oxford ratings with vaginal pressure measures for pelvic muscle assessment by several investiga- obtained from a vaginal balloon device using a tors.\":\" DeLancey has reported MRI evidence of small sample of young females with a mean age levator abnormalities in nearly 30% of women of 25 years, mostly nulliparous, and the majority following vaginal delivery.\" In a subset of such without symptoms of pelvic floor dysfunction.\" women, Miller et al. reported that women without The Oxford scale had only fair intertester agree- visible pubococcygeus muscle in MRIs are less ment. Vaginal squeeze pressure, measured by the likely to be able to voluntarily increase their ure- balloon device, did not differ between women thral closure pressure greater than 5em H20 categorized as having weak, moderate, good, or on standardized urodynamic sphincter assess- strong muscle contractions; however, the study ment.\" Although the clinical significance of such was limited by the small sample size. findings requires further analysis, clearly the pubococcygeus is an important pelvic muscle . Brink et al. reported the interrater reliability, Hoyte et al.\" has highlighted the differences in test-retest reliability, and validity of the Brink levator ani thickness in asymptomatic and symp- scale from a sample of 208 women attending pre- tomatic women using color thickness mapping treatment clinic visits. Test-retest had moderate technique (Fig. 104.7, A and B).However, given the correlations (r= 0.51-0.65) for pressure, displace - expense of these investigations, MRI is not cur- ment, duration, and total score. Interrater reli- rently recommended as a clinical tool. ability in 36 women was also moderate, ranging from 0.52 for duration to 0.74 for pressure. Bo et al. have reported a small series of female physical therapists who were assessed by tradi- A combined approach using visual and digital tional palpation techniques, as well as ultra- assessment was tested for interobserver reliabil- sound.\" In addition, they compared two sets ity in two groups of women, continent and in- of instructions - one aimed at the transverses continent.\" These investigators reported high abdominis and one aimed at pelvic floor muscles. reliability in both groups. One commonly cited They suggest that in such healthy women, ultra- limitation of digital grading systems is the lack sound is more valid than palpation and that of discrimination between clinically important instructions aimed at pelvic floor muscles are groups.32-35 Comparisons of the digital methods more useful than instructions aimed at trans- have been compared with intravaginal pressure verses abdominis muscles. Aswith much research measurements with conflicting findings .t\":\" in pelvic floor muscle assessment, this finding awaits reproduction in a clinical population. Electromyographic (EMG) measures of pelvic Thompson and O'Sullivan used ultrasound in muscle strength typically use intravaginal surface probes that may receive signals from other pelvic muscles, such as gluteus or adductors. Digital assessments are only modestly correlated with

56 B. Russell and L. Brubaker o Clinical Relevance Fron Vaginal parity affects the appearance and func- tion of the pelvic floor muscles.Y\" Multiple authors have reported statistically significant decreases in the pelvic floor muscle strength of incontinent women compared with continent controls. 51-53 Bo compared the pelvic floor muscle RighI strength of physical educat ion students in Norway and was unable to detect significant differences in strength in her small sample.\" In several clini- cal case series, investigators have reported that women may not correctly perform a voluntary contraction of their pelvic floor muscles.P \":\" mm Front F-Ught Opportunities for Prevention or Clinical Treatment FIGURE 1.4.7. A. Areconstructed levator is shownin brown, with the symphysis (S). Views of the front, left, and right sides are Several investigators have assessed the role of shown. In thefront view, theinner layerfaces thelabell, and the pelvic muscle training in the prevention of symp- outer layer faces thelabel O. Additional images and video can be toms, especially during pregnancy\"? ' In addi- found online at www.us.elsevierhealth.com/ajog. B. Three views tion , one novel randomized trial assessed the ofa color-mapped levator areshown. The color bar on the left effect of pelvic muscle training on the duration shows thethickness (in millimeters) corresponding to thecolors of the second stage oflabor, finding that although seen. Additional images and video can befound online at www. training did not reduce the duration of the second us.elsevierhealth.com/ajog. (Source:Reprinted from Hoyte et al. stage overall, women in the training group had a Copyright 2004, with permission from Elsevier.) lower rate of prolonged second stage labor (train- ing group 34% vs. no training 21%}.62 104women with incontinence and/or prolapse to assess levator plate movement.\" The relationship Kegelis credited with the first observation that between the instructions to elevate the levator a structured tra ining program may reduce clini- plate and the ultrasound appearance was variable cal symptoms of incontinence.\" He described a and inconsistent. Relationships to specific clini- strengthening program that is now known to cal conditions, such as prolapse, require further increase muscle tone and may elevate or improve analysis. However, the investigators raise aware- support of the pelvic organs in selected women. ness that muscle dysfunction may playa role in the genesis, propagation, or treatment outcomes A recent Cochrane review concludes that pelvic of common pelvic floor disorders such as pro- floor muscle exercise is consistently superior to lapse and incontinence. Bernstein reported that no treatment (or placebo).\" Miller et al. report ultrasound is able to detect increasing muscle that performing a voluntary contraction of the thickness in women who are compliant with pelvic floor muscles before and during increases pelvic muscle training.\" He also confirmed that in abdominal pressure reduced cough leakage by levator muscles are thicker in asymptomatic 73-98%, depending on the strength of the cough.\" women than those with stress urinary inconti- A separate Cochrane review regarding weighted nence. This finding is consistent with the later vaginal cones for urinary incontinence suggests work using MRI techniques. that there may be a role for these devices in con- servative treatment.\" These reviewers recom- mend that larger, well-conducted studies should be performed in order to detect differences in several techniques of muscle training. The optimal techniques for muscle training in the pelvis are not established. However, experts

1.4. Muscle Function and Ageing 57 agree that individualized programs are essential. The regenerative properties of most tissues Such programs must take into account the current decline with age because of changes in the stem skills and strength of the individual woman, and cells and to environmental cues from the sur- further strength training must be specific for rounding extracellular matrix. The finding that each individual. Sapford et al. report that con- youthfulness can be returned to old satellite cells traction is associated with an increase in pelvic has long been known to depend on the age of the floor muscle activity in health volunteers.\" Saps- tissue matrix, which is partially attributable to ford et al. further reported that abdominal con- the finding that remodeling of the extracellular traction is a normal response to pelvic floor hydrolytic and proteolytic systems differs in exercises in health subjects.\" Neumann and Gil muscles of old animals compared to young also reported this finding.\" Thus, the often taught animals.\" In muscle, satellite cell activation and technique of abdominal relaxation during pelvic cell fate determination are controlled by the muscle contraction may be incorrect. In Neumann Notch signaling pathway,\" Interestingly, the and Gil's small series of four nulliparous lean reduced activation and proliferative capacity of women, testing was performed twice, one week satellite cells in the elderly human population apart; they noted that strong pelvic floor muscu- means that the same bout of exercise leads to a lar contractions invariably activated the abdomi- smaller increase in muscle mass and damage is nal wall muscles. To date, these findings have not much less readily repaired.\" These ageing pro- been reproduced in a clinical population. Saps- cesses may be tightly coupled to the muscle- ford emphasizes the importance of trunk stabili- specific growth factors, which are important for zation in training\" although this belief has not the division of the satellite cells.\" undergone scientific testing. Beliefs and biases strongly impact descriptions of pelvic floor Clinical Impact ofMuscle Dysfunction muscle training, similar to the impact of expert opinion and bias in many other areas of pelvic Striated urethral sphincteric contraction is an floor health. This area is ready for multiple high important part of maintaining normal conti- quality research trials to determine the optimal nence . It may also play a role in compensatory techniques for pelvic muscle training . techniques for maintaining continence. This is particularly true during moments of increased Normal Ageing Changes abdominal pressure, such as cough. This has led investigators to describe the \"cough anal Systemic changes in the nerve and cardiovascular reflex.'>6,n systems result in concomitant decline in muscle function.\" However, the muscle fibers themselves The role of muscle dysfunction in pelvic floor become atrophic because some growth factors and disorders is often discussed as an important etio - hormones decline with age.\" At present, there are logical contributor. Stress urinary incontinence intense studies on growth hormones to enhance is increasingly recognized as a neuromuscular muscle growth with age and in disease. The hope disorder with concomitant anatomical altera- for a boost in the muscle growth rate that can tions. Regardless of \"which came first,\" measur- compensate for the deficits in muscular dystro- able neuromuscular dysfunction is documented phies is a major instigator for these hypertrophy by multiple modes of evaluation. studies. The insulin growth factor has muscle- specific isoforms that are clearly important for Amarenco et al. describe the relationship increasing muscle mass.\" Furthermore, in males, between intravesical pressure and pelvic floor testosterone jumps as puberty begins, but reverses muscle electromyographic activity using both in the latter decades oflife, which can be compen- urodynamic assessment and electrophysiologic sated for by anabolic and natural steroids. None- techniques. In a small series, 16women who were theless, the major application for muscle mass referred for frequency and/or urgency without increases is in the sports industry where steroids urge or stress incontinence underwent urody- and other drugs are widely abused. namics with patch electrodes recording from the three and nine o'clock perianal positions.\" At

58 B. Russell and L. Brubaker five different volumes (0, 100, 200, 300, and 400) in modeling. However, DeLancey et al. have a series of successively increasing coughs oc- previously pointed out the limitations of cer- curred. These investigators report a close rela- tain embalming techniques and the significant tionship between the intravesical pressure (used artifacts that may arise from measurements to compare the intensity of the cough effort) and and observations using cadaveric specimens the integrated perianal EMG signal. Theyreported that have been embalmed in the supine, non- that bladder filling did not alter the recruitment suspended positions.\" curve, but, instead, the perianal EMG signal increased only with increases in intravesical Conclusion pressure. The muscles of the pelvic floor are an intriguing Aukee et al. reported their series of 31 women area of physiology.In health, these muscles assist with urodynamic stress incontinence and a com- with pelvic functions, including urinary and parable group of 35 women without urinary bowel control, as well as sexual function. In symptoms.\" Using vaginal EMG measures, they disease, these muscles may suffer from primary recorded three rapid contractions in both supine muscular injury or secondary dysfunction when and standing positions . They reported a signifi- neuropathy is present. Given their central role in cant difference across groups, with incontinent pelvic floor health , continued emphasis on under- women demonstrating a lower mean decrease in standing the anatomy, physiology, and patho - EMG activity with the standing position (incon- physiology is important. Research regarding the tinent, 12.9 [5.0-33.0] vs. continent, 18.2 [8.0- optimal methods of muscle assessment will be an 43.5]). Because of the small number of subjects essential prerequisite to meaningful prevention and the use of a relatively indirect assessment and clinical treatment. Our understanding of with the vaginal EMG probe, they could not optimal clinical treatment requires high-quality substantiate further claims about muscle clinical trials in well-characterized populations. dysfunction. However, their data is suggestive of differences between groups by continence status . Future Directions References Multiple investigators are creating three- 1. Salmons S. Striated muscle . In: Gray's Anatomy. dimensional models of the pelvic muscles to 38th Edition. Bannister LH, Berry MM, Collins P, simulate the clinical situations of birth and et aI., editors. London: Churchill Livingstone; surgery with the hope of further understanding 1995:739. the pathophysiology ofpelvicfloordisorders.P'\":\" Our understanding of pelvic muscle morphology 2. Eisenberg BR. Section 10.Quantitative ultrastruc- and function is critical to the accurate creation of ture of mammalian skeletal muscle . In: Handbook appropriate models. Janda et al. describe their of Physiology. Peachey LD and Adrian RH, editors. efforts to obtain a complete data set to describe Bethesda, MD: American Physiological Society; the morphological parameters of the pelvic floor 1983:73112. muscles structures using a single embalmed cadaver from a 72-year-old female. Through a 3. Russell B, Motlagh D, Ashley WW. Form follows carefully described series of sequential tech- function: how muscle shape is regulated by work. niques, the investigators attempted to measure J Appl Physiol. 2000;88:1127-1132. and summarize muscle parameters for all muscles and all muscle elements of the levator ani 4. Tidball JG. Mechanical signal transduction in complex.\" These investigators have demon- skeletal muscle growth and adaptation. J Appl strated the technical feasibility of transferring Physiol. 2005;98:1900-1908. cadaveric data to an MRI data set for ultimate use 5. Eisenberg BR, Salmons S. The reorganization of subcellular structure in muscle undergoing fast to slow type transformation: a stereological study. Cell Tissue Res. 1981;220:449-471. 6. Deindl FM, Vodusek DB, Heese U, et al. Activity patterns of pubococcygeal muscles in nulliparous continent women . Br J Urol. 1993;72:46-51.

