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94 Benign Anorectal Diseases
a
c
and specificity of EAUS was 100% for EAS defects and 100% and 95.5%, respectively,for IAS lesions. Sultan et al. [12] compared preoperative
ultrasonographic findings with intraoperative results in 12 consecutive patients who underwent surgical repair for fecal incontinence. EAUS cor­rectly identified all sphincters defects at time of surgery. Sentovich et al. [34] examined the accu­racy and reliability of EAUS. In 22 incontinent women with known anal sphincter injury, the accuracy was 100%. However, in nulliparous women, EAUS falsely identified sphincter injury in 5–25% of normal anal sphincters. In this group, intact internal sphincters were more accurately predicted than intact external sphinc­ters (95% vs. 85%). Overall,clinical agreement in
the interpretation of the ultrasound between
b
Fig. IV.16. Anterior external sphincter repair (a). Three-
dimensional images in the coronal plane demonstrating the lower (b) and the upper (c) sling of the overlap
experienced ultrasonographers (interobserver reliability) was good (81% agreement). Agreement was significantly better for the IAS (74%, fair) than the EAS (61%, poor; p=0.0002) and in evaluating the distal anal canal (0–1.5cm) (78%) than the proximal anal canal (2.0–2.5cm from the anal verge) (48% agreement; p <0.0001). However, Gold et al. [35] reported that interobserver agreement for diagnosis of sphinc­ter disruption was very good (k=0.80). There was no disagreement with respect to combined or isolated IAS tears although there was some disagreement regarding isolated EAS tears.
Abramowitz et al. [36] demonstrated interob­server concordance in 98.9% of cases.
Three-dimensional (3-D) EAUS may improve
diagnostic confidence of detecting damage to the
Section IV • Endoanal Ultrasonography in the Assessment of Patients with Fecal Incontinence 95
a
Fig. IV.17. Large internal sphincter defect in the anterior part of the anal canal (a). Three-dimensional sagittal view showing
that this extends the full length of the internal sphincter, with a length of 29 mm (arrow) (b)
anal sphincter complex, and the relationship between the radial angle and longitudinal extent of a sphincter tear can be assessed [13] (Figs. IV.17–20). An additional advantage of 3-D reconstructions is the possibility of measuring the length of the remaining intact sphincter mus­cle. Christensen et al. [37] investigated the differ­ences between 3-D and two-dimensional (2-D) EAUS in visualizing damage to the anal sphincter complex. The overall agreement between two observers was 98.2% using 3-D and 87.9% using 2-D. In our institution (unpublished data), we assessed the differences between 2-D and 3-D
EAUS in defining the longitudinal extent of a sphincter defect in 33 patients with fecal inconti­nence due to obstetrical injury. The longitudinal extent of an EAS tear was graded as either proxi-
mal, central, or distal only, or a combination of two levels or full-length involvement. Two­dimensional EAUS localized the defect in the mid anal canal in most patients (94%), and in two patients, the defect was localized in the upper plus mid or mid plus distal anal canal,respective­ly. After 3-D reconstruction, the defects were localized the upper plus mid anal canal in four patients (12%), in the mid anal canal only in 22
b
a
Fig. IV.18. Large internal sphincter defect in the left side of the anal canal (a). Three-dimensional coronal view showing that this
extends the full length of the internal sphincter, with a length of 25 mm (b)
b
96 Benign Anorectal Diseases
Fig. IV.19. Obstetric trauma with a well-defined defect of the external sphincter at 2 o’clock. Multiview reconstruction showing
the defect in the coronal (a), axial (b), and sagittal (c) planes
patients (67%), and in the mid plus distal anal
canal in six patients (18%). In one patient (3%),it detected a full-length involvement. The overall agreement between 2-D and 3-D EAUS was mod­erate (k=0.25) for EAS tears in the upper plus mid anal canal, good (k=0.71) for mid anal canal only lesions, and poor (k=0.14) for defects extending to the mid plus distal anal canal or for full-length involvement. Three-dimensional EAUS allows a better evaluation of the longitudinal extent of EAS defects and may improve the selection of patients for surgical repair of the anal sphincter complex,helping the surgeon to judge how far the repair should extend.
West et al. [38] examined whether 3-D EAUS measurements (EAS length, thickness, area, and volume) can be used to detect EAS atrophy and
compared the results with MRI measurements. Agreement between 3-D EAUS and endoanal MRI was 61% for IAS defects and 88% for EAS defects. However, correlation was poor for EAS atrophy, suggesting that 3-D EAUS measurements are not suitable parameters for assessing EAS atrophy.
