Background Lacerations of the anal sphincter or injury to sphincterinnervation during childbirth are major causes of fecal incontinence,but the incidence and importance of occult sphincter damageduring routine vaginal delivery are unknown. We sought to determinethe incidence of damage to the anal sphincter and the relationof injury to symptoms, anorectal physiologic function, and themode of delivery.
Methods We studied 202 consecutive women six weeks before delivery,150 of them six weeks after delivery, and 32 with abnormal findingssix months after delivery. Symptoms of anal incontinence andfecal urgency were assessed, and anal endosonography, manometry,perineometry, and measurement of the terminal motor latencyof the pudendal nerves were performed.
Results Ten of the 79 primiparous women (13 percent) and 11of the 48 multiparous women (23 percent) who delivered vaginallyhad anal incontinence or fecal urgency when studied six weeksafter delivery. Twenty-eight of the 79 primiparous women (35percent) had a sphincter defect on endosonography at six weeks;the defect persisted in all 22 women studied at six months.Of the 48 multiparous women, 19 (40 percent) had a sphincterdefect before delivery and 21 (44 percent) afterward. None ofthe 23 women who underwent cesarean section had a new sphincterdefect after delivery. Eight of the 10 women who underwent forcepsdelivery had sphincter defects, but none of the 5 women whounderwent vacuum extractions had such defects. Internal-sphincterdefects were associated with a significantly lower mean (±SD)resting anal pressure (61 ±11 vs. 48 ±10 mm Hg,P<0.001) six weeks post partum, and external-sphincter defectswere associated with a significantly lower squeeze pressure(increase above resting pressure, 70 ±38 vs. 44 ±13mm Hg; P<0.001). There was a strong association (P<0.001)between sphincter defects and the development of bowel symptoms.
Conclusions Occult sphincter defects are common after vaginaldelivery, especially forceps delivery, and are often associatedwith disturbance of bowel function.
Childbirth may be accompanied by mechanical or neurologic injuryto the anal sphincter. Overt sphincter damage due to a third-degreeor fourth-degree tear1 occurs in approximately 0.7 percent ofwomen undergoing vaginal delivery in centers where posterolateralepisiotomy is practiced2,3. Inadequate primary repair of thesesphincter injuries can lead to early fecal incontinence3,4.Pudendal-nerve conduction can also become impaired after vaginaldelivery,5 and the later development of fecal incontinence hasbeen attributed to progressive denervation of the anal-sphinctermuscles6,7,8. Some women sustain both mechanical and neurologictrauma during vaginal delivery9.
Until recently, defects of the external anal sphincter weredetected by electromyography,10 and defects of the internalsphincter were inferred from measurement of a low resting analpressure11. Anal endosonography, however, has allowed accurateimaging of both sphincter muscles,12,13 leading to the recognitionof unsuspected defects of the external sphincter in women thoughtto have purely neurogenic fecal incontinence14 and the detectionof internal-sphincter damage when only an external-sphincterdefect was suspected15. In a study of 62 women with fecal incontinencerelated to obstetrical procedures, anal endosonography revealedan external-sphincter defect in 90 percent and an internal-sphincterdefect in 65 percent15.
Because most previous studies of anal-sphincter function wereeither retrospective14,15 or attributed the development of fecalincontinence directly to pudendal-nerve damage,5,6,16 we undertooka prospective study of women before and after delivery, usinganal endosonography and anorectal neurophysiologic tests toestablish the incidence of mechanical and neurologic traumaduring childbirth.
Methods
Subjects
We studied 202 unselected, consecutive women (median age, 28years; range, 18 to 43) who had been pregnant for more than34 weeks. Of the 202 women, 135 had never had a vaginal delivery(including 2 who had had a cesarean section) and 67 had hadone or more vaginal deliveries.
This study was approved by the Research Ethics Committee ofthe City and Hackney District Health Authority, and all thewomen gave informed consent.