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60 B. Russell and L. Brubaker 35. Herbison GJ,Cohen ME, et al. Strength post-spinal Estrogen receptor studies. Neururol Urodyn . cord injury: myometer vs. manual muscle test. 1997;16:237-275. Spinal Cord. 1996;34:543-548. 48. Miller JM, Perucchini D, Carchidi LT, et al. Pelvic floor muscle contraction during a cough and 36. Hahn I, Milsom I, Ohlsson BL,et al. Comparative decreased vesical neck mobility. Obstet Gynecol. assessment of pelvic floor function using vaginal 2001;97:255-260. cones, vaginal digital assessment and vaginal 49. Peschers U, Schaer G, Anthuber C, et al. Changes pressure measurements. Gynecol Obstetric Invest. in vesical neck mobility following vaginal deliv- 1996;41:269-274. ery. Obstet Gynecol. 2001;88:1001-1006. 50. Haderer JM, Pannu HK, Genadry R, et al. Contro- 37. Kerschan-Schindl K, Uher E, Wiesinger G, et al. versies in female urethral anatomy and their sig- Reliability of pelvic floor muscle strength mea- nificance for understanding urinary continence: surement in elderly incontinent women. Neuro- observations and literature review. Int Urogyne- urol Urodyn . 2002;21:42-47. col J. 2002;13:236-252. 51. Gunnarsson M. Pelvic floor dysfunction: a vaginal 38. Bo K, Fickenhagen HB. Vaginal assessment of surface EMG study in healthy and incontinent pelvic floor muscle strength: Inter-test reproduc- women. Lund, Sweden: Lund University; 2002. ibility and comparison between assessment and 52. Hahn I, Milsom I, Ohlson BL, et al. Comparative vaginal squeeze pressure. Acta Obstet Gynecol assessment of pelvic floor function using vaginal Scand. 2001;80:883-887. cones, vaginal digital palpation and vaginal pres- sure measurement. Gynecol Obstetric Invest. 1996; 39. Romanzi L, Polaneczky M, Glazer HI. Simple test 41:269-274. of pelvic muscle contraction during pelvic exami- 53. Morkved S, Salvesen K, Bo K, et al. Pelvic floor nation: Correlation to surface electromyography. muscle strength and thickness in continent Neurourol Urodyn. 1999;18:603-612. and incontinent nulliparous women. Neurourol Urodyn . 2002;21:358-359. 40. Dumoulin D, Bourbonnais D, Lemiuex M-C. 54. Bo K, Stien R, Kulseng-Hanssen S, et al. Clinical Development of a dynameter for measuring the and urodynamic assessment of nulliparous young isometric force of the pelvic floor musculature. women with and without stress incontinence Neurourol Urodyn. 2003a;22:648-653. symptoms: a case-control study. Obstet Gynecol. 1994;84:1028-1032. 41. Thompson DL, Smith DA. Continence nursing: a 55. Benvenuti F, Caputo GM, Bandinelli S, et al. Reed- whole person approach. Holist Nurs Pract. ucative treatment of female genuine stress incon- 2002;16:14-31. tinence. Am J ofPhys Med. 1987;66:155-168. 56. Bo K, Larsen S, Oseid S, et al. Knowledge about the 42. Thompson JA,O'Sullivan PB. Levator plate move- ability to correct pelvic floor muscle exercises in ment during voluntary pelvic floor muscle con- women with urinary stress incontinence. Neurou- traction in subjects with incontinence and rol Urodyn. 1988;7:261-262. prolapse: a cross-sectional study and review. Int 57. Hesse U, Schussler B, Frimberger J, et al. Effective- Urogynecol J. 2003;14:84-88. ness of a three step pelvic floor reeducation in the treatment of stress urinary incontinence: a clini- 43. DeLancey JO, Kearney R, Chou Q, et al. The cal assessment. Neurourol Urodyn. 1990;9:397- appearance oflevator ani muscle abnormalities in 398. magnetic resonance images after vaginal delivery. 58. Kegel AH. Stress incontinence and genital relax- Obstet Gynecol. 2003;101:46-53. ation. Ciba Clin Sympos. 1952;2:35-51. 59. Morkved S, Bo K, Schei B,et al. Pelvic floor muscle 44. Miller JM, Umek WH, DeLancey JOL, et al. Can training during pregnancy to prevent urinary women without visible pubococcygeal muscle in incontinence: a single-blind randomized con- MR images still increase urethral closure pres- trolled trial. Obstet Gynecol. 2003;101:313- sures? Am J Obstet Gynecol. 2004:171-175. 319. 60. Reilly ET,Freeman RM, Waterfield MR, et al. Pre- 45. Hoyte L, Jakab M, Warfield SK, et al. Levator ani vention of postpartum stress incontinence in pri - thickness variations in symptomatic and asymp- migravidae with increased bladder neck mobility: tomatic women using magnetic resonance-based a randomised controlled trial of antenatal pelvic 3-dimensional color mapping . Am J Obstet and floor exercises. BJOG. 2002;109:68-76. Gynecol. 2004;191:856-861. 46. Bo K, Sherburn M, Allen T. Transabdominal ultra- sound measurement of pelvic floor muscle activity when activated directly or via a transversus abdo- minis muscle contraction. Neururol Urodyn . 2003; 22:582-588. 47. Bernstein IT. The pelvic floor muscles: muscle thickness in healthy and urinary-incontinent women measured by perineal ultrasonography with reference to the effect of pelvic floor training.

1.4. Muscle Function and Ageing 61 61. Sampselle CM, DeLancey JO. The urine stream 73. Bar-Shai M, Carmeli E, Coleman R, et al. The interruption test and pelvic muscle function . Nurs effect of hindlimb immobilization on acid phos- Res. 1992;41:73-77. phatase, metalloproteinases and nuclear factor- kappaB in muscles of young and old rats . Mech 62. Salvesen KA, Morkved S. Randomised controlled Ageing Dev. 2005;126:289-297. trial of pelvic floor muscle training during preg- nancy. BMJ. 2004;329:378-380. 74. Conboy 1M, Rando TA. Ageing, stem cells and tissue regeneration: lessons from muscle. Cell 63. Kegel AH. Progressive resistance exercise in the Cycle. 2005;4:407-410. functional restoration of the perineal muscles. Am J Obstet Gynecol. 1948;56:238-249. 75. Goldspink G, Harridge SD. Growth factors and muscle ageing. Exp Gerontol. 2004;39(10):1433- 64. Hay-Smith E, Bo K, Berghmans L, et al. Pelvic 1438. floor muscle training for urinary incontinence in women. Available in the Cochrane Library [data- 76. Machida S, Booth FW. Insulin-like growth factor base on disk and CD ROM) . Updated quarterly. 1 and muscle growth: implication for satellite cell The Cochrane Collaboration, 2001. proliferation. Proc Nutr Soc. 2004;63:337-340. 65. Miller JM, Ashton-Miller JA, DeLancey JO. A 77. Bo K, Stien R. Needle EMG registration of striated pelvic muscle precontraction can reduce cough - urethral wall and pelvic floor muscle activit y related urine loss in selected women with mild patterns during cough, Valsalva, abdominal, SUI. J Am Geriatr Soc. 1998;46:870-874. hip adductor, and gluteal muscle contractions in nulliparous healthy females. Neurourol Urodyn. 66. Herbison P, Plevnik S, Mantle J. Weighted vagi- 1994;13:35-41. nal cones for urinary incontinence. [update of Cochrane Database Syst Rev. 2000;(2):CD002114; 78. Amarenco G, Ismael SS, Lagauche D, et al. Cough PMID: 10796862). Cochrane Database of System- anal reflex: strict relationship between intravesi- atic Reviews, 2002;1. cal pressure and pelvic floor muscle electromyo - graphic activity during cough. Urodynamic and 67. Sapsford RR, Hodges PW. Contraction of the pelvic electrophysiological study. J Urol. 2005;173:149- floor muscles during abdominal maneuvers. Archs 152. Phys Med Rehab. 2001;82:1081-1088. 79. Aukee P, Penttinen J, Airaksinen O. The effect of 68. Sapsford RR, Hodges PW, Richardson CA, et al. ageing on the electromyographic activity of pelvic Co-activation of the abdominal and pelvic floor floor muscles. A comparative study among stress muscles during voluntary exercises. Neurourol incontinent patients and asymptomatic women. Urodyn .2001;20:31-42 . Maturitas. 2003;44:253-257. 69. Neumann P, Gill V. Pelvic floor and abdominal 80. Janda S, van der Helm FC, de Blok SB. Measuring muscle interaction: EMG activity and intra- morphological parameters of the pelvic floor for abdominal pressure. Int Urogynecol J.2002;13:125- finite element modelling purposes. J Biomech. 132. 2003;36:749-757. 70. Brooks SV, Faulkner JA. Skeletal muscle weakness 81. Parikh M, Rasmussen M, Brubaker L, et al. Three in old age: underlying mechanisms. Med SciSports dimensional virtual reality model of the normal Exerc. 1994;26:432-439. female pelvic floor. Ann Biomed Eng. 2004;32: 292-296. 71. Goldspink G, Harridge SD. Growth factors and muscle ageing. Exp Gerontol. 2004;39:1433-1438. 82. DeLancey JO, Sampselle CM, Punch MR. Kegel dyspareunia: levator ani myalgia caused by over- 72. Goldspink G. Age-related loss of skeletal muscle exertion. Obstet Gynecol. 1993;82:658-659. function; impairment of gene expression. J Mus- culoskelet Neuronal Interact. 2004;4:143-147.

1.5 Urinary Incontinence and Voiding Dysfunction Annette Kuhn and Bernhard Schussler Key Messages sphincter control of these two organs is a manda- tory prerequisite for adequate social behavior. In this chapter, normal bladder function and its neurological control, as well as the types of incon- The hardware driving these reflexes consists tinence, are classified and explained. Voiding of different centers within the central nervous dysfunction is similarly classified, and its symp- system, as well as of a network of autonomous toms, etiology, and outline of treatment are and somatic nerves; as a consequence , the system presented. involves smooth and skeletal muscles. Introduction Based on careful perception of an individual's bladder cycle during filling, storage, and voiding, a few examples may help for a better understand- ing of the close entanglement of all of these structures: Physiological bladder function consists of two • No sensation at the very beginning of bladder phases; the storage phase, defined by the Interna- filling indicates a central threshold of bladder tional Continence Society (ICS) as \"the phase in perception. which the bladder volume increases without a significant rise in pressure (accommodation),\" • First sensation of the fluid in the bladder and and the voiding phase as when \"a bladder con- its voluntary suppression is carried out by the traction is initiated and bladder neck, urethra, cortical control mechanism. and pelvic floor are relaxed in synchrony.\"! • Earlier and more intensive urgency to void in These definitions are what they should be: situations of psychic agitation apparently indi- short, precise, and easy to comprehend. In con- cates connections to emotional areas within trast, the physiological mechanism of bladder the brain. This mechanism is also active in sit- function is complicated and not yet completely uations when the bladder is adequately filled elucidated. and voiding is urgently intended, but the indi- vidual could not voluntarily initiate the process It consists of two separate reflex circuits for because of social embarrassment (e.g, passing storage and voiding, which the cortical brain is urine during urodynamic assessment) . able to control and modify. This voluntary inter - ference is distinct from most other visceral • Voluntary suppression of an urgent need to organs, such as the heart, intestine, etc., which void by contracting the pelvic floor muscle for are regulated exclusively by involuntary (auto- a short period of time, relaxation of the pelvic nomic) reflexes. As with the anal sphincter, corti - floor as a mandatory prerequisite for the initia- cal control highlights the fact that voluntary tion of voiding, and the ability to interrupt voiding voluntarily by a contraction of the 62

