시원항병원
051) 331-7275논문발표
| 번호 | 제목 | 등록일 | 조회수 |
|---|---|---|---|
| 35 | Pelvic Floor Disturbance After Childbirth [2001년 8월 DCR] | 2011-11-17 | 3414 |
|
Vaginal Delivery Damages the Upper Levels of Sphincter Innervation
Tomoyuki Sato, M.D., Fumio Konishi, M.D., Hisanori Minakami, M.D.
From the Departments of Surgery, Obstetrics and Gynecology, and tClinical Laboratory Medicine, Jichi
Medical School, Tochigi-ken, Japan PURPOSE: Vaginal delivery disturbs pelvic floor innervation, which has previously been studied as a single mechanism. The effects of childbirth on innervation at different levels of the anal sphincter system were studied after childbirth.
METHODS: Both anal manometry and motor latencies were measured in 67 females. Twenty-nine females (30.8 -+ 4.4 years) were examined four days after vaginal delivery. Eleven of these 29 females were re-examined five months after vaginal delivery. Nineteen females (33.6 +- 4.6 years) who were examined five to nine days after undergoing an elective cesarean section and 19 asymptomatic, nonpregnant females (26.8 _+ 6.9 years) served as controls. Motor latencies were bilaterally measured within the anal sphincter system at 5, 3.8, 2.6, and 1.5 cm from the perineal skin by using a concentric needle electrode after sacral magnetic stimulation. Means of the bilateral latencies were analyzed. RESULTS: In postpartum females who gave birth vaginally, motor latencies at 5 and 3.8 cm, although not those at 2.6 and 1.5 cm, from the perineal sMn were significantly prolonged, and anal pressure monitored by maximum resting and squeeze pressures was significantly decreased compared with that in control females. The decreased anal pressure normalized spontaneously. The prolonged motor latencies at the upper two levels of the anal sphincter system persisted in these females for five months after vaginal delivery. CONCLUSIONS: The disturbance of irmervation of the upper anal sphincter system af*er vaginal
delivery may last for a long time, whereas the decreased anal pressure normalizes in a short time. Tim protracted disturbance of innervation of the upper anal sphincter system may be associated with later development of fecal incontinence. Childbirth is a natural event for females. Vaginal delivery, however, has been reported to disturb the anal sphincter system and its innervation: the anal sphincter may be disrupted and / or pudendal nerve conduction may become impaired after vaginal delivery. These phenomena may result in the later
development of fecal incontinence. Pudendal nerve terminal motor latency is examined predominantly to assess neurogenic disorders of the pelvic floor or the anal sphincter system of skeletal muscle. This method, used to assess the distal motor innervation of the anal sphincter system of skeletal muscle as a single unit, records the evoked contraction response of the external anal sphincter with a special surface electrode after transrectal stimulation of the pudendal nerve. Many previous studies have assessed the disturbance of innervation of the anal sphincter system of skeletal muscle after childbirth as a single unit by using this measurement system. The anal sphincter system of skeletal muscle, however, is not homogeneous but is composed of different sphincter muscles, including the puborectalis muscle and the external anal sphincter(s). An anatomic division of the external anal sphincter into three, two, or only one continuous mass depends on the perspective of the surgeon, gross anatomist, physiologist, or histologist.
We have already" developed a new method by which to examine the innervation of the pelvic floor,
which involves measuring the motor latencies of the anal sphincter system of skeletal muscle at four different levels, separately, after magnetic sacral nerve stimulation, a2 This method has revealed that the motor latency varied significantly among levels in middie-aged individuals. Thus, the newly developed method may allow specific assessment of the dysfunction of parts of the anal sphincter system. In this report, using this new technique, we studied the anal sphincter system of skeletal muscle and its
innervation at four different levels in females after childbirth and thus clarified which nerves and innervating muscles were damaged or impaired in the anal sphincter system after vaginal delivery. In addition, we investigated the time difference between the recovery of manometric data and that of the motorevoked potential latencies after vaginal delivery. DISCUSSION
We observed that vaginal delivery disturbed the nerve system of the pelvic floor at certain levels from
the perineal skin; i.e., vaginal delivery injured the upper two levels of the peripheral nerves in the anal sphincter system, which were assumed to reach the levels of the puborectalis muscle and the deep external anal sphincter muscle, respectively. Simultaneously the manometric data, including MRP, MSP, and LAC, showed deterioration after vaginal delivery but showed a good recovery within five months, whereas the deterioration in the motor-evoked potential latencies of the upper two levels of the pelvic floor persisted for more than five months after vaginal delivery. The pudendal nerve terminal motor latency was measured with a surface electrode in previous studies, thus the damage to the pudendal nerve after vaginal delivery has heretofore been considered homogeneous in the pelvic floor. Our findings strongly suggest that vaginal delivery is likely to injure innervation in the upper parts of the anal sphincter system but not that in the lower parts. These results may indicate that vaginal delivery injures the innervation in larger sphincter muscles such as the puborectalis muscle, which is reported to play a pivotal role in fecal continence. The larger the denervated sphincter muscle, the greater the influence on the defecatory function. The re-examination was elective, and only 11 of 29 females who gave birth vaginally were re-examined