Delivery and Evaluation
All women were examined during the last six weeks of pregnancyand were asked to return for reevaluation six to eight weeksafter delivery. At each assessment an interviewer completeda detailed questionnaire that reported any symptoms of fecalurgency (the inability to defer defecation for more than fiveminutes) and anal incontinence. Anal endosonography, manometry,studies of pudendal-nerve terminal motor latency, and perineometrywere then performed. Information on labor and delivery was obtainedfrom hospital records.
Delivery was managed as deemed appropriate by the attendingphysician. All episiotomies were posterolateral. Uncomplicatedepisiotomies were repaired by senior house officers and qualifiedmidwives, whereas complicated episiotomies were repaired bymore senior physicians. Tears related to delivery were classifiedas follows: first-degree tears involved only vaginal epithelium(women with such tears were included among those with no laceration);second-degree tears involved the perineal body but not the externalsphincter; third-degree tears involved the external sphincter;and fourth-degree tears involved both the external sphincterand the anal epithelium.
Women with defects on ultrasonography or prolonged terminalmotor latency of the pudendal nerves six weeks after deliverywere asked to return for reevaluation six months post partum.
Anal Endosonography
Endosonography was performed with an ultrasound scanner witha rotating rectal probe, a 7-MHz transducer (focal range, 2to 4.5 cm), and a hard sonolucent plastic cone (Bruel and Kjaer,Naerum, Denmark),12 while the woman lay on her left side. Serialimages of the upper, middle, and lower anal canal were recorded(Umatic video recorder, Sony, Tokyo, Japan). The endosonographicinterpretation of the appearance of muscle layers has been previouslyvalidated13: an external-sphincter defect appears as a breakin the normal texture of this muscle ring17,18 (Figure 1), andan internal-sphincter defect as a gap in the hypoechoic ring18,19(Figure 2). All investigations were performed and the resultsinterpreted by one operator; the results were reviewed independentlyby a second observer unaware of the first interpretation.
Figure 1. Results of Anal Endosonography before and after Delivery in a Primiparous Woman with a Postpartum Defect of the External Anal Sphincter.
Panel A shows a normal image of the middle portion of the anal canal at 34 weeks of pregnancy. R denotes right, L left, IAS internal anal sphincter (hypoechoic), EAS external anal sphincter (hyperechoic), post posterior, sm submucosa (hyperechoic), and V vagina. The probe lies medial to the submucosa. Panel B shows the canal six weeks after delivery. The woman had incontinence of flatus after a forceps delivery with an episiotomy. A hypoechoic defect of the external anal sphincter is present between the open arrows. The damage to the anal sphincter was not recognized during repair of the episiotomy.
Figure 2. Results of Anal Endosonography before and after Delivery in a Primiparous Woman with a Postpartum Defect of the Internal Anal Sphincter.
Panel A shows the middle portion of the anal canal at 34 weeks of pregnancy. R denotes right, L left, IAS internal anal sphincter, EAS external anal sphincter, post posterior, and V vagina. Panel B shows the canal six weeks after delivery. The woman had no symptoms after a spontaneous vaginal delivery but had a second-degree tear (not involving the anal sphincter). The hyperechoic defect in the internal anal sphincter is present between the open arrows.
Anal Manometry
Anal manometry was performed with an intracompartmental-pressuremonitor (Stryker, Kalamazoo, Mich.) attached to an air-filledmicroballoon20. The maximal resting pressure and the maximalsqueeze pressure (i.e., the maximal increase above the restingpressure) were measured according to a stationary pull-throughtechnique21.
Measurement of Terminal Motor Latency of the Pudendal Nerves
The terminal motor latency of each pudendal nerve was measuredafter an electronic stimulus (Medelec stimulator, Old Woking,United Kingdom) from an electrode (Dantec, Skovlunde, Denmark)mounted on a gloved index finger22,23. Latency is the time betweenstimulation of the pudendal nerve at the level of the ischialspine and contraction of the anal sphincter. Prolongation oflatency is indicative of damage to the fastest conducting nervefibers24.