1.5. Urinary Incontinence and Voiding Dysfunction 63 pelvic floor muscles all indicate a connection fibers. These circuits act as \"On/Off' switches between the autonomous system and the skel- that are controlled by the presence or absence of etal muscle system and brain, the latter one glutamate at the level of the sacral micturition further highlighted by recent PET studies that center. The central control of these reflexes is revealed that the most medial portion of the located in the brain stem at the pontine micturi- motor cortex is activated during pelvic floor tion center and the pontine voiding center. contraction.' The pelvic parasympathetic nerves, which Physiology ofStorage and arise at the sacral level of the spinal cord, excite Voiding Phase the bladder. The thoracolumbar sympathetic nerves, which arise at the thoracolumbar level of As shown in Figure 1.5.1, A and B, storage and the spinal cord, inhibit the bladder body and voiding of urine is controlled by 2 reflex arcs and excite the bladder base and urethra. The puden- involve descending nerves, the thoracolumbar dal nerves, which arise at 53-55 (Onuf's nucleus), sympathetic and pelvic parasympathetic nerves, excite the urethral sphincter. Direct somatic the pudendal nerves, and the afferent nerve nerve branches, which stem from the same area, excite the pelvic floor muscles. All of these nerves contain sensory (afferent) fibers. Pontine micturition centre External External Pudendal B sphincter nerve A sphincter FIGURE 1.5.1. A. Storage reflex.During thestorage phase, disten- B. Voiding reflex. During elimination of urine, intense bladder sion of the bladder produces low-level vesical afferent firing, afferent firing activates spino-bulbo-spinal pathways passing which stimulates the sympathetic outflow ofthe bladder outlet through the pontine micturition center, which stimulates the and pudendal outflow to the external urethral sphincter. These parasympathetic outflow to the bladder and inhibits thesympa- responses occur by spinal reflex pathways and represent \"guard- thetic and pudendal outflow to the urethral outlet. (Source: ing reflexes,\" which promote continence. (Source : Adapted with Adapted with permission from Abrams PH, Cardozo L, Khoury 5, permission from Abrams PH, Cardozo L, Khoury 5,Wein A, editors. Wein A, editors. Incontinence. Plymouth, UK: Health Publication Incontinence. Plymouth, UK: Health Publication Ltd.; 2005:370.) Ltd.; 2005:370.)

64 A. Kuhn and B. Schiissler During storage of urine while glutamate is pathway to the urethra that triggers the release of present at Onuf's nucleus, distension of the nitric oxide, which is an inhibitory transmitter, bladder wall produces low-level vesical afferent and by the removal of adrenergic and somatic firing, which in turn stimulates sympathetic cholinergic excitatory inputs to the urethra.' outflow to the bladder outlet (bladder neck and urethra) and outflow of the pudendal nerves to Studying these reflexes by constantly measur- urethral sphincter and direct branches to the ing intravesical pressure during filling and pelvic floor respectively, increasing the tone of voiding parallel to a sphincter/pelvic floor elec- smooth and skeletal muscle at these sites. These tromyograph (EMG), as well as uroflow, illus- responses occur by spinal reflex pathways and trates how these reflex circuits interact with each represent the \"guarding reflexes,\" which promote other in harmony (Fig. 1.5.2 A). continence. It is further enhanced before a cough and other events challenging the continence As already mentioned, centers above the mechanism, thus, preparing the sphincter mech- pontine micturition center control and volun- anism adequately. Sympathetic firing also in- tarily interfere with these two reflex circuits. hibits the detrusor muscle and modulates Although lesions in this area are not able to transmission in bladder ganglia. A region in the abolish the reflex activity, they do, however, dis- pontine storage center increases urethral sphinc- connect cortical interference. This is why patients ter activity (Fig. 1.5.1 A). with cortical brain damage (e.g., after a stroke) may suffer from detrusor overactivity and/or may During elimination of urine while glutamate is lose the ability to delay voiding at an appropriate absent, intense bladder afferent firing activates place and time. Lesions below the pontine mictu- spino-bulbo-spinal pathways passing through rition center and above the level of the sacral the pontine micturition center, which stimulates reflex arc, as they occur in paraplegic patients, the parasympathetic outflow to the bladder lead to reflexincontinence combined with a detru- muscle and internal sphincter smooth muscle, sor sphincter dyssynergia (Fig. 1.5.2 B). thus, inhibiting the sympathetic and pudendal outflow to the urethral outlet (Fig. 1.5.1 B). Recently, interest has been focused on the layer as a further independent mode of bladder func- Relaxation of the urethral smooth muscle is tion . To date, there is good evidence, at least from also mediated by activation of a parasympathetic animal data, that there are local interactions between the smooth muscle, urothelium, afferent 60 60 Parapleg ic Bladder pressure Bladder pressure 0 0 EMG EMG A 0 100 200 300 0 100 200 300 B FIGURE 1.5.2. A. Voluntary voiding response in an adult. On the bladder and sphincter is abolished and detrusor sphincter leftsideofthe trace thearrows indicate the startofthe bladder dyssynergiaoccurs. During bladder filling, transient uninhibited filling. Note increased pelvic floor activity (EMG) with increas- bladder contractions occur in association with sphincter activity. ing bladder filling. No pelvic floor activity during voiding is Further filling leads to more prolonged and simultaneous physiological. (Source: Reproduced with permission from contractions ofthe bladder and sphincter. (Source: Reproduced Abrams PH, Cardozo L, Khoury S, Wein A, editors. Incontinence. with permission from Abrams PH, Cardozo L, Khoury S, Wein A, Plymouth, UK: Health Publication Ltd.; 2005:371.) B. Voiding in editors. Incontinence. Plymouth, UK: Health Publication Ltd.; a paraplegic patient. The reciprocal relationship between 2005:371.)

1.5. Urinary Incontinence and Voiding Dysfunction 65 nerve terminals, and various neurotransmitters. increase this pressure, as could contraction of the The result seems to be an information system for striated sphincter muscle. The situation changes the central nervous system and for phasic activity when physical stress (e.g., sneezing and cough- of the bladder wall during filling . The latter might ing) increases the intraabdominal pressure dra- be able to better explain the phenomena of matically and, depending on its extent, easily bladder wall compliance, as it is not yet well exceeds any urethral closure pressure. The intact- understood how the bladder is able to keep ness of the following two mechanisms is critical: normal bladder pressure increments as low as the \"guarding reflex,\" which actively increases 30-40 em H20 during bladder filling of 400 ml muscle tone, and the simultaneous passive trans- and more. mission of the abdominal pressure (e.g. during a cough) to the urethra. It is obvious that the greater Incontinence the loss of pressure transmission to the urethra the greater the likelihood of stress incontinence. Incontinence is a pathological condition of the It is also clear that a very low resting closure storage phase and could be divided into func- pressure needs excellent pressure transmission tional and anatomical types. Various epidemio- to maintain continence. Pressure transmission logical studies have shown that stress urinary is dependent not only on muscle tone but also on incontinence is the predominant type. Its preva- the elasticity of the connective fibers both within lence has been shown to range between 27-50%Y and adjacent to the muscle. The laxer and more The overactive bladder syndrome (OAB) ranges mobile the pelvic floor and urethra are, the less between 14%5 and 26%,6 and patients suffering likely it is that continence is maintained in a stress from mixed incontinence, e.g. a combination of situation. stress urinary incontinence and the OAB, con- tribute between 22%4 and 55% .6 When stress urinary incontinence occurs it is the result of three main causes: Overflow incontinence is a rare form of urinary incontinence, especially in females, mostly a 1. Pregnancy and delivery (see Chapter 1.3) result of a longstanding overdistension of the 2. Ageing (see Chapter 1.4) bladder either by subvesical obstruction, e.g. pro- 3. The individual continence threshold (see lapse or obstructive incontinence surgery, or caused by bladder denervation following radical Chapter 1.5, Fig. 1.5.2). pelvic surgery. It is obvious that the lower the individual thresh- Fistulae, as well as remnants of the embryonic old, the more an individual is prone to develop kidney system, may also lead to incontinence, but stress urinary incontinence later in life. are not functional disorders. There is good evidence that the closure thresh- Stress Urinary Incontinence old varies individually. This is supported by data from young nulliparous female athletes who Stress urinary incontinence is defined by the ICS present evidence for sphincter insufficiency in as the complaint of involuntary leakage on effort high-impact situations. Urine leakage occurred or exertion, or on sneezing and coughing, at the in 50% of them while playing tennis, 67% during absence of any bladder contraction.' This implies gymnastics, and 29% during athletics.\" that weakness of the urethral closure mechanism is the underlying pathology of this condition. There are other risk factors besides high- impact sports, such as pregnancy,\" parity, and an At rest, involuntary urinary leakage is pre- increased body mass index.P'\" as well as influ- vented by the maximum urethral closure pres - ences such as cigarette smoking, hysterectomy, sure, which ranges between 50 and 80 ern H20 and and menopause, but evidence in support of these decreases with age.' As the bladder pressure - factors is mixed.\" as a result of bladder wall compliance - is kept very low, even when the bladder is full, very low As stress continence is the result of ade- urethral closure pressures are sufficient for con- quate urethral closure pressure and a stabilized tinence. Voluntary pelvic floor contraction could urethra at the very moment when stress occurs, decreased closure pressure (intrinsic urethral insufficiency) and hypermobility, both of which can occur with a funneled bladder neck, are the

66 A. Kuhn and B. Schussler Increased bladder neck mobility AB FIGURE 1.5.3. A. Anormal competent sphincter unit keeps the urethra closed during physical stress (e.g. coughing) despite a certain mobility ofthe urethra. B.Hypermobility ofthe urethra and bladder neck during physical stress (e.g. coughing) can lead to an opening ofthe urethra and bladder neck despite an ade- quate activity ofthe urethral sphincter. C. Decrease in urethral sphincter activity can lead to an opening of the urethra and ( bladder neck without increase of normal mobility of the urethra. critical challenges to continence. When stress pubic bone. Consequently, this form of stress urinary incontinence occurs, either ofthese issues urinary incontinence is often combined with may be the underlying pathology alone, but it is voiding disorder. usually a combination of both (Fig. 1.5.3,A-C). Overactive Bladder Syndrome It is obvious that in patients with stress urinary incontinence caused by a low-pressure urethra Overactive bladder syndrome is defined by the (intrinsic sphincter insufficiency) alone, physio- ICS as any involuntary detrusor contraction therapy is less likely to be successful. The same during the filling phase, which may be spontane- is true for another entity of stress urinary incon- ous or provoked, and that the patient cannot tinence that is often the final result of recurrent completely suppress .' incontinence surgery or pelvic irradiation. In these cases, the urethra is scarred and completely The OAB occurs either with (OAB/wet) or immobile, mostly fixed to the back surface of the without (OAB/dry) urinary leakage. Overactive