five months later. However, the small number of reexamined subjects is unlikely to have altered our results because data on MRP, MSP, LAC, and latencies A, B, C, and D on postpartum Day 4 did not differ significantly between the 18 females who were not re-examined and the 11 females who were re-examined five months after delivery. The significantly decreased MRP and MSP seen in the 11 females at the initial examination had normalized at five months after delivery, whereas the significantly prolonged latencies A and B seen in these 11 females had not improved even five months after delivery. Previous studies reported that the deterioration of pudendal nerve latency recovered by two to three months, whereas our findings indicate that the deterioration in the nerve conduction velocity of the upper sphincter could last more than five months. In previous studies, the pudendal nerve latent T was measured at the terminal part of the pudendal nerve by using the special surface electrode on the anal canal mucosa. In contrast, in our study the motor-evoked potential latency was measured separately for S2 and S3 and at four different levels of the anal sphincter by using a concentric needle electrode. The specificity of our method may explain why the motor-evoked potential latency was prolonged in our study, the findings of which are discrepant with those of previous reports. In the present study, the anal pressure recovered within five months after vaginal delivery, at which
time recovery in the prolongation of the motorevoked potential latencies was not observed at the upper two levels of the anal sphincter system. The discrepancy of recovery between the anal pressure and the motor-evoked potential latencies was considered to indicate that the deterioration of the manometric data observed four days after vaginal delivery was not caused by the disturbance of the nerve system but by a possible direct injury to the anal sphincter, although ultrasound imaging was not performed to confirm this. Generally speaking, a decrease in MRP indicates a deterioration in the internal anal sphincter, whereas MSP represents damage to the external anal sphincter. Some compensatory mechanisms other than neural factors may work to improve anal pressure in these postpartum females with decreased anal pressure. The discrepancy of recovery between the anal pressure and the motor latencies may also mean that the
disturbance of the nerves innervating the upper anal sphincters is an ongoing process without any immediate effect. Although not verified, this protracted problem in innervation to the upper sphincters may cause delayed atrophy of the larger sphincter, including the puborectalis muscle and the deep external anal sphincter, leading to fecal incontinence later in life. This hypothesis is consistent with epidemiologic facts that fecal incontinence is likely to develop in middle-aged females (i.e., several years after vaginal delivery). The long second term of labor, the use of obstetric forceps, and the use of a vacuum extractor have been reported to be associated with deterioration of the anal function. In the present study, four days after vaginal delivery, MRP was lower in primiparous females than in multiparous females (P < 0.05;
Table 3). This may indicate that direct damage to the anal canal was more severe in primiparous females than in multiparous females; nevertheless, no significant difference was observed in the motor latencies based on parity (Table 3). Why does vaginal delivery selectively injure the nerves innervating the upper parts of the anal sphincter
system without disturbing tile nerves innervating the lower parts? We offer two possible explanations. First, during vaginal delivery the fetus may compress the pelvic floor to different degrees, depending on its anatomic location. Previous studies have suggested that the motor nerve supply of the upper parts of the pelvic floor, or the puborectalis muscle, comes from direct branches rising above the pelvic floor and that the nerve supply of the caudal sphincter, or the external anal sphincter, lies below the pelvic floor. Thus, different modes of nerve injury may arise and affect the sphincters in different ways. Second, this phenomenon may be caused by a basic biologic rule regarding the vulnerability of the peripheral nerves is (i.e., the nerves with faster conduction velocity are vulnerable to physical foreign power or stretching power), The conduction velocity of the nerve innervating the upper levels of the anal sphincter system is originally greater than that innervating the lower levels. Alternatively, these explanations may work in tandem. Different latency results in different females after vaginal delivery may depend on their innervation to the sphincter system. Variations in innervation to the puborectalis muscle and the external anal sphincters
may make one female more susceptible to injury than another. In summary, the pressure in the anal canal became lower and the peripheral nerves innervating the upper parts of the pelvic floor were damaged four days after vaginal delivery. About five months later, the
pressure in the anal canal had recovered but the disturbance of the nerve innervating the upper parts of the pelvic floor persisted. In contrast, anal pressure and motor latencies were not damaged after a cesarean section. |
|||