Perineometry
The perineal plane (the level of the perineal soft tissues atthe point of the anal verge, relative to the bony ischial tuberosities)was measured with a perineometer at rest and during maximalstraining effort in the left lateral position25. The differencebetween the two measurements indicates the degree of perinealdescent. Descent of the perineum below the level of the ischialtuberosities at rest or on straining was considered abnormal25.
Statistical Analysis
Antepartum measurements were compared with postpartum measurementsby paired t-tests. Associations between categorical variableswere assessed with the chi-square test or Fisher's exact test.Continuous variables in independent groups were compared bytwo-tailed t-tests. A P value of less than 0.05 was consideredto indicate statistical significance. All results are reportedas means ±SD.
All variables shown to be significantly associated with sphincterdefects on univariate analysis were then entered in a multiplelogistic-regression analysis in a stepwise fashion to determinethe combination of variables that best predicted sphincter damage.An odds ratio was also calculated.
The statistical analyses were performed with software from MinitabData Analysis (Minitab, State College, Pa.) and SAS (SAS Institute,Cary, N.C.).
Results
One hundred fifty women (of whom 100 were primiparous and 50multiparous) returned for postpartum examination a median of49 days (range, 35 to 105) after delivery. Twenty-three women(21 primiparous and 2 multiparous) had delivered by cesareansection, and 127 vaginally (73 women were white, 71 black, and6 of other races).
Vaginal Delivery
Of the 127 women who had a vaginal delivery, 79 were consideredprimiparous (including 2 women who had had previous children,but by cesarean section) and 48 multiparous, of whom 38 (79percent) had only one previous vaginal delivery. Two primiparouswomen (3 percent) and 10 multiparous women (21 percent) hadsymptomatic urinary stress incontinence on examination at sixweeks.
Bowel Symptoms
None of the 79 primiparous women had diabetes mellitus or neurologicor anorectal disease. Post partum, 10 women (13 percent) reportedhaving one or more new bowel symptoms; 8 (10 percent) had fecalurgency, and 4 (5 percent) had anal incontinence (3 had flatus,and 1 had flatus and liquid stool). Two women had temporaryincontinence of flatus for less than three weeks post partum.Among the 48 multiparous women, 9 (19 percent) had one or morebowel symptoms before delivery. These symptoms began after aprevious vaginal delivery (seven women had fecal urgency, threewere incontinent of flatus, and five were incontinent of liquidstool). After delivery, three women (6 percent) had new symptoms(two had urgency and incontinence of flatus, and one had urgencyalone). One woman with incontinence of liquid stool before deliveryhad no symptoms afterward. Therefore, after delivery, 11 (23percent) of the multiparous women had bowel symptoms.
Altogether, of the 127 women who delivered vaginally, 13 (10percent) had one or both bowel symptoms (urgency and incontinence)after delivery.
Anal Endosonography
No sphincter defect was detected before delivery in any primiparouswoman. Six weeks after delivery, 28 women (35 percent) had defectsof either the internal sphincter (Figure 2B), the external sphincter(Figure 1B), or both (Table 1). Twenty-three women (29 percent)had a defect of the internal sphincter; the defect involvedthe entire length of the internal sphincter in 14 women andthe distal portion in 9. Among the 15 women (19 percent) witha defect of the external sphincter, the defect involved thefull length of the sphincter in 11 women, the proximal portionin 2, and the distal portion in 2. Nine women had only partialthickness defects, and six had complete defects. Ten of the15 women with an external-sphincter defect also had an internal-sphincterdefect.
Table 1. Incidence of Anal-Sphincter Defects in Women Evaluated by Anal Endosonography after Vaginal Delivery, According to Parity.
Nineteen (40 percent) multiparous women had a sphincter defectbefore delivery, and 21 (44 percent) after delivery (Table 1).Two women had a new defect, and two with an internal-sphincterdefect before delivery had a new, external-sphincter defectafter delivery. All three multiparous women who reported newbowel symptoms after delivery had combined sphincter defects,which were new in two of the women. All these defects occurredin the anterior portion of the sphincter.