1.5. Urinary Incontinence and Voiding Dysfunction 67 TABU 1.5.1. Common causes for the development ofanoveractive bladder Gynecological Prolapse Pregnancy Urological Pelvic surgery Radiation Infections Atrophy Endocrine Pelvic mass Medical Intravesical tumor, Carcinoma in situ Psychological Interstitialcystitis Chronic urinary retention Tuberculosis Bladder calculus or other foreignbodies Urinarytract infection Diabetes mellitus Diabetes insipidus Drugs Congestiveheart failure Impaired renal function Neurological disorders Anxiety Drinkinghabit bladder syndrome/wet refers to motor and much earlier and without the ability of the indi- sensory urge incontinence, whereas OAB/dry vidual to suppress the need to void. The best refers to frequency and urgency syndrome with example for sensory urge incontinence is an acute the unsuppressible need to void as a predominant urinary tract infection. OAB/dry mayor may symptom. The maximal capacity of the bladder not be accompanied by autonomous detrusor is almost always reduced. Consequently, these contractions. patients suffer from a bothersome increased daytime and nighttime frequenc y. Frequency and Mixed Incontinence urgency caused by high fluid intake (which is fashionable today and sometimes exceeds more Mixed incontinence is a combination of stress than three liters per day) is not a pathological urinary incontinence and overactive bladder. It condition, as long as bladder capacity at micturi- has been defined by the Ies as the complaint of tion is normal. involuntary leakage of urine associated with urgency and also with exertion and effort, like The etiology of the OAB is not completely sneezing or walking.' The diagnosis is usually understood today. Although there are diseases made after careful review of the patient's history. that are accompanied by OAB, in the majority of In patients with a predominant motor urge incon- patients it is an idiopathic condition (Table tinence component presenting with a low bladder 1.5.1). capacity, care has to be taken to diagnose mixed incontinence. In these cases, neither the patient's Urodynamically, two different forms ob OAB/ symptoms nor clinical examination or urody- wet could be dist inguished: Motor urge inconti- namics are able to categorize the stress compo- nence and, very rarely, sensory urge inconti- nent correctly. nence. In motor urge incontinence, an involuntary detrusor contraction leads to a rise in bladder Between individuals with mixed incon - pressure and, hence , to an immediate inconti- tinence, both components vary in regard to nence episode. High-pressure motor urge epi- the extent of the incontinence and the bother to sodes are more likely to be affiliated with the patient, which has implications for the neurological diseases. treatment. Sensory urge incontinence totally mimics the voiding phase apart from the fact that it occurs

68 A. Kuhn and B. Schussler Voiding Dysfunction It commonly presents with residual urine of at least 50% of normal capacity. Voiding in the female occurs as a result of a syn- chronized autonomic contraction of the detrusor An acute retention is the condition of a palpa- muscle and relaxation of urethral smooth and skel- ble or percussable bladder when the patient is etal muscles. Although relaxation of the pelvic unable to pass any urine and requires catheter- floor muscle is necessary for an unimpeded mictu- ization. Whether it is painful or painless depends rition, voluntary gradual contraction is able not on the neurological status of the patient. only to steer urine outflow but also to influence the direction of the urine stream. Increasing the The etiology of voiding dysfunction is repre- abdominal pressure by a Valsalva maneuver also senting defects at any conceivable level of contributes to an increase in urine flow. the normal micturition reflex, expanding from mechanical infravesical obstruction as the most Retention occurs when the basic mechanism common cause via muscular and neurogenic fails, e.g., when the detrusor is unable to contract, failure up to psychogenic causes (Table 1.5.3). the urethra fails to relax, additional infravesical resistance is present, or when there is a failure in Voiding dysfunction, even if it is caused by the synchronization of detrusor contraction and infravesical obstruction, does not exclude symp- urethral relaxation. toms of any kind of urinary incontinence, and the patient may end up with incontinence once Voiding normally leads to an empty bladder the pressure of the overdistended bladder wall without residual urine. However, constant resid- exceeds urethral pressure (overflow inconti- ual urine whatever the origin and its extent is, is nence) . Based on the underlying pathology, a medical concern only if leading to symptoms physiotherapy may play an important role in that can mimic a variety of other lower urinary reestablishing micturition or improving voiding tract pathology (Table 1.5.2). dysfunction. Pelvic floor relaxation techniques may not only improve detrusor/pelvic floor dys- Although not as prevalent as in men, voiding synergia conditions but also emptying of a hypo- difficulties in women are not uncommon, with contractile bladder. prevalence rates of 12-17%.14.15 Prevention and Treatment Chronic retention is the condition of a non- painful bladder that remains palpable or per- Prevention or early recognition of retention may cussable after the patient has passed urine. avoid long term voiding difficulties. Not only TABLE 1.5.2. Classification of voiding difficulties and retention Condition Symptom Asymptomatic voiding difficulty Frequency Symptomatic voiding difficulty Urgency due tourinary infection ornosymptoms Acute retention Poor stream Chronic retention Incomplete emptying Straining Acute chronic retention Frequency Painful orpainless Sudden onset Reduced sensation Hesitancy Straining tovoid Frequency, nocturia Urgency, incontinence Urinary tract infection Painful orpainless Sudden onset Incontinence Source: Modified from Shag and Dasgupta, 2002.\"

1.5. Urinary Incontinence and Voiding Dysfunction 69 TABLE 1.5.3. Etiology of voiding dysfunction Mechanism Etiology Postsurgical causes Any continence procedure orsurgery close tothebladder neck can provoke retention by physical obstruction and postoperative edema. Prolapse Acute inflammation Because ofurethral kinking, cystourethrocelemay cause inability tovoid,\" Pharmacological Patients with acute vulvitis, cystitis, urethritis may retain urine because ofpainful micturition. Age Tricyclic antidepressants, alpha-adrenergic substances, anticholinergics and spinal orepidural anesthetic. Widespread degenerative changes inall components ofthedetrusor, assmooth muscle cells and axons are the Neurological Fowler'ssyndrome morphological equivalent for impaired contractility. Detrusor/pelvic floor Upper orlower motor neurone disease Aprimary defect within thestriated urethral sphincter which ishypertrophied and fails torelax.\" dyssynergia This isa learned orfunctional voiding dysfunction, which sometimes isalso called nonneurogenic neurogenic bladder. Psychogenic The patient contracts her pelvic floor while there isa detrusor contraction, which leads toanintermittent stream Infravesical obstruction and high micturition pressure. Psychogenic causes for impaired voiding are well known in hysteria.,,·1. Endocrine Urethral stenosis is uncommon infemale patients, butpossible after traumatic catheterization. Distal urethral stenosis may becaused by urogenital atrophy in postmenopausal women. Extrinsic causes for obstruction may beflbrolds,\" Diabetic neuropathy long-time but also acute overdistension of the 3. Bennett BC, Kruse MN, Rappolo IR, et al. Neural detrusor may result in chronic voiding disorders control of urethral outlet activity in vivo: the role of nitric oxide. I Urol. 1995;53:2004-2009. because of detrusor muscle damage.\" 4. Diokno AC, Brock BM, Brown MB, et al. Preva- Therefore, surgery which may lead to voiding lence of urinary incontinence and other urologic difficulties, e.g. incontinence operations or ex- symptoms in the noninstitutionalized elderly. tensive reconstructive or radical pelvic surgery, I Urol. 1986;136:1022-1025. will require prophylactic postoperative bladder drainage. Suprapubic catheterization is superior 5. Hannestad YS, Rortveid G, Sandvik H, et al. A to a transurethral catheter, as it allows easy community base epidemiologicalsurvey of female trials of postoperative voiding without traumatic urinary incontinence: the Norvegian EPICONT transurethral recatheterization if voiding at- study. I Clin Epidemiol. 2000;53 :1150-1157. tempts are unsuccessful. The catheter can be clamped and unclamped according to the patient's 6. Wells TI, Brink CA, Diokno AC. Urinary inconti- progress. nence in the elderlywomen:clinical findings. I Am If adequate voiding could not be reestablished, Geriatr Soc. 1987;35:933-939. clean intermittent self-catheterization is the primary treatment for long-term voiding diffi- 7. Sorensen 5, Waechter PB, Constantinou CE, culties. Patients who are properly counseled by professional staff will easily learn the technique, Kirkeby HJ, Djuruus JC. Urethral pressure which allows them to lead an independent, and pressure variations in healthy fertile and normal life. postmenopausal women with reference to the Sacromodulation involves stimulation of the S3 root using a nerve stimulator. Encouraging female sex hormones. JUrol. 1991;146(5):1434- early results have been reported. 1440. References 8. Nygaard IE, Thompson FL, Svengalis SL, et al. 1. Abrams P, BlaivasIC, Stanton SL. Standardization Urinary incontinence in elite nulliparous athletes. of terminology of lower urinary tract function. Obstet Gynecol. 1994;84(3):342. Neurourol Urodyn. 2002;21:167-178 . 9. Hunskaar S, Arnold EP, Burgio K,et al. Epidemiol- ogy and natural history of urinary incontinence. 2. Blok BF, Willemsen AT, Holstege G. A PET study Int Urogyn I Pelvic Floor Dysfunct. 200;11:301- on brain control of micturition in humans . Brain. 319. 1997;120:111. 10. Rortveit G, Daltveit AK, Hannestad YS, et al. Urinary incontinence after vaginal delivery or caesarean section. New Engl I Med. 2003;348: 900-907. 11. Sampselle CM, Harlow SD, Skurnick I, et al. Urinary incontinence predictors and life impact in ethnically diverse perimenopausal women. Obstet Gynecol. 2002;100(6) :1230-1238.

70 A. Kuhn and B. Schussler 12. Sampselle CM,Hunskaar S, Burgio K, et aI. Epide- 16. Monga AK, Woodhouse C, Stanton SL. A case of miology and natural history of urinary inconti- simultaneous urethral and ureteric obstruction. nence. In: Incontinence. Second edition. Abrams Br J UroI. 1996;77:606-607. P, Cardozo L, Khoury S, et al., editors. Plymouth, UK: Plymbridge Distributors Ltd.; 2002. 17. Fowler CJ, Kirby RS. Abnormal electromyographic 13. Shag PJR, Dasgupta P. Voiding difficulties and activity in the striated urethral sphincter in 5 retention in Clinical Urogynaecology. Stanton SL, women with urinary retention. Br J UroI. 1985;57: Monga A, editors. London: Churchill Livingstone; 67-70. 2000. 18. Barrett DM. Evaluation of psychogenic urinary retention. J UroI. 1978;120:191-192. 14. Stanton SL, Ozsoy C, Hilton P. Voiding difficulties 19. Krane R, Siroky M. Psychogenic voiding dysfunc- in the female: prevalence. Clinical and urody- tion In: Clinical neurourology. Krane R, Siroky M, namic review. Obstet GynecoI. 1983;61:144-147. editors. Boston: Little, Brown & Co; 1978:275- 284. 15. Brieger GM, Yip SK, Lin LY, et aI. The prevalence 20. Dean AM, Worth PHL. Female chronic urinary of urinary dysfunction in Hong Kong Chinese retention. Br J UroI. 1985;57:24-26. women. Obstet GynecoI. 1996;88:1041-1044.

1.6 Pelvic Organ Prolapse Peggy A. Norton Key Messages ing, lower back pain, which improves after lying down, and dyspareunia. Unlike urinary and fecal In this chapter, the prevalence of prolapse and incontinence, POP is difficult to assess in study the causative factors are reviewed. Important fea- populations by symptom questionnaire; this tures of the clinical examination are described, means that for epidemiological or outcome and the objective Pelvic Organ Prolapse Quanti- research into POP an examination is the only way fication (POP-Q) and Schussler Quantitative to assess whether a woman has the condition or systems of clinical examination are illustrated not. Two quality of life instruments specific to and explained. POP have been described;' although these instru- ments correlate with physical findings in women Introduction with POP presenting for evaluation, they have not been validated as outcome measures or as popu- Pelvic organ prolapse is a common clinical entity lation screening tools. that may affect 1 in 3 women, where the pelvic structures lose their support and descend to and Etiology and Risk Factors beyond the vaginal introitus. In the United States, it accounts for 3 times as many surgical procedures Similar to other pelvic floor disorders, the etiol- as stress urinary incontinence, despite the fact that ogy of POP is multifactorial.' The biggest risk much of the condition is managed without surgery,' factor remains childbirth injury, but contribut- The number of women who seek treatment for ing factors include conditions of chronic increased pelvic floor disorders is expected to increase by intraabdominal pressure: chronic pulmonary approximately 50% in the near future.' disease (asthma, COPD), chronic constipation, obesity, and occupations involving heavy lifting. 5 Clinical Findings The natural history of POP remains to be described; it is known that some women have Pelvic organ prolapse includes defects of the significant levels of pelvic organ descent without anterior vaginal wall (cystocele), vaginal apex symptoms, and that some women have identifi- (uterine prolapse, vaginal vault prolapse, and able defects that do not progress over many years enterocele), and posterior vaginal wall (rectocele of observation. Several large-scale studies have and enterocele.) The major symptoms associated included a physical assessment for POP with with POP include a sensation of fullness, pres- some surprising findings; 30% of parous women sure, bulging, or a lump in the vagina or at the in the Heart and Estrogen/Progestin Replace- introitus. Patients report difficulties with voiding ment study had a cystocele to within 1em of the or defecation, which is sometimes relieved by hymenal ring, and of these, only 30% were symp- splinting with a finger or thumb to effect empty- tomatic. Thus, an anatomical finding of descent 71

