David E. Beck, Steven D. Wexner, Tracy L. Hull, Patricia L. Roberts, Theodore J. Saclarides, Anthony J. Senagore, Michael J. Stamos and Scott R. Steele (eds.)The ASCRS Manual of Colon and Rectal Surgery2nd ed. 201410.1007/978-1-4614-8450-9_3
© Springer Science+Business Media New York 2014
3. Anorectal Physiology
(1)
Division of Colon and Rectal Surgery, Department of Surgery, University of Minnesota, 6363 France Ave S # 212, Edina, MN 55435, USA
Abstract
Normal bowel continence and evacuation are complex processes that involve the coordinated interaction between multiple different neuronal pathways and the pelvic and perineal musculature.
Understanding of anorectal anatomy and physiology is challenging due to the complex series of neural and behavioral-mediated interactions and the lack of ideal studies to evaluate the anatomy and physiology.
Complicating this understanding are other factors such as systemic disease, sphincter integrity, bowel motility, stool consistency, evacuation efficiency, pelvic floor stability, and cognitive and emotional affects.
Conventional anorectal physiology testing using techniques such as manometry, endoanal ultrasound, electrophysiologic studies, and defecography help to elucidate anorectal structures and function.
However, diagnostic dilemmas occur when patients report normal function with grossly abnormal test results or abnormal function with a normal test profile.
Introduction
Normal bowel continence and evacuation are complex processes that involve the coordinated interaction between multiple different neuronal pathways and the pelvic and perineal musculature.
Understanding of anorectal anatomy and physiology is challenging due to the complex series of neural and behavioral-mediated interactions and the lack of ideal studies to evaluate the anatomy and physiology.
Complicating this understanding are other factors such as systemic disease, sphincter integrity, bowel motility, stool consistency, evacuation efficiency, pelvic floor stability, and cognitive and emotional affects.
Conventional anorectal physiology testing using techniques such as manometry, endoanal ultrasound, electrophysiologic studies, and defecography help to elucidate anorectal structures and function.
However, diagnostic dilemmas occur when patients report normal function with grossly abnormal test results or abnormal function with a normal test profile.
Muscles of the Pelvic Floor and Sphincter Complex
Control of stool can be thought of as a pressure vector diagram, with continence represented as a balance of propulsive and resistive forces.
Contraction of the muscles of the pelvic floor and sphincter complex provides resistance, and tone is noted during periods of rest or deep sleep.
Voluntary contraction of the puborectalis and external sphincter increases resistance and defers defecation.
The anal sphincter is not a paired muscle structure, like the biceps and triceps in the arm; there is no extensor ani muscle.
Evacuation occurs when propulsive forces (increased intra-abdominal pressure and peristalsis of the colon and rectum) overcome the resistance of the pelvic floor and sphincter muscles.
The pelvic floor consists of a striated muscular sheet through which viscera pass.
This striated muscle, the paired levator ani muscles, is actually subdivided into four muscles defined by the area of attachment on the pubic bone.
The attachments span from the pubic bone, along the arcus tendineus (a condensation of the obturator fascia), to the ischial spine.
The components of the levator ani are therefore named the pubococcygeus, ileococcygeus, and ischiococcygeus. The pubococcygeus is further subdivided to include the puborectalis.
Between the urogenital viscera and the anal canal lies the perineal body.
The perineal body consists of the superficial and deep transverse perinei muscles and the ventral extension of the external sphincter muscle to a tendinous intersection with the bulbocavernosus muscle.
The fourth sacral nerve innervates the levator ani muscles.
Controversy continues regarding the innervation and origin of the puborectalis muscle.
Cadaver studies differ from in vivo stimulation studies as to whether the puborectalis muscle receives innervation only from the sacral nerve or also from the pudendal nerve.
Comparative anatomy and histological studies of fiber typing also support the inclusion of the puborectalis muscle with the sphincter complex and not as a pelvic floor muscle. In addition, electromyography (EMG) studies of the external anal sphincter (EAS) and puborectalis muscle indicate that the muscles function together with cough and strain.
The rectal smooth muscle consists of an outer muscularis mucosa, inner circular muscle, and the outer longitudinal layer.