Manometry
The maximal resting anal pressure fell significantly after deliveryin both the primiparous and the multiparous women (Table 2).It was also significantly lower in women with an internal-sphincterdefect than in those without such a defect (Table 3). The decrementin resting pressure (the difference between the value afterdelivery and the value before delivery) was significantly greaterin women with an internal-sphincter defect than in those without(Table 3). The relation between resting pressure and external-sphincterdefects was not significant (Table 3).
Table 2. Anal Pressure, Perineal Descent, and Pudendal-Nerve Terminal Motor Latency before and Six Weeks after Childbirth, According to Type of Delivery.
Table 3. Anal Pressure in Relation to the Presence or Absence of Sphincter Defects in 79 Women Six Weeks after Vaginal Delivery.
The squeeze pressure fell significantly after delivery in boththe primiparous and the multiparous women (Table 2). It wasalso lower in women with an external-sphincter defect than inthose without such a defect (Table 3). The decrement in squeezepressure after delivery was greater in the women with an external-sphincterdefect than in those without (Table 3). There was no relationbetween the squeeze pressure and internal-sphincter defects(Table 3).
The 23 women in whom an internal-sphincter defect developedhad a significantly shorter anal canal before delivery thanthe 56 women in whom such a defect did not develop (36 ±5vs. 39 ±5 mm, P = 0.01). No such relation was found amongthe women with external-sphincter defects.
Pudendal-Nerve Terminal Motor Latency
The terminal motor latency of each pudendal nerve was measuredin 63 primiparous and 33 multiparous women. Latency was significantlyincreased in both nerves in women from both groups who underwentvaginal delivery (Table 2). The values were higher than theupper limit of the antepartum normal range in 10 primiparouswomen (16 percent) and 5 multiparous women (15 percent) sixweeks post partum; only 1 multiparous woman (3 percent) hadabnormal values before delivery.
There was no relation between the change in the pudendal-nerveterminal motor latency and the development of symptoms or theresults of anal manometry. However, there was a significantassociation (P = 0.02) between abnormal latency and the developmentof a sphincter defect in primiparous women.
Perineometry
Perineal descent increased significantly after vaginal deliveryin both primiparous and multiparous women (Table 2). The 36women with abnormal perineal descent on straining after deliveryhad a significantly longer mean pudendal-nerve motor latencypost partum than the 35 with normal descent (2.1 ±0.2vs. 2.0 ±0.2 msec, P = 0.01).
The duration of active pushing during the second stage of laborcorrelated significantly with the plane of the perineum at rest(P = 0.04, r = 0.23) and during straining (P = 0.008, r = 0.30):the women with a longer active second stage of labor had a greaterdescent.
Sphincter Defects in Relation to Obstetric Variables
A defect involving at least one of the sphincter muscles occurredin 8 of the 10 women (80 percent) who had forceps deliveries(9 with outlet [low] deliveries and 1 with a rotational delivery),but in none of the 5 who had vacuum-extractor deliveries (Table 4).All instrumental deliveries were carried out when the infantpresented below the ischial spines.
Table 4. Obstetrical Variables in Relation to the Development of Anal-Sphincter Defects in 79 Women with Vaginal Deliveries.
The deliveries of two women were complicated by shoulder dystocia;one of these women had a forceps delivery and was later foundto have an external-sphincter defect. In addition, one womanunderwent a twin delivery (no defects), another a breech delivery(internal-sphincter and external-sphincter defects), and a thirdan occipitoposterior delivery (external-sphincter defect).
Internal-sphincter defects developed in three women althoughtheir perineum was intact after delivery. External-sphincterdefects were detected only in women who underwent episiotomyor sustained a spontaneous perineal tear.