72 P.A. Norton from \"normal\" pelvic support may have no clini- cal significance unless the woman has associated symptoms. Examination A vaginal examination with a speculum is neces- FIGURE 1.6.1. The pelvic organ prolapse quantification system for sary for the evaluation of POP. Abivalve Graves or description ofpelvic organ prolapse. In POP-Q, all measurements a Sims speculum is used to identify the cervix or arerelative tothehymen.The two anterior vaginal wall measure- vaginal cuff after hysterectomy, and is withdrawn ments areAa and Ba. Aa isthepoint 3 cm cephalad (internal) from while the woman bears down until the point of external urethral meatus, meant to represent thelocation ofthe maximum descent is reached (i.e., the cervix or bladder neck. Ba is thepoint in theanterior wall which descends cuff descends no further). All distances are mea- most. The apical measurements areC, D, and total vaginal length sured in centimeters relative to the hymenal ring, orTVL. Cmeasures the position the uterine cervix orinthecase the remnants of which can be identified in all of hysterectomy, thevaginal cuff, while Dmeasures theposterior women. Although the vaginal apex (cervix or fornix when theuterus is present. The two posterior vaginal wall cuff) is optimally found at 8-10 ern above the measurements are Ap and Bp. Ap is thepoint 3 cm cephalad from hymenal ring, there can be considerable descent theposterior forchette (at thehymen), and Bp isthatpoint in the toward the hymen without symptoms. The poste- posterior wall which descends most. Additionally, genital hiatus rior vaginal wall is retracted with a Sims specu- (gh) and perineal body length (pb) are recorded.' lum or the posterior half of a Graves speculum, while watching the anterior wall descend to its stage 0 being no prolapse, and stage I being pro- maximum point, and is used again to retract the lapse less than stage II (not to within 1cm of anterior wall while watching the posterior wall the hymenal ring.) Although some specialist descend. Finally, the genital hiatus (distance from gynecologists would prefer a system with more midurethra to posterior fourchette) and perineal detail that includes vaginal capacity, bladder neck body (distance from posterior fourchette to mobility, and the presence of a lateral wall defect, midanal opening) are measured. All measure- the POP-Q system may be too detailed for ments are taken with the patient while strainingl other clinicians. One useful modification is Valsalva; examining a patient in the supine lithot- the Schiissler diagram (Fig. 1.6.2), devised by omy position demonstrates less prolapse than Schiissler as part of the original POP-Q system.\" examining in a birthing chair at a 45 degree sitting In this diagram, the vagina is represented dia- position or in the standing position.\" Some clini- grammatically with an obtuse representation of cians examine in the standing position as well if the introitus, and an outline of the leading edge the supine or sitting positions fail to reproduce of the prolapse with including measurements. the woman's symptoms of bulging. Unless precise measurements are needed for research purposes, the measurements for pro - The International Continence Society devised lapse, including a Schiissler diagram, should take the POP-Q system in 1994 in an effort to stan- no more than a few minutes. dardize the measurement of pop,7 The system records two points in the anterior wall, two points in the posterior wall, one to two points in the apex, total vaginal length, and the measurements of the genital hiatus and perineal body (Fig. 1.6.1). The leading edge of the prolapse defines the overall stage, with stage II being defined as the leading edge being within 1ern of the hymenal ring (above or below), stage IV being complete eversion of the vagina, stage III being prolapse greater than stage II but not complete eversion,

1.6. Pelvic Organ Prolapse 73 FIGURE 1.6.2. Schussler diagram demon- A Hymenal remnants Anterior vaginal wall strating (A) astage III anterior vaginal wall +10 -7 -10 prolapse IAa + 3 and Ba + 3) and (B) a +3 0 stage III posterior vaginal wall prolapse lAp+ 3and Bp + 4). II\" I\\.... 100-'\" Posterior vaginal wall B --Hymenal remnants Anteriorvaginal wall +10 +4 0 -5 -10 r-,po-. r-r- ~ ~ f0- to- r-, ..... Posterior vaginal wall Descending Perineal Syndrome significant stretching during such straining to move the stool bolus back to the anal sphincter, Perineal descent refers to the movement of the thus, causing a chronic nerve damage in addi- perineal body (the area between the posterior tion to that seen with childbirth injury. Such fourchette of the vagina and the anu s) with val- perineal descent may be compensated by salva, especially during evacuation. At rest, the instructing patients to manually splint the perineal body should be several centimeters perineum or rectovaginal septum during defeca- above the ischial tuberosities, which are bony tion. The Mayo Clinic reviewed their experience prominences that are easily palpated in supine with pelvic floor education for descending lithotomy. Terminal branches of the pudendal perineum syndrome;\" many patients still expe - nerve insert into the perineal body. In child- rienced constipation or excessive straining two birth, the fibromuscular wall of the rectovaginal years after their regimen for pelvic floor train- septum may become deta ched from the perineal ing, especially where the perineal body move body; thus, with any straining the perineal body more than 4 ern (relative to the ischial spines) descends several centimeters below or beyond with straining. the ischial tuberosities, further injuring these nerves as they stretched with the movement of POP and the Pelvic Floor their insertion site.\" It has been suggested that the clinical finding of perineal descent may actu- Does pelvic floor muscle dysfunction cause POP? ally represent a hernia of the levator ani. \" Some This has been the subject of much conjecture, but surgeons have referred to a \"perineal rectocele \" little definitive research. The hypothesis is well and have advocated repair by pulling bulbocav- founded; as long as the muscles remained intact, ernosus tissue to the midline in a surgical repair pelvic organs were supported without tension on and reattaching the fibromuscular wall to its thei r suspensory ligaments. This idea originated insertion site on the perineal body.\" Loss of as long ago as the beginning of the twentieth pelvic floor muscle support may lead to more century with Paramore, who suggested that the than POP. Defecation can become disordered as support of pelvic organs was similar to a boat in the stool bolus follows the path of least resis- dr ydock (Fig 1.6.3), where the water (pelvic floor tance and pushes the rectovaginal septum and muscles) supports the boat (pelvic structures), per ineal body in a caudal direction. The puden- while the moorings (connective tissue supports dal nerve end ings on the perineal bod y undergo

74 P.A. Norton after the prolapse has developed is unlikely to reverse the process of POP. A References FIGURE 1.6.3. Boat in drydock concept for the development of 1. Olsen A, Smith V,Bergstrom J, et a1. Epidemiology pelvic organ prolapse. of surgically managed pelvic organ prolapse and urinaryincontinence. ObstetGyneco1.1997;89:501- such as ligaments) help to suspend and stabilize 506. the boat. If the water is withdrawn to work on the underside of the boat, much strain is placed on 2. Luber K, Boero S, Choe J. The demographics of the moorings, which now support the entire boat pelvic floor disorders: current observations and through its suspensions. Similarly, loss of some future projections. Am J Obstet Gyneco1. 2001; or all of the pelvic floor support may place exces- 184:1496-1501. sive strain on the connective tissue suspensions in the pelvis. Although good pelvic floor function 3. Barber MD, Kuchibhatla MN, Pieper CF, et a1. would be expected to preserve pelvic organ Psychometric evaluation of 2 comprehensive support, it is unknown whether such muscle condition-specific quality of life instruments for training could be expected to improve support, women with pelvic floor disorders. Am J Obstet once damage (stretching or breaking) of the sus- Gyneco1. 2001;185(6):1388-1395. pensory components has occurred. 4. Bump R, Norton P. Epidemiology and natural Although it may be difficult to show a cause history of pelvic floor dysfunction. Obstet Gynecol and effect relationship for pelvic floor dysfunc- Clin North Am. 1998;25(4):723-46. tion and POP,a related question is whether pelvic floor muscles prevent POP. The American College 5. Spence-Jones C, Kamm M, Henry M, Hudson C. of Obstetrics and Gynecology's patient education Bowel dysfunction: a pathogenic factor in utero- bulletin on pelvic relaxation recommends that vaginal prolapse and urinary stress incontinence. patients employ Kegel exercise to improve their Br J Obstet Gynaeco1. 1994;101(2):147-152. POP, although no published studies exist to confirm this. If the pelvic floor prevents undue 6. Barber MD, Lambers A, Visco AG, et a1. Effect of burden on the pelvic suspensory/connective patient position on clinical evaluation of pelvic tissue components, then one might hypothesize organ prolapse. Obstet Gyneco1. 2000;96(1):18- that strengthening the pelvic floor would have a 22. very positive impact on prolapse. However,appre- ciation of a damaged pelvic floor may come late 7. Viereck V, Peschers U, Singer M, Schuessler B. in the process; if the injury to the muscles is at Metrische Quantifizierung des weiblichen Geni- the time of childbirth and the woman is able to talprolapses: Eine sinnvolle Neuerung in der compensate somewhat to achieve normal func- Prolapsdiagnostik? GeburtshFrauenheik. 1997;57: tion, the lack of support may begin the process of 177-182. POP. Teaching these muscles to contract better 8. Bump R, Mattiasson A, BO K, et a1. The standard- ization of terminology of female pelvic organ pro- lapse and pelvic floor dysfunction. Am J Obstet Gyneco1. 1996;175:10-17. 9. Henry M, Parks A, Swash M. The pelvic floor mus- culature in the descending perineum syndrome. Br J Surg. 1982;69:470-472. 10. Gearhart SL, Pannu HK, Cundiff GW, et a1. Peri- neal descent and levator ani hernia: a dynamic magnetic resonance imaging study. Dis Colon Rectum. 2004;47(8):1298-1304. 11. Richardson A. The anatomic defects in rectocele and enterocele . J Pelvic Surg. 1995;4:214-221. 12. Harewood GC, Coulie B, Camilleri M, et a1. Descending perineum syndrome: audit of clinical and laboratory features and outcome of pelvic floor retraining. Am J Gastroentero1. 1999;94(1): 126-130.

1.7 Anal Incontinence, Constipation, and Obstructed Defecation Abdul H. Sultan and A. Muti Abulaffi Key Message an objective constipation scoring system using a 100-question symptom analysis which correlated The definitions and prevalence of anal incon- well with colon transit, anal manometry, proc- tinence and constipation are discussed. The tography, and electromyography. anatomy, physiology, and pathophysiology of bowelmotilityand sphincter control are reviewed. Anal incontinence has an estimated prevalence The relationship between posterior compartmen- of 0.42%, rising to more than 1% in the over 65 tal prolapse, rectal prolapse, and uterovaginal age group.' The condition is more common in prolapse is discussed. women than men of young and middle age, although in the elderly, it affects both sexes Introduction equally. Constipation is far more common, with an estimated prevalence of 2% with women being Anal incontinence is defined as the loss of normal affected 3 times more often than men.' control of bowel action leading to the involuntary passage of flatus and feces. Incontinence can Although constipation and incontinence would range from a minor leakage of feculent fluid, seem to be at the opposite extremes of the spec- occasional leakage of stool during passage of trum, there are scenarios where constipation can flatus, to a complete loss of bowel control. Con- lead to incontinence (see the following sections). stipation, on the other hand, has no universally accepted definition . About 80% of people suffer Anatomy and Physiology from constipation at some time during their lives, and brief periods of constipation are normal. The Large Bowel Widespread beliefs, such as the assumption that everyone should have a movement at least once The large bowel is 1.5m long from the ileocecal each day, have led to overuse and abuse of laxa- valve to the anus . It is arbitrarily divided into tives. Some of the most frequently used defini- the cecum, ascending colon, transverse colon, tions include infrequent bowel movements, descending colon, sigmoid colon, and rectum. typically 2 or less per week, difficulty in defeca- The transverse and sigmoid colon always have a tion (straining at passing stools for more than mesentery, but the ascending and descending 25% of bowel movements or a subjective sensa- colons have a mesentery in 12%and 22%, respec- tion of hard stools), or the sensation of incom- tively. The function of the large bowel is to mix plete bowel emptying. Agachan et al.' proposed and propel its contents and to absorb water and electrolytes . Bowel activity (peristalsis) is in- voluntary and is mediated by a combination of extrinsic and intrinsic nervous systems. The 75

