External Anal Sphincter

The external anal sphincter fibers develop from the anal tubercules. The fibers are not circularly arranged, which may impair concentric contraction. They can easily be identified by electrical stimulation and are usually situated in a line between the ischial tuber-osities. However, they can also be antepositioned. There are no longitudinal muscle fibers penetrating the smooth muscle fibers of an internal anal sphincter, as in normal individuals, and inserting into the skin. Therefore, there is no corrugator ani muscle for the so-called fine continence helping to avoid staining or smearing, and fixing the mucosa to the surrounding tissue, which avoids mucosal prolapse. Rectal prolapse with a protrusion of all muscle layers of the pulled-down rectum, on the other hand, is unusual if the lateral wings continue to fix the neorectum inside the pelvis or the colon is fixed to the presacral fascia. The hemorrhoidal plexus is developed on a higher level and therefore not supporting fine continence by obstructing the lower anal canal by filling its vessels.

Abnormalities of innervation of the external sphincter are another important factor affecting postoperative anorectal function. Yuan et al. investigated 45 patients with ARM by neural electrophysiologic methods [41]. They found the latencies of the pudendoanal reflex, the spinoanal response, and the conduction times of sacral spinal centers are significantly prolonged in patients with ARM. There was a significant difference between the rectourethral fistula group and the vestibular fistula group, as well as the low-type deformity group on the other side. There was significant negative correlation between the latencies and clinical scores. Although pudendoanal reflex latency was longer in patients who had PSARP than those who had abdominoperineal pull-through procedures, the difference was not significant. The neuronal lesions resemble those of lumbosacral deformity but vary for each type of anal lesion. Nevertheless, they are important for clinical outcome.

Abbaso et al. came to the same result [42]. Five out of eight children showed well-preserved electrical activity of the external sphincter muscle in postoperative electromyographic studies. In one patient there was no activity and in only two patients the activity was normal. Six out of eight children showed a normally localized anus.

This is contradictory to studies in rats performed by Yuan et al. in 2003 showing that the innervation to the sphincter mechanism is defective and should be regarded as a primary anomaly that coexists with the alimentary tract anomaly in ARM during fetal development [43]. However, in the animal model of ethy-lenethiourea (ETU)-treated rats, the development of the muscle complex is decreased, especially in type II deformities showing only a muscular cord without any intestinal tube [44]. ETU-induced malformations are more complex, showing additional neural tube defects in 24 out of 29 animals studied by Qi et al. [45]. In addition, in Bai's ETU experiments the only types of ARM induced were the rectourethral fistula and common cloaca [46]. According to Mortell et al. adriamycin induces notochord hypertrophy, resulting in a significant increased volume of notochord during the critical phase of development [47,48]. This may interfere with organogenesis, resulting in vertebral, anorectal, cardiac, tracheoesophageal, renal, and limb (VACTERL) association. ETU-induced ARM cannot, therefore, be compared with human alterations.

Constipation Prescription

Constipation Prescription

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