Univariate analysis showed that internal-sphincter defects weresignificantly associated with forceps delivery (P = 0.004),epidural analgesia (P = 0.005), and the presence of an episiotomy(P = 0.04). Stepwise logistic-regression analysis revealed thatforceps delivery was associated with a significant risk of aninternal-sphincter defect (odds ratio, 7.0). When this factorwas controlled for, epidural analgesia was not found to contributeto the development of an internal-sphincter defect.
External-sphincter defects were associated with augmentationof labor (P = 0.03), epidural analgesia (P = 0.03), posterolateralepisiotomy (P = 0.02), and forceps delivery (P = 0.001) on univariateanalysis. On stepwise logistic-regression analysis, the singleindependent factor associated with the development of an external-sphincterdefect was forceps delivery (odds ratio, 11.1).
The infant's weight, the infant's head circumference, inductionof labor, the length of each stage of labor, spontaneous perinealtears, the mother's age, and race were not significantly relatedto the development of sphincter defects.
Sphincter Defects in Relation to Bowel Symptoms
All women except one (a primiparous woman) who had either fecalurgency or anal incontinence after delivery had sphincter defects.There was a strong association (P<0.001) between the developmentof either symptom and sphincter defects (Table 5).
Table 5. Symptoms of Fecal Urgency or Anal Incontinence in Relation to the Presence of Any Anal-Sphincter Defect after Vaginal Delivery in 127 Women.
Cesarean Section
No woman who underwent cesarean section had any bowel symptomafter delivery or any significant change in anal pressure (Table 2).Pudendal-nerve terminal motor latency was measured in 16of these women. None of the seven in whom this procedure waselective had a significant change in latency; however, the ninewomen in whom the procedure was indicated after labor had begunhad a significant increase in the latency of the left pudendalnerve (Table 2).
There was no significant change in perineal descent in 16 ofthese women (Table 2). However, the perineal plane on strainingwas significantly lower after delivery in the nine women whounderwent a cesarean section after the onset of labor (P = 0.05).
Follow-up Evaluation at Six Months
Thirty-two women returned a mean of six months after deliveryfor a third evaluation. This group included 10 women with fecalurgency and 7 with anal incontinence six weeks post partum.Fecal urgency was no longer a problem in 4 of the 10 women withthis symptom, but it developed in 2 others. Two of the sevenwomen with anal incontinence had improvement, and another woman(with no sphincter defect) had had no further episodes of incontinence.
Repeat anal endosonography performed at six months in womenwith sphincter defects six weeks after delivery showed no changein the defects. Anal manometry did not reveal any significantchange from the values recorded six weeks post partum. Measurementof pudendal-nerve terminal motor latency was repeated in 22women and showed a significant decrease in latency in both theright (P = 0.002) and left (P = 0.04) pudendal nerves. Latencyhad returned to normal in 8 of the 12 women who had abnormalvalues six weeks after delivery.
Discussion
We found that vaginal delivery is frequently associated withmechanical disruption of the anal sphincters. Three percentof the primiparous women studied, but none of the multiparouswomen, sustained an injury to the anal sphincters during deliverythat was apparent on clinical examination -- i.e., a third-degreeor fourth-degree tear. Endosonography, however, revealed sphincterdamage in 35 percent and 44 percent, respectively. The incidenceof sphincter defects among the primiparous women six weeks afterdelivery was comparable to that among the multiparous womenbefore delivery, most of whom had had only one previous vaginaldelivery. There was only a slight increase in the incidenceamong the multiparous group post partum (4 percent), suggestingthat the risk of sphincter damage is greatest during the firstvaginal delivery.
External-sphincter damage occurred only in the presence of atear or episiotomy, suggesting that it occurs as part of a directcontinuation of perineal disruption. As others have reported,1a posterolateral episiotomy did not appear to protect the patientagainst the development of sphincter defects (Table 4). Midlineepisiotomies are associated with a higher incidence of third-degreeor fourth-degree tears than posterolateral episiotomies1,26.There is therefore no reason to suspect that our findings wouldhave been any different in women who underwent a midline episiotomy.