76 A.H. Sultan andA.M. Abulaffi extrinsic innervation is made up of sympathetic teric reflex), and then only for a short time. The and parasympathetic nerves. The intrinsic inner- external sphincter, puborectalis, and levator ani vation is made up of the enteric nervous system, are constantly active, even during sleep. This which is a network of nerve cells in the bowel activity in the external sphincter further contrib- wall comprising the myenteric and submucosal utes to the resting tone of the anal canal. The plexuses. activity in these muscles is increased by volun- tary squeezing, but usually only for short periods The Anal Sphincter and Pelvic Floor (up to 60 seconds) and is lowered during defeca- tion (initial straining effort). The anal canal is 3-4 em in length. It is sur- rounded by two muscles (Fig. 1.7.1):4 (1) the inter- The anorectal angle is created and maintained nal sphincter, a smooth muscle that represents by the constant active contraction of the levator the expanded distal portion of the circular ani and its most central portion, the puborecta- smooth muscle of the rectum and is innervated lis, which passes around the rectum in aU-shaped by the autonomic nerves, and (2) the external fashion, thus, pulling it forward. This allows the sphincter, a striated muscle that is situated anterior wall of the rectum to cover the top of around the internal sphincter and extends supe- the anal canal as a flap valve. Any increase in the riorly to blend with the puborectalis, which is an intraabdominal pressure causes the flap valve to important constituent of the levator ani. It is close more tightly, preventing rectal contents divided descriptively into three parts; subcutane- from entering the anal canal. ous, superficial, and deep. The innervation of the external sphincter is from the pudendal nerves Continence and Defecation (52, 53, 54), and that of the puborectalis is from direct branches of 53 and 54. Normal continence and defecation is achieved by the interplay between a host of sensory and motor The internal sphincter is almost always con- inputs. The rectum maintains low intraluminal tracted and contributes up to 70% of the resting pressure (rectal compliance) and accommodates tone. Relaxation occurs in response to certain slowlyto the fecal contents, which are propagated stimuli such as rectal distension (rectosphinc- slowly down the colon by colonic peristalsis. l.onR\"udmal ( 'trcular sm oo th smooth muscle muscle IIl ococC)'g FIGURE 1.7.1. Diagrammatic representa- Levator ani { tion of the anal sphincter mechanism, (Thakar and Sultan, 2003.) Puborectalts E.lt~T,\"11 {Dap anal Supu{ll' lal SphmCI<T Subcutaneous --~

1.7. Anal Incontinence, Constipation, and Obstructed Defecation 77 FIGURE 1.7.2. The mechanism of maintaining continence and Bowel evacuation Colonicaccommodation Qdefecation. (Sultan and Nugent, 2004.) Q EAS & puborectalis EAS & puborectalis relaxation contraction Once a certain volume is reached (usually 200ml), In general, passive soiling and lor flatus inconti- a sensation of rectal fullness occurs, which is nence is associated with internal sphincter dys- mediated by sensory stretch receptors in the function. By contrast, urgency and/or urge puborectalis and levator ani. The rectosphinc- incontinence is associated with external sphinc- teric inhibitory reflex (anorectal inhibitory reflex) ter dysfunction. However, more frequently dys- is activated, causing relaxation of the internal function involves both sphincters, giving rise to anal sphincter. The fecal bolus descends towards mixed symptoms. the anal canal, but is prevented from progressing further by the voluntary contraction of the exter- When anal incontinence is attributed to anal nal sphincter. At this point, sensory sampling by sphincter dysfunction, it is usually caused by the profuse sensory receptors of the anal canal either mechanical disruption or neuropathy, but permits the individual to distinguish between sometimes both may coexist. Obstetric trauma is flatus, liquid, or solid (Fig. 1.7.2). When socially a major etiological factor, and there is a double convenient, the external sphincter and puborec- peak incidence of anal incontinence; the first is talis are relaxed and combined with straining, in the postpartum period and the second is in the the anorectal angle straightens, allowing the perimenopausal years. After the advent of anal rectal contents to be expelled . If the timing is endosonography it has been shown that approxi- inconvenient, the external sphincter and puborec- mately one third of primiparous women develop talis remain contracted, returning the luminal anal sphincter injury that is not recognized contents back to the rectum, and the contents are during vaginal delivery,\" However, even when then reaccommodated in the colon.\" it is recognized and repaired, the outcome is suboptimal, as one third continue to suffer Pathophysiology im-paired continence.' This may be related to concurrent neuropathic damage or inadequate Anal Incontinence repair. However, there are other factors, such as the effect of ageing, collagen weakness, progres- Most of the resting anal pressure is contributed sion of pelvic neuropathy, estrogen deficiency, by the internal anal sphincter (up to 70%), the concurrent irritable bowel syndrome (IBS), anal cushions (up to 15%), and the external primary degeneration of the internal anal sphinc- sphincter (the remaining percentage of pressure). ter, severe constipation, and uterovaginal/rectal prolapse that may contribute to a deterioration in anorectal function.

78 A.H. Sultan and A.M. Abulaffi TABLE 1.7.1. Causes ofConstipation Causes ofconstipation Colonic constipation OrganiclAnatomic Diverticular disease Colonic tumors Functional Benign colonic strictures Colonic (slow transit) IBS Idiopathic Anorectal constipation OrganiclAnatomic Drugs Endocrine causes Functional causes Psychiatric Environmental Rectal Cancer Fissure inano Extrinsic compression ofrectum Rectal intussusception and prolapse Rectocele Enterocele Diminished sensation Anismus Constipation Functional Causes There may be several, possibly simultaneous, In these situations, the colon is structurally factors leading to constipation, including normal looking during a contrast examination inadequate fiber and fluid intake, a sedentary or a colonoscopy. However, the problem lies lifestyle, psychosocial issues, history of sexual with disordered motor activity of the colon abuse, and environmental changes. Constipation caused by factors and conditions affecting both may be aggravated by travel, pregnancy, or a the extrinsic and intrinsic nervous systems. change in diet. In some people, it may result from Perhaps one of the most common conditions repeatedly ignoring the urge to have a bowel belonging to this group is IBS. In these patients, action. there is colonic hypermotility producing nonpro- pulsive haustral waves that hinder transport of Constipation results from disorders of the feces rather than promote it. In contrast, colonic large bowel and anorectum and, for the purposes hypomotility or colonic inertia can also be a of this chapter, can be classified into colonic and cause of severe constipation, such as in idiopathic anorectal constipation. Each can then be subdi - slow-transit constipation. Other factors affecting vided into organic and functional causes\" (Table motor activity include endocrine, metabolic, 1.7.1). environmental, psychiatric, neuromuscular, and drugs. Colonic Constipation Organic Causes Anorectal Constipation (Outlet Obstruction) In these situations, there is a physical or a struc- tural abnormality in the colon that hinders or Organic Causes interferes with the passage of stools, causing con- stipation. Tumors of the colon and rectum, diver- As with colonic causes, there is an associated ticular disease, and benign strictures are but a anatomical abnormality. This includes condi- few good examples.

1.7. Anal Incontinence, Constipation, and Obstructed Defecation 79 tions in the pelvis outside the anorectum, such as stools. The individual feels the urge to open large fibroids, uterine tumors, endometriosis, the bowels, but is unable to do so even though and pregnancy pressing on the rectum and the stools are soft . It should be noted, however, causing luminal narrowing. Within the ano- that there is a small group of patients with rectum, evacuatory difficulties occur with anorectal constipation who rarely feel the urge to tumors of the lower rectum, large hemorrhoids, defecate because of diminished sensation in the rectal prolapse, rectocele, enterocele, and anal anorectal zone. fissures. Relationship Between Redal Prolapse and In rectal prolapse, part of the rectum protrudes Advanced Uterovaginal Prolapse through the anus. The prolapse may be made of rectal mucosa only (mucosal prolapse) or the full There is no evidence to support a clear asso cia- thickness of the rectal wall including the muscu- tion between rectal prolapse with complete laris (full-thickness prolapse). In few instances, uterine prolapse. Reports in the literature are the prolapse is internal or occult and is only limited to case reports and small series.\":\" The seen on sigmoidoscopy or during defecation largest series is by Goligher,\" where only 8 out of proctography. 83 patients with rectal prolapse had a significant uterine prolapse requiring surgery. Unlike fecal Intussusception is a type of a full-thickness incontinence, the prevalence of rectal prolapse internal rectal prolapse that involves one seg- does not appear to be lower in nulliparous women. ment of the rectal circumference and is only In one series of 183 women treated for rectal seen during sigmoidoscopy or defecation pro- prolapse, 40% were nulliparous. It would there- ctography. fore appear that although uterovaginal prolapse and rectal prolapse may present simultaneously, A rectocele is a herniation of the rectum creat- there are different mechanisms in the ir ing a bulge in the posterior vaginal wall. Recto- pathogenesis. celes are described in detail in Chapter 4.8. Many such posterior wall defects are asymptomatic Anismus is a condition where the aforemen- and are often identified during concurrent exam- tioned normal defecator process is lacking. In ination of prolapse in other compartments. this condition, the anal sphincter muscles (exter- Symptoms include a vaginal bulge (lump), con- nal and puborectalis) fail to relax and, in some stipation, a feeling of incomplete emptying, and instances, there is paradoxical contraction during the need to perform rectal or vaginal digit ations straining. The condition can develop at any age or digital splinting in order to facilitate bowel and frequently there is an associated psychologi- emptying.\" cal element (see Chapter 1.8). Other posterior compartment prolapse, such Functional Causes as an enterocele (herniation of the small intestine into the vagina), may occur concurrently; there- Abnormal motility occurs in anismus and fore, careful evaluation is essential before Hirschsprung's disease. Abnormal sensitivity embarking on surgery. Rectoceles may be a sec- occurs in cerebrovascular accidents, lesions of ondary manifestation of outlet obstruction the ascending nerves, as in diabetes, and after caused by intussusception; therefore, a defecat- damage to pudendal nerves. ing proctogram should be performed under these circumstances. In a study of 69 patients with an Relationship Between Constipation and enterocele, Mellgren et al'? found that 55% had Fecal Incontinence concurrent rectal intussusception, and 38% had rectal prolapse. There are several scenarios where dysfunction can lead to either constipation or incontinence Functional Causes (Fig. 1.7.3). Indeed, constipation itself can lead to incontinence (Fig. 1.7.4). Patients with fecal In this type of constipation, the colonic transit is normal, but the abnormality is within the ano - rectal mechanism responsible for expelling the

80 A.H. Sultan and A.M. Abulaffi ~-------- brain - frequent prolonged retention: constipation - chronic excessive straining: constipationlincontinence - CVA: incontinence - dementia: incontinence spinalcord: - acutetransverse cord lesion orlocal lesion:constipation (overflow)incontinence colon: - impaction: constipation! overflow incontinence - diarrhoea: incontinence rectum: - Hirschsprung's disease: constipation pudendalnerve: - damage: incontinence puborectal muscle: - anismus: constipation levatoranimuscle: - excessive perineal descent: constipationlincontinence - anismus:constipation rectoanaljunctionand lAS: - adultHirschsprung's disease: constipation - disturbed rectoanal inhibition reflex: constipation EAS: - anismus:constipation - damage: incontinence haemorrhoidectomy: - leakage FIGURE 1.7.3. Pathogenesis ofconstipation and/or incontinence. (Smout and Akkermans, 1994.) impaction can develop paradoxical diarrhea Descending perineal syndrome is a term intro- caused by overflow, and this can be profuse and duced by Sir Alan Parks\" to describe a group of severe enough to leak through the anus even patients with various anal symptoms who showed though the sphincter function is normal. In marked descent of the perineum when asked to another much debated condition, it is suggested strain. One of the findings in this condition is an that patients with chronic constipation and anterior rectal mucosal prolapse into the upper habitual straining develop damage to the puden- anal canal that is interpreted as bowel contents, dal nerves as a result of traction neuropathy result ing in excessive straining. It is suggested (stretch injury), and that this in turn causes that the pelvic descent in these groups of patients weakness of the anal sphincter and pelvic floor may lead to traction neuropathy and, ultimately, muscles leading to incontinence (Fig. 1.7.5). incontinence (Fig. 1.7.4).