EAUS is the anorectal physiology study most likely to change a patient’s management plan. Liberman et al. [20] reported that EAUS detected anal sphincter defects in five (11%) of 45 patients within the medical group of fecal incontinence
who changed from medical to surgical manage­ment. In the surgical management group, 7% of patients changed from surgical to medical thera­py because of normal EAUS findings, and 2% changed from sphincteroplasty to neosphincter surgery.
Section IV • Endoanal Ultrasonography in the Assessment of Patients with Fecal Incontinence 97
a
c
Fig. IV.20. Three-dimensional images with volume render mode showing the extent of a sphincter tear in different planes (a–d)
References
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2. Bartram CI (2003) Ultrasound. In: Bartram CI, DeLancy JOL. Imaging pelvic floor disorders.Springer, Berlin Heidelberg New York
3. Burnett SJD, Bartram CI (1991) Endosonographic vari­ations in the normal internal anal sphincter. Int J Colorect Dis 6:2
4. Williams AB, Bartram CI, Halligan S et al (2001) Multiplanar anal endosonography – normal anal canal anatomy. Colorectal Dis 3:169–174
5. Frudinger A, Halligan S, Bartram CI et al (2002) Female anal sphincter: age-related differences in asymptomatic volunteers with high-frequency endoanal US. Radiology 224:417–423
6. Williams AB, Cheetham MJ, Bartram CI et al (2000) Gender differences in the longitudinal pressure profile of the anal canal related to anatomical structure as
demonstrated on three-dimensional anal endosonog­raphy. Br J Surg 87:1674–1679
7. Nielsen MB, Hauge C, Rasmussen OO et al (1992) Anal sphincter size measured by endosonography in healthy volunteers. Effect of age, sex and parity. Acta Radiol 33:453–456
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98 Benign Anorectal Diseases
8. Kumar A, Scholefield JH (2000) Endosonography of the anal canal and rectum. World J Surg 24:208–215
9. Gold DM, Halligan S, Kmiot WA, Bartram CI (1999) Intraobserver and interobserver agreement in anal endosonography. Br J Surg 86:371–375
10. Enck P,Heyer T, Gantke B et al (1997) How reproducible are measures of the anal sphincter muscle diameter by endoanal ultrasound? Am J Gastroenterol 92:293–296
11. Thakar R, Sultan A (2004) Anal endosonography and its role in assessing the incontinent patient. Best Pract Res Clinic Obstet Gynaec 18:157–173
12. Sultan AH, Kamm MA, Talbot IC et al (1994) Anal endosonography for identifying external sphincter defects confirmed histologically.Br J Surg 81:463–465
13. Gold DM, Bartram CI, Halligan S et al (1999) Three­dimensional endoanal sonography in assessing anal canal injury. Br J Surg 86:365–370
14. Bollard RC, Gardiner A,Lindow S et al (2002) Normal female anal sphincter: difficulties in interpretation explained. Dis Colon Rectum 45:171–175
15. Rociu E, Stoker J, Eijkemans MJC et al (1999) Fecal incontinence: endoanal US versus endoanal MR imag­ing. Radiology 212:453–458
16. Felt-Bersma RJ, van Baren R, Koorevaar M et al (1995) Unsuspected sphincter defects shown by anal endosonography after anorectal surgery. Dis Colon Rectum 38:249–253
17. Vaizey CJ, Kamm MA, Bartram CI (1997) Primary degeneration of the internal anal sphincter as a cause of passive faecal incontinence. Lancet 349:612–615
18. Felt-Bersma RJ, Cuesta MA, Koorevaar M (1996) Anal sphincter repair improves anorectal function and
endosonographic image: a prospective study. Dis
Colon Rectum 39:878–885
19. Voyvodic F, Rieger NA, Skinner S et al (2003) Endosonographic imaging of anal sphincter injury. Does the size of the tear correlate with the degree of dysfunction? Dis Colon Rectum 46:735–741
20. Liberman H, Faria J, Ternent CA et al (2001) A prospective evaluation of the value of anorectal physi­ology in the management of fecal incontinence. Dis Colon Rectum 44:1567–1574
21. Gantke B, Schafer A, Enck P, Lubke H (1993) Sonographic, manometric and myographic evaluation of the anal sphincters morphology and function. Dis Colon Rectum 36:1037–1041
22. Bennett RC, Friedman MHW, Goligher JC (1963) Late results of haemorrhoidectomy by ligature and exci­sion. BMJ 2:216–219
23. Speakman CT, Burnett SJ, Kamm MA, Bartram CI (1991) Sphincter injury after anal dilatation demon­strated by anal endosonography. Br J Surg 78:1429–1430
24. Khubchandani IT, Reed JF (1989) Sequelae of internal sphincterotomy for chronic fissure in ano. Br J Surg 76:431–434