The internal sphincter was injured more frequently than theexternal sphincter and was sometimes damaged when the perineumremained intact. Shearing forces produced by the descent ofthe infant's head may cause isolated damage to the internalsphincter, a mechanism different from that causing injury tothe external sphincter. Women with a shorter anal canal maybe more prone to this form of trauma, since internal-sphincterdisruption was positively associated with a shorter canal beforedelivery.
Endosonographic examination suggested that the structural damageto the sphincters was permanent, since the defects were presentat six months, and the incidence of defects among the primiparouswomen after delivery was similar to that among the multiparouswomen before delivery.
There was a definite relation between the presence of sphincterdefects, anal pressure (Table 3), and bowel symptoms (Table 5).These ultrasonographically identified sphincter defectstherefore appear to have physiologic and clinical importance.The single best predictive test of clinical dysfunction wasanal endosonography. Although anal pressures were reduced inwomen with sphincter defects, there was considerable overlapof values between the women with symptoms and those withoutthem.
Only about one third of the women with sphincter defects hadbowel symptoms. Women with defects who do not have symptomsmay have sufficient residual sphincter function to maintaincontinence. Long-term follow-up of such women will be necessaryto determine whether they are at greater risk for incontinencelater in life. Since the peak incidence of fecal incontinenceamong women occurs in the fifth and sixth decades,27 the cumulativeeffect of subsequent deliveries, the effects of aging,27,28the menopause,27,28 and the progression of a neuropathy6 mayall contribute to sphincter weakness in the long term. Womenwith an occult sphincter defect may be at greater risk.
None of the women with disturbances of bowel function had spontaneouslyreported their symptoms or sought medical attention. Underreportingof such symptoms is well known29 and may explain why these problemsare not widely recognized in obstetrical practice.
Sphincter defects developed in 8 of the 10 primiparous womenwho had a forceps delivery but in none of the 5 who had a vacuum-extractordelivery. These findings are consistent with those of otherreports indicating that vacuum extraction is associated withless trauma to the perineum than forceps delivery30,31.
In two previous studies,5,16 pudendal-nerve terminal motor latencyin women who delivered vaginally was not increased two monthspost partum, as compared with latency in a control group ofwomen5; latency had not been measured before delivery. Whenwe compared postpartum values directly with antepartum values,we found that vaginal delivery, particularly a first vaginaldelivery, resulted in a significant increase in pudendal-nerveterminal motor latency and in perineal descent six weeks afterdelivery. There was no association between bowel symptoms andprolonged pudendal-nerve terminal motor latency or abnormalperineal descent, which is not the case with idiopathic fecalincontinence32 that develops in middle age and is believed tobe related to neuropathy8. The association of a prolonged pudendal-nerveterminal motor latency with a sphincter defect probably reflectsa traumatic cause common to these two factors, rather than acausal relation between them.
In conclusion, vaginal delivery causes bowel symptoms, mechanicaltrauma to the anal sphincter, and injury to the pudendal nervein many women. The use of the obstetrical forceps is particularlyassociated with a higher risk of sphincter damage.
Supported by the Joint Research Board of St. Bartholomew's Hospital,a travel grant from the Wellcome Trust (Dr. Sultan), and St.Mark's Research Foundation (Dr. Kamm).
We are indebted to Professor Tim Chard (Department of ReproductivePhysiology, St. Bartholomew's Hospital) for his helpful advice,to the obstetrical consultants who allowed us to study theirpatients, and to the women who participated in this study.
Source Information
From St. Mark's Hospital (A.H.S., M.A.K., C.I.B.) and St. Bartholomew's (Homerton) Hospital (A.H.S., C.N.H., J.M.T., C.I.B.), both in London. Presented at the annual meeting of the American Gastroenterological Association, San Francisco, May 10-13, 1992, and published in abstract form (Gastroenterology 1992;102(4):A522).
Address reprint requests to Dr. Bartram at St. Mark's Hospital, City Rd., London EC1V 2PS, United Kingdom.
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