1.7. Anal Incontinence, Constipation, andObstructed Defecation 81 Primary sensory motor disorder Possible diagnosis 11 .1 !f Disordered colonic motor activity IIanismus Hirschsprung's disease Constipation .. 1 -- - -1-'\\ .1 Impa ction Damage to Frequent and autonomic hard straining - nerves T rau ma difficult labour '1'\\ Damage to ~ sacral nerves, anal sphincters Par ad ox ica l n d iar rho ea Damage to pudendal nerve , - -anal sphincters Pr imary sensory Secondary Secondary motor disorder motor disorder anatomical abnormality Myogen ic ~ t1 Prolapse, ulcer, ne u ro ge ni c , Disordered ~ perineal descent idiopathic closing of syndrome anal sph incter Overflow incontinence n Fecal incontinence FIGURE 1.7.4. Interrelationship and pathophysiology of constipation and anal incontinence. (Smout and Akkermans, 1994.) ~ Prolonged straining . - ~ Abnormal perinealdescent ~ Traction injury to pudendal nerve ! Pudendal neuropathy ! Atrophy of striated anorectal muscles ! I Anorectal incontinence I FIGURE 1.7.5. The mechanism of neurogenicanal incontinence. (Sultan and Nugent, 2004.)

82 A.H. Sultan and A.M. Abulaffi Conclusion 7. Sultan AH, Thakar R. Lower genital tract and anal sphincter trauma. Best Pract Res Clin Obstet Gyn- The mechanisms that maintain continence are aeco!. 2002;16(1):99-116. complex and the cause is often multifactorial. Constipation, obstructed defecation, prolapse, 8. Smout AJP, Akkermans LMA. Normal and and anal incontinence are disorders that may be disturbed motility of the gastrointestinal tract. interrelated; therefore, a careful history and eval- Petersfield, UK: Wrightson Biomedical; 1994:175- uation is essential. When dysfunction involves 189. multiple compartments, a multidisciplinary ap- proach should be adopted .IS 9. Karlbom U, Graf W, Nilsson S, et al. Does surgical repair of rectocele improve rectal emptying? Dis References Colon Rectum. 1996;39:1296-1302. 1. Agachan F, Chen T, Pfeifer J, et al. A constipation 10. Mellgren A, Johansson C, Dolk A, et al. Enterocele scoring system to simplify evaluation and man- demonstrated by defecography is associated with agement of constipated patients. Dis Colon other pelvic floor disorders. Int J Colorect Dis. Rectum. 1996;39:681-685. 1994;9:121-124. 2. Thomas TM, Egan M, Walgrove A, et al. The prev- 11. Azpuru CEo Total rectal prolapse and total genital alence of faecal and double incontinence. Com- prolapse: a series of 17 cases. Dis Colon rectum. munity Med. 1984;6(3):216-220. 1974;17:528-531. 3. Sonnenberg A, Koch TR. Physician visits in the 12. Dekel A, Rabinerson D, Ben Rafael ZY. Concurrent United States for constipation. 1958 to 1986. Dig genital and rectal prolapse: two pathologies - one Dis Sci. 1989;34:606-611. joint operations. BJOG. 2000;107:125-129. 4. Thakar R, Sultan AH. Management of obstetric 13. Goligher JC. Prolapse of the rectum. In: anal sphincter injury. Obstet Gynaecol. 2003;5(2): Goligher JC, Duthie HL, Nixon HH, editors. 72-78. Surgery of the anus, rectum and colon. Fifth Edition . London: Baillere Tindall; 1984:246- 5. Sultan AH, Nugent K. Pathophysiology and 284. non-surgical treatment of anal incontinence. Br J Obstet Gynaecol. 2004;111(Supp 1):84-90. 14. Parks AG,Porter NH, Hardcastle J. The syndrome of the descending perineum. Proc R Soc Med. 6. Sultan AH, Kamm MA, Hudson CN, et al. Anal 1966;59:477. sphincter disruption during vaginal delivery. N 15. Sultan AH, Abulafi MA. The role of the gynaecolo- Engl J Med. 1993;329:1905-1911. gist in faecal incontinence. In: Sturdee R, Olah K, Keane D, editors. Yearbook of Obstetrics and Gynaecology. Volume 9. London: RCOG press; 2001:170-87.

1.8 Overactive Pelvic Floor Muscles and Related Pain Wendy F. Bower Key Message Pain In this chapter, the condition of overactive pelvic Local floor (OAPF) is defined, and its resultant symptom of pain and its effect on bladder and bowel func- Patients with OAPF experience aching or cramp- tion are explained. The clinical findings are ing pain in the coccygeal region and a heavy reviewed. The causat ion is multifactorial. feeling in the rectal or vaginal area (Fig. 1.8.1).3,4,5 Pain is often triggered or exacerbated by sitting, Introduction intercourse, or defecation, which are activities that stretch the pelvic floor musculature.\" Overactive pelvic floor is a term synonymous with a dysfunctional/spastic/short pelvic floor, Other patients will complain of a nonspecific puborectalis syndrome, paradoxical sphincter tenderness. Urethral pain or hyperalgesia may be reaction, and nonrelaxing/hypertonic pelvic reported, and they are likely caused by local floor. By definition, the patient with OAPF has mucosal ischemia , secondary to forceful closure impaired use of the pelvic skeletal muscles in the of the urethral sphincter.' absence of neurological disease . The entire pelvic floor, rather than one muscle group , is in a state Referred of sustained contraction.' Overactive pelvic floor may also be described as the absence or partial Pain may be felt in structures that are distant presence of relaxation after a pelvic floor con- from the pelvic floor muscles but innervated by traction.' It is unlikely that OAPF is a primary the same spinal nerve. Referred OAPF pain is disorder occurring in isolation, but rather part of commonly reported in the perineum and labia, a cascade of symptoms precipitated by dysfunc- and, less frequently, in the rectum, suprapubic tion within the pelvis and reactive changes in region, abdomen, lower limbs, or lower back.\" muscle fibers. The site of referral may become hyperalgesic and display trophic changes such as edema, altered blood flow, subcutaneous thickening, or muscle atrophy. Symptoms Bladder The symptoms of OAPF that may be encountered The effect of an OAPF on the urinary tract is in clinical practice fall into three categories, but dynamic. Symptoms include hesitancy or diffi- can occur in concert: pain , effect on the bladder, culty initiating a void, slow or intermittent urine and consequences for bowel function. flow, pain with micturition, significant residual urine after voiding, urgency, frequency, and 83

84 W.F.Bower TABLE 1.8.1. Urinarytract morbidity associated with OAPF ) • OABdry • OABwet • Straining tovoid • Recurrent urinary tract infections • Hydroureteronephrosis • Vesicouretericreflux • Grossly trabeculated large capacity bladder • Detrusordecompensation urethral sphincter hyperalgesia (Table 1.8.1).9.S.1O A significant number of patients also have a diag- nosis of interstitial cystitis.' Bowel Patients with OAPF perceive appropriate perineal FIGURE 1.8.1. Areas oftissue abnormality in patients with OAPF. fullness and fecal urge, but have trouble passing (Reprinted from Fitzgerald and Kotarinos, 2003.) stools. Because the puborectalis may fail to relax during attempted evacuation, defecation may be points can be identified within the pelvic floor painful and mechanically difficult, often requir- muscle group, as well as in the abdominal wall ing external assistance, and rectal emptying may and hip girdle.' be incomplete. II Constipation and obstructed defecation are common in patients with OAPF OAPF may be secondary to local inflamma- and can precipitate further anorectal pathology, tion, disease, introital or vaginal infection, such as anal fissures and hemorrhoids. In some or abscess. v\":\" Trauma to the perineum or patients, irritable bowel syndrome and slow- pelvic floor from falls, sexual abuse, vaginal transit constipation may be noted .\" delivery, episiotomy, or surgical scarring can also precipitate the OAPF.3.4·14 Pudendal nerve entrap- Causes ment and musculoskeletal limitations may be implicated.v\" It is likely that the OAPF is both a consequence of pelvic dysfunction and a cause of pain and Heightened activity in the pelvic floor muscle discomfort. Effects may be mechanical, inflam- group and urethral and anal sphincters suggests matory, or histochemical. Repetitive, acute, or an underlying dysfunction of neural control. sustained muscle overload, such as occurs when Various theories exist. Mechanosensitive units the pelvic floor is maintained in a shortened may develop either a lower threshold of firing or (contracted) position, can injure the motor end stronger discharge suprathreshold. Cross com- plate. Tonic contraction results in decreased local munication, convergence within the dorsal horn blood flow, heat, and accumulation of potassium of the spinal cord, or the presence of dichotomiz- ions, lactic acid, histamine, and bradykinin.' ing neurons could explain referred pain. Alterna- High local concentrations of these metabolites tively the release of excitotoxic neurotransmitters are known to generate pain . Over time, the muscle in the pelvic floor could facilitate a change in becomes habitually shortened and may develop foci of tethering, or trigger points. These struc- tural changes within the muscle fiber anchor regions prevent pelvic floor lengthening and gen- erate local and referred pain. In up to 88% of female patients with pelvic pain, such trigger

1.8. Overactive Pelvic Floor Muscles and Related Pain 85 central drive that allows a drift toward memo- intended to provide primary support or move- rized high-pressure activity in pelvic skeletal ment and are themselves vulnerable to imbalance muscle.\" Increased excitability of central neurons and pain . It is common to find obturator inter- may be maintained independent of initiating nus, psoas, gluteal, abdominal, and piriformis peripheral input, e.g., by cross-system visceroso- muscle abnormality and pain. 3,4,6,20 matic interaction, and precipitate change in vis- ceral behavior. Findings of Pelvic Floor Overactivity It has been shown that emotions affect sphinc- Patients with OAPF have short and weak pelvic ter tension, and that patients with disordered floor muscles. When visualizing the perineum, timing of the puborectalis have significantly the genital hiatus may appear small and the higher anxiety, depression, and panic scores than perineal body may be displaced anteriorly. controls.\" There is clearly a psychological com- On a request to contract the pelvic floor mus- ponent to OAPF, but whether or not it is causative cles, the OAPF patient is likely to demonstrate is contentious. poor proprioception, minimal or absent move- ment, descent in place of elevation, and early Findings of Pelvic Floor Pain fatigue. 3,4,8,14,21 Accessory muscle activity is fre- Associated with Pelvic Floor quently seen in the thigh adductor muscles, hips, Muscle Dysfunction buttocks, and thorax, as patients attempt to locate the pelvic floor muscles. Chronic pelvic floor dysfunction is often associ- ated with lower urinary tract dysfunction, and it One of the most common findings of OAPF is possible that both are maintained by an up is a high level of pelvic floor muscle activity at regulation of the sacral reflex arc.\" Motor plan- rest, and marked difficulty returning the muscle ning and performance is altered by the expecta- to a relaxed state.':\" Patients may be unable tion of pain . The tight and often painful pelvic to sense pelvic floor relaxation or take several floor muscle displays obvious change in recruit- efforts before tension is released . Successful ment patterning, timing, proprioception, and treatment not only ameliorates pain but also resting muscle length. Functional use of the results in posttreatment reduction of vaginal pelvic floor is also modified by memory of pain . resting pressure.\" For example, the alteration of micturition after urinary tract infection or dyssynergic defecation A less commonly reported finding in OAPF after constipation illustrates the ability of the patients is the thickening of subcutaneous con- higher centers to override earlier learning. nective tissues around perineal or suprapubic trigger points or their regions of pain referral. Palpation of the normal pelvic floor should not These trophic changes are identifiable on palpa- produce pain; however, OAPF patients frequently tion as altered tissue bulk, contour, elasticity, and report moderate to severe tenderness on exami- temperature, along with variation in color.' nation of the pelvic floor muscle group, particu- larly when trigger points are present . Pressure Association with Micturition from the examiner's finger is interpreted as painful, and pain is often noted to spread to the Initially slow or nonrelaxation of pelvic floor hips and lower abdomen.v' Palpation of muscle skeletal muscle is most problematic during spasm often results in pain. 9•' 8 voiding, creating a hesitancy and resistance to the outflow of urine. The flow of urine may be Other muscles of the pelvic girdle may com- intermittently slowed, stop and start, or the pensate for limitations of the pelvic floor in neu- detrusor may cease contracting prematurely tralizing intraabdominal pressure rises, stiffening (Table 1.8.2). Associated residual urine after the sacroiliac joint, allowing backward rotation voiding is common, and patients report a need to of the sacrum, and stabilizing the spine. '9,20 double void. However, these compensatory muscles are not