25. Kennedy HL, Zegarra JP (1990) Fistulotomy without external sphincter division for high anal fistula. Br J Surg 77:898–901
26. Farouk R, Bartolo DCC (1994) The use of endoluminal ultrasound in the assessment of patients with fecal incontinence. J R Coll Surg Edinb 39:312–318
27. Burnett SJ, Spence-Jones C, Speakman CT et al (1991) Unsuspected sphincter damage following childbirth revealed by anal endosonography. Br J Radiol 64:225–227
28. Nielsen MB,Rasmussen OO, Pedersen JF, Christiansen J (1993) Anal endosonographic findings in patients with obstructed defecation. Acta Radiol 34:35–38
29. Stoker J, Rociu E, Zwamborn AW et al (1999) Endoluminal MR imaging of the rectum and anus: tech­nique, applications and pitfalls. Radiographics
19:383–398
30. Williams AB, Bartram CI, Modhwadia D et al (2001) Endocoil magnetic resonance imaging quantifictaion of external anal sphincter atrophy. Br J Surg 88:853–859
31. Nielsen MB, Dammegaard L, Pedersen JF (1994) Endosonographic assessment of the anal sphincter after surgical reconstruction. Dis Colon Rectum 37:434–438
32. Savoye-Collet C, Savoye G, Koning E et al (1999) Anal endosonography after sphincter repair: specific patterns related to clinical outcome. Abdom Imaging 24:569–573
33. Deen KI, Kumar D, Williams JG (1993) Anal sphincter defects: correlation between endoanal ultrasound and surgery.Ann Surg 218:201–205
34. Sentovich SM, Wong WD, Blatchford GJ (1998) Accuracy and reliability of transanal ultrasound for
anterior anal sphincter injury. Dis Colon Rectum
41:1000–1004
35. Gold DM, Halligan S, Kmiot WA, Bartram CI (1999) Intraobserver and interobserver agreement in anal
endosonography. Br J Surg 86:371–375
36. Abramowitz L, Sobhani I, Ganansia R et al (2000) Are
sphincter defects the cause of anal incontinence after vaginal delivery? Results of a prospective study. Dis Colon Rectum 43:590–598
37. Christensen AF, Nyhuus B, Nielsen MB,Christensen H (2005) Three-dimensional anal endosonography may improve diagnostic confidence of detecting damage to the anal sphincter complex.Br J Rad 78:308–311
38. West RL, Dwarkasing S, Briel JW et al (2005) Can three-dimensional endoanal ultrasonography detect external anal sphincter atrophy? A comparison with endoanal magnetic resonance imaging. Int J Colorectal Dis 20:328–333
IV.3.
Update in Perineal Anatomy and its
Relevance to Obstetric Trauma
G.A. Santoro, L. Pellegrini, G. Di Falco
The prevalence of anal incontinence in women is strongly associated with obstetric history [1–5]. However, the mechanisms by which obstetrical events induce anal incontinence remain contro­versial [6–10]. The etiology of fecal incontinence has largely been attributed to damage to the innervation of the anal sphincter musculature sustained during vaginal childbirth, and Snooks et al. [11] could demonstrate the existence of pudendal nerve injury in 60% of patients with anal incontinence due to obstetric tearing. Sultan
et al. [5] found that although pudendal nerve ter­minal motor latency (PNTML) was significantly prolonged after vaginal delivery, it was not asso­ciated with the defecatory symptoms, and Lee et al. [10] reported that pathologic postpartum PNTML recovers to the predelivery level within 2 months.
With the introduction of endoanal ultrasonog­raphy (EAUS), the role of anal sphincter disrup­tion emerged, and the effect of pudendal nerve injury during vaginal delivery became less impor­tant [5, 6, 12–20]. Anal sphincter lacerations should be considered the main cause of fecal
incontinence in women after vaginal delivery [5, 6, 12–20] and are strongly associated with primi­parity, macrosomia, abnormal presentation, pro­longed second-stage labor, and operative vaginal delivery [1, 2,6–8, 21,22]. Prospective studies [5,6] before and after childbirth have also shown that up to one third of women sustain a sphincter defect that is not recognized after delivery but will be the primary cause of anal incontinence in later life. This late-onset incontinence is due to the compensation of pelvic floor muscles in younger women. With aging and weakening of these adju-
vant pelvic supports, however, these defects become clinically evident [10, 22–24].
This chapter focuses on the mechanism of delivery and its relevance to pelvic floor injuries. We also review the role of EAUS in the assess­ment of anal sphincter injuries following obstet­ric trauma.