The inner circular muscle forms the valves of Houston proximally and distally extends down into the anal canal becoming the internal anal sphincter (IAS).
This is not a simple extension of muscle as there are histologic differences between the upper circular muscle and the IAS.
For instance, the IAS is thicker than the circular muscle due to an increased number of smaller muscle cells.
The outer longitudinal layer surrounds the sigmoid colon coalescing proximally into thicker bands called taenia coli.
This same layer continues down to the anorectal junction where it forms the conjoined longitudinal muscle along with fibers from the pubococcygeus muscle.
Distally, this muscle lies in the intersphincteric plane, and fibers may fan out and cross both the internal and EAS muscles.
In an ultrasound view of the anal canal, the longitudinal muscle is seen as a narrow hyperechoic line in the intersphincteric space.
The puborectalis muscle, EAS, and IAS muscles are easily viewed with endoanal ultrasound. In the hands of an experienced ultrasonographer, the technique is highly sensitive and specific in identifying internal and external sphincter defects.
External Anal Sphincter (EAS)
Anatomical and sonographic studies indicate that the EAS begins development, along with the puborectalis muscle, at 9–10 weeks gestation.
At 28–30 weeks it is mature, and the anal sphincter then consists of three components, the striated puborectalis muscle, the smooth IAS muscle, and the smooth and striated EAS muscle.
Further differentiation of the EAS into two or three components is highly debated.
In 1715, Cowper described it as a single muscle. Later, Milligan and Morgan promoted the naming of the components as subcutaneous, superficial, and deep. Recently, Dalley makes a convincing point that the three components can only be seen in the exceptionally dissected specimen, and, in most cases, the muscle is one continuous mass and should be considered as such.
The EAS is innervated bilaterally by the pudendal nerve arising from S2 to S4. Motor neurons arise in the dorsomedial and ventromedial divisions of Onuf’s nucleus in the ventral horn of the spinal cord.
Crossover of the pudendal innervation was first suggested in studies by Swash and Henry on rhesus monkeys.
Hamdy and associates evaluated corticoanal stimulation of humans and found variable crossover which was symmetric in some and either right- or left-sided dominant in others.
This has been offered as one possible explanation for the inconsistent relationship between unilateral pudendal neuropathy and fecal incontinence.
The EAS maintains tonic activity at rest due to monosynaptic spinal reflex.
The tone can be abolished with spinal anesthesia and in conditions such as tabes dorsalis, where large-diameter afferent sensory fibers are destroyed, and over distension of the rectum, due to the inflation response.
Maximum tone, due to phasic activity in the EAS, can be maintained for only about 1 min, before fatigue is encountered.
Of interest, the only other striated muscles that maintain continuous low-level resting activity are the abductor of the larynx, the cricopharyngeus, and the external urinary sphincter.
Internal Anal Sphincter (IAS)
The IAS is an involuntary smooth muscle. It is the major source of anal resting pressure and is relatively hypoganglionic.
There are nerve fibers expected in an autonomic muscle – cholinergic, adrenergic, and nonadrenergic noncholinergic fibers.
It receives sympathetic innervation via the hypogastric and pelvic plexus. Parasympathetic innervation is from S1, S2, and S3 via the pelvic plexus.
There is considerable evidence that the sympathetic innervation is excitatory but conflicting information regarding the parasympathetic effect.
The IAS contributes 55 % to the anal resting pressure.
The myogenic activity that contributes 10 and 45 % is due to the sympathetic innervation.
The remainder of the resting tone is from the hemorrhoidal plexus (15 %) and the EAS (30 %).
Spinal anesthesia decreases rectal tone by 50 %, and the decreased resting tone seen in diabetic patients may be due to an autonomic neuropathy.
The IAS has slow waves occurring 6–20 times each minute increasing in frequency toward the distal anal canal.
Ultraslow waves occur less than two times a minute and are not present in all individuals occurring in approximately 5–10 % of normal individuals.
Ultraslow waves are associated with higher resting pressures, hemorrhoids, and anal fissures.
The occurrence of anal slow-wave activity with rectal pressure waves exceeding anal resting pressure suggests a role for anal slow waves in preserving continence.Related posts:
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