86 W.F.Bower TABLE 1.8.2. Patterns ofvoiding seen in patients with OAPF Flow curve shape Bell Void type Urethral relaxation Valsalva evident Pelvic flooractivity Detrusor contraction Staccato/steep No Yes rise 1= Normal Yes No Yes Partial Intermittent 2=Abnormal Yes No Yes No 3= Abnormal Yes Yes Functional obstruction to complete emptying time, the call to stool is perceived at higher of the bladder generates escalating detrusor pres- volumes. Thus, it is probable that in some indi- sures. The feed-forward loop triggers further viduals with OAPF the ability to relax puborecta- pelvic floor activity to \"brake\" additional detru- lis and funnel stool through an appropriate sor pressure rise. Eventually, the micturition aperture was never acquired. reflex becomes destabilized during bladder filling, evidenced on urodynamic investigation Pontine projections between the reticular for- as an overactive bladder and on a frequency mation and nucleus retroambiguus allow the volume chart as frequent low-volume voids.\" abdominal and pelvic floor muscles to influence each other, making it possible for abdominal Pelvic floor contraction is a common method pain to lead to dysfunction of the pelvic floor and used to inhibit urgency; however, in the OAPF vice versa.\" patient with a shortened muscle very little pres- sure may be generated. Prescription of pelvic Association with Sexual Function or floor exercises to increase urethral closure pres- Sexual Abuse sure and maximize detrusor inhibition is inap- propriate, as it exacerbates both pain and muscle Sexual pain and orgasm are the components of imbalance and is minimally effective. female sexual dysfunction most likely to be influ- enced by OAPF.26 Pain associated with sexual Association with defecation activity may be either dyspareunia or vaginismus (see Chapter 4.4), whereas orgasmic dysfunction Smaller, more acute straining angles are seen in includes infrequent or nonorgasmic response.\" OAPF patients than in normal defecation attempts; this is a direct consequence of the slow There is a higher prevalence of prior sexual or nonrelaxing pelvic floor,\":\" Anal manometry abuse among patients with functional disorders is essentially normal for both resting and squeeze in comparison to patients with organic disease.\" pressure.' On straining, there is obvious perineal Genitourinary and gastrointestinal symptoms descent and marked EMG activity in place of are the most common somatic complaints.\" relaxation in puborectalis and the external anal Although there is no specific data in respect to sphincter,\" There is delayed initiation of evacua- patients with OAPF, both women with pelvic pain tion, prolonged duration of passage of stool, and and patients with dysfunctional voiding have incomplete emptying of rectum in OAPFpatients, high prevalence rates of childhood or other sexual compared with control subjects.' abuse.\":\" Clinicians should be aware of this association when treating women with OAPF (see In some cases flawed inhibitory gating within Chapter 4.4, text box #3). the central nervous system may have been laid down during the toilet training process.\" References Children who experience large, hard stools learn to respond to fecal urge with a rise in pelvic floor 1. Halligan S, Bartram Cl, Park HJ, et al. Procto- activity. Withholding of stool, although initially graphicfeatures ofanismus. Radiol. 1995;197:679- a response to the fear of pain, becomes a learned response to rectal distension. Over a period of 682 .

1.8. Overactive Pelvic Floor Muscles and Related Pain 87 2. Messelink B, Benson T, Berghmans B, et al. Stan- 16. Zermann DH, Manabu I, Schmidt RA. Pathophysi- dardization of term inology of pelvic floor muscle ology of the hypertonic sphincter or hypertonic function and dysfunction: report from the pelvic urethra. In: Corcos I and Schick E, editors. The floor clinical assessment group of the Interna- urinary sphincter. New York: Marcel Dekker ; tional Continence Society. Neurourol Urodyn 2001:201-218 . 2005;24:374-380. 17. Zermann DH, Manabu I, Schmidt RA. Manage- 3. Fitzgerald MP, Kotarinos R. Rehabilitation of the ment of the hypertonic sphincter or hyperpathic short pelvic floor: Background and patient evalu- urethra. In: Corcos I and Schick E, editors. The ation. Int Urogynecol 1.2003;14:261-268. urinary sphincter. New York: Marcel Dekker; 2001:679-686. 4. Shelly B, Knight S, King P, et al. Aetiology of pelvic 18. Hetrick DC, Ciol MA, Rothman I, et al. Musculo- floor muscle pain syndromes. In: Laycock I and skeletal dysfunction in men with chronic pelvic Haslam I, editors. Therapeutic management of pain syndrome type III: a case-control study. I Urol. 2003;170(3):828-831. incontinence and pelvic pain. London: Springer- Verlag; 2002:167-170. 19. Pool-Goudzwaard A, Hoek Van Dijke G, Van Gurp 5. Meadows E. Treatment for patients with pelvic M, et al. Contribution of pelvic floor muscles to pain . Urolog Nurs . 1999;19(1):33-35. stiffness of the pelvic ring. Clin Biomech. 2004; 19(6):564-57 1. 6. Segura IW, Opitz IL, Greene LF. Prostatosis, pros - tatitis or pelvic floor tension myalgia. I Urol. 1979; 20. Sapsford RR, Hodges PW. Contractions of the pelvic floor muscles during abdominal maneu- 122:168-169. vers. Arch Phys Med Rehabil. 2001;82(8):1081- 1088. 7. Everaert K, Devulder I, De Muynck M, et al. The 21. Ab E, Schoenmaker M, van Empelen R, et al. Para- pain cycle: Implications for the diagnosis and doxical movement of the pelvic floor in dysfunc- tre atment of pelvic pain syndromes. Int Urogyne - tional voiding and the results of biofeedback training. BIU Int. 2002;89(SuppI2):I-13 . col I. 2001;12:9-14. 8. Schmidt RA, Vapnek 1M. Pelvic floor behavior and 22. [arvis SK, Abbott lA, Lenart MB, et al. Pilot study interstitial cystitis. Semin Urol. 1991;9(2):154- of botulinum toxin type A in the treatment of 159. chronic pelvic pain associated with spasm of the levator ani muscles . Aust N Z I Obstet Gynaecol. 9. Weiss 1M. Pelvic floor myofascial trigger points: 2004;44(1):46-50. 23. Yeung C. Pathophysiology of bladder dysfunction. manual therapy for interstitial cystitis and the urgency-frequency syndrome. I Urol. 2001;166(6): In: Pediatric urology. Gearhart IP, Rink R, Mouri- 2226-2231. 10. Zermann DH, Manabu I, Doggweiler R, et al. Neu- quand P, editors. WB Saunders: Philadelphia; rological insights into the etiology of genitouri- 2001. 24. Lee HH, Chen SH, Chen DF, et al. Defeco- nary pain in men. I Urol. 1999;161:903-908 graphic evaluation of patients with defecation dif- ficulties. I Formos Med Assoc. 1994;93(11-12): 11. Bleijenberg G, Kuijpers HC. Treatment of the 944-949. spastic pelvic floor syndrome with biofeedback. 25. Kuijpers HC, Bleijenberg G. The spastic pelvic Dis Col Rec. 1987;50(2):108-111. floor syndrome. Dis Col Rec. 1985;28(9):669- 12. Walker EA, Gelfand AN, Gelfand MD, et al. 672. Chronic pelvic pain and gynecological sym- 26. Munarriz R, Kim NN, Goldstein I, et al. Biologyof ptoms in women with irritable bowel syndrome. I Psychosom Obstet Gynaecol. 1996;17(1):39- female sexual function. Urol Clin N Am. 2002; 46. 29:685-693. 27. Bachmann GA, Phillips NA. Sexual dysfunction. 13. Chung AK, Peters KM, Diokno AC. Epidemiology of the dysfunctional urinary sphincter. In: Corcos In: Steege IF, Metzger DA, Levy BS, editors. I and Schick E, editors. The urinary sphincter. New York: Marcel Dekker; 2001:183-191. Chronic pelvic pain . Philadelphia: WB Saunders; 1998:77-90. 14. Glazer HI, Rodke G, Swencionis C, et al. Treatment 28. Jacob MC, De Nardis MC. Sexual and physical of vulvar vestibulitis syndrome with electromyo- graphic biofeedback of pelvic floor musculature. abuse and chronic pelvic pain. In: Steege IF, I Reprod Med. 1995;40(4):283-290. Metzger DA,Levy BS,editors. Chronic pelvic pain . Philadelphia: WB Saunders; 1998:13-24. 15. Antolak SI, Hough DM, Pawlina W,et al. Anatomi- cal basis of chronic pelvic pain syndrome: the ischial spine and pudendal nerve entrapment. Med Hypotheses. 2002;59(3):349-353.

88 W.F.Bower 29. Drossman DA. Physical and sexual abuse and gas- 31. Salonia A, Zanni G,Nappi RE, et al. Sexual dysfunc- tion is common in women with lower urinary fract trointestinal illness: What is the link? Am JMed. symptoms and urinary incont inence: Results of a cross-sectional study. Euro Urol. 2004;45:642- 1994;97:105. 648. 30. Ellsworth PI, Merguerian PA, Copening ME. Sexual abuse: another causative factor in dysfunc- tional voiding. JUrol. 1995;153:773-776.

Part II Evaluation of the Pelvic Floor

2.1 Clinical Evaluation of the Pelvic Floor Muscles Diane K. Newman and Io Laycock Key Message and relax the PFMs and to determine the pres- ence of a muscle hypertonus. Clinical examination is the basis of diagnosis of urogynecological disorders. It is important that This evaluation or examination is performed this examination is performed by a well-trained by a variety of health care clinicians: doctors, person with the appropriate skills. The patient nurses , and physical therapists that specialize in should actively participate in the examination the area of pelvic floor dysfunction. Physicians and be able to carry out pelvic floor muscle (PFM) who treat pelvic floor disorders include urolo- contractions in a coordinated waywhen required. gists, gynecologists, fellowship-trained urogyne- This will form the basis of subsequent pelvic floor cologists and female urologists, geriatricians, exercises and is how the woman will learn the family practitioners, and other interested clini- different types of muscle contraction which are cians . Nurses' background and skills are unique integral to this. Digital self examination is an because they encompass the full spectrum of important part of pelvic floor re-education, and evaluation and treatment, especially in the area a woman should be able to do this herself. There of comprehensive pelvic examination. Physio- are various grad ing methods, and, in particular, therapists or physical therapists (PTs) have long the P.E.R.F.E.C.T. scheme is an important assess- played a part in incontinence and pelvic floor ment technique, and necessary when planning a care, and involvement in this area is often through treatment program. The Knack is a useful maneu- association with women's hospitals or obstetric ver that can be taught to guard against stress departments, rather than as part of a general incontinence. Mechanical devices, such as a peri- physiotherapy practice . As such, they tend to be neometer with the addition of electromyographic highly motivated and enthusiastic. (EMG) recording and vaginal cones, can help in the retraining process. It is important to set a Beginning the Evaluation ofthe program of exercises and re-evaluate them after Pelvic Floor a reasonable time period, aided by a urinary diary. Before examining the pelvic floor, the clinician should explain the procedure to prevent embar- Introduction rassment and the woman should empty her bladder. Several positions are used, with the Women who present with pelvic floor disorders lithotomy position considered ideal. This posi- should undergo a pelvic evaluation to determine tion requires that the patient be supine, with hips abnormalities, the patient's ability to contract and knees bent and abducted; most clinicians' choose this position because PFM assessment may be part of a bimanual speculum pelvic 91