Mechanism of Delivery and its Relevance to Pelvic Floor Injuries
The natural process of childbirth carries inherent risks to the perineum. However,the precise mech­anisms of anal sphincter injury during deliveries have still to be elucidated [6–10].Labor is divided into three stages: (1) first stage – start to full dilatation of the cervix, (2) second stage – full dilatation to birth of baby, and (3) third stage – birth of baby to delivery of placenta. The fetus is descending during first and second stages of labor. The birth canal is formed by dilatation of the cervix and vagina and by stretching and dis­placement of the muscles of the pelvic floor and
perineum. The bladder is pulled above the pubis because of its attachment to the uterus; the ure­thra is stretched and the bowel is compressed. By the end of the second stage, the birth canal has been fully formed (Fig. IV.21). Descent continues, and the occiput reaches the pelvic floor (Fig. IV.22). The occiput rotates to the front (inter­nal rotation) and the head become occipitoanteri­or (Fig. IV.23). This process of pushing the head through the vaginal introitus results in downward descent of the pelvic floor,and most of the uterine pressure is direct toward the perineal body and
100 Benign Anorectal Diseases
Urethra
Bulbospongiosus muscle
White line
Levator ani muscle
a
{
Anus
Dilated birth canal
Ischial
spine
Ischial
tuberosity
b
Transverse perineal
c
muscle
Urethra
Vagina
Coccyx
Anus
Fig. IV.21. Schematic representation of
the birth canal at the end of the second stage of labor (a). Canal from the outside (b), and from hereback (c)
Section IV • Endoanal Ultrasonography in the Assessment of Patients with Fecal Incontinence 101
Fig. IV.22. Schematic representation showing mechanism of
labor in left occipitoanterior position: the occiput reaches the pelvic floor
anorectum (Fig. IV.24). During the second stage of labor, the structures of pelvic floor are at highest risk of injury. Further descent of the fetus pushes the head forward with a movement of extension, and the occiput is delivered. Increasing extension round the pubis delivers the bregma, brow, and face (Fig. IV.24). Descent and delivery of the head has brought the shoulders into the pelvic cavity. The head on delivery is oblique to the line of the shoulders and rotates to the natural position rela-
tive to the shoulders with a movement known as “restitution” (Fig. IV.25a, b). Descent continues, and the shoulders rotate to bring the bisacromial diameter into the anteroposterior diameter of the pelvic outlet. This descent and rotation causes the head to rotate so that the occiput lies next to the left maternal thigh (external rotation) (Fig. IV.25c). The anterior shoulder now slips
a
Bladder
Cervix
beginning
to open
Fig. IV.23. Schematic representation
Normal
b
anus
showing mechanism of labor in left occipitoanterior position: descent and flexion (a); internal rotation (b)
102 Benign Anorectal Diseases
Physiological retraction ring
Upper
segment
(thick)
Lower
segment
(thin)
a
Bladder
Cervix fully dilated
Vagina distending
Anus stretching
b
under the pubis, and with lateral flexion of the fetal body,the posterior shoulder is born. The rest
of the body follows easily. Two thirds of the cases will deliver spontaneously as occipitoanterior (Fig. IV.26).
Abnormal Presentation
If flexion of the head remains incomplete in descent,then rotation of the occiput anteriorly on
the pelvic floor may not occur, and rotation will occur posteriorly (occipitoposterior position) (Fig. IV.27). The mechanism now is difficult, for flexion of the head is restricted by the fetal chest. The soft tissues are stretched more than in occip­itoanterior, and the fetus is delivered face to pubis (Fig. IV.28). Occipitoposterior position may lead
Fig. IV.24. Schematic representation of the mechanism of
pelvic floor injury during vaginal delivery (a). Uterine force acts downward and the pelvic resistance upward (b)
to increased risk of pelvic floor injuries [22]. Moreover, the perineum is distended by the occipitofrontal diameter, and often, delivery has to be completed by large episiotomy, by forceps rotation (Fig. IV.29), or by use of the ventouse. The incidence rate of occipitoposterior delivery
is 12%.
Episiotomy
Episiotomy is an incision in the perineal body at
the time of delivery. There are three types of inci­sions (Fig. IV.30): (1) median – a linear surgical incision is made is the midline of the vagina and perineum to increase vaginal capacity; it is asso­ciated with a much higher rate of third-degree injury [2, 7], (2) posterolateral – more difficult to
Section IV • Endoanal Ultrasonography in the Assessment of Patients with Fecal Incontinence 103
a
b
c
Fig. IV.25. Schematic representation showing mechanism of labor in left occipitoanterior position: delivery of head (a); resti-
tution (b); external rotation (c)