Physiology of the Rectum and Anus

Fig. 6.1

Pelvic view of the levator ani demonstrating its three main components: puborectalis, pubococcygeus, iliococcygeus. Reprinted with permission from (Canda et al. 2010)

Fig. 6.2

Diagram of a coronal section of the rectum, anal canal, and adjacent structures. The pelvic barrier includes the anal sphincter complex and the pelvic floor muscles. Reprinted with permission from (Canda et al. 2010)

Lateral to the subepithelial layer, the caudal continuation of the circular smooth muscle of the rectum thickens and forms the internal anal sphincter (with its innervation from the myeneteric plexus or Auerbach plexus) , which terminates caudally with a well-defined border at a variable distance from the anal verge. Continuous with the outer layer of the rectum the longitudinal layer of the anal canal lies between the internal and external anal sphincters and forms the medial edge of the intersphincteric space. The longitudinal muscle comprises smooth muscle cells from the rectal wall, augmented with striated muscle from a variety of sources, including the levator ani, puborectalis, and pubococcygeus muscles. Fibers from this layer traverse the external anal sphincter forming septa that insert into the skin of the lower anal canal and adjacent perineum as the corrugator cutis ani muscle.

The striated muscle of the external sphincter surrounds the longitudinal muscle and between these lays the intersphincteric space. The external sphincter is arranged as three supposed structure, originally described by Holl and Thompson and later adopted by Gorsch and by Milligan and Morgan. In this system, the external sphincter is divided into deep, superficial, and subcutaneous portions, with the deep and subcutaneous sphincter forming rings of muscle and, between them, the elliptical fibers of the superficial sphincter running anteriorly from the perineal body to the coccyx posteriorly. Some consider the external sphincter to be a single muscle contiguous with the puborectalis muscle , while others have adopted a two-part model. The latter proposes a deep anal sphincter and a superficial anal sphincter, corresponding to the puborectalis and deep external anal sphincter combined, as well as the fused superficial and subcutaneous sphincter of the tripartite model. Anal endosonography and magnetic resonance imaging have not resolved the dilemma, although most authors report a three-part sphincter where the puborectalis muscle is fused with the deep sphincter.

The blood supply to the anorectal region is rich. The terminal branch of the inferior mesenteric artery is the superior hemorrhoidal (rectal) artery. The superior hemorrhoidal artery branches into right and left branches; the right branch further divides into anterior and posterior branches. The classic hemorrhoidal plexes are then located at the left later, right anterolateral and right posterolateral locations. The middle hemorrhoidal (rectal) arteries are direct branches from the internal iliac arteries. The inferior hemorrhoidal (rectal) arteries are branches off the pudendal arteries which also arise from the internal iliac arteries. The superior, middle, and inferior hemorrhoidal arteries then complete the rich arterial supply to the anorectal region.

The venous drainage of the anorectal region consists of superior hemorrhoidal veins draining into the portal venous system (by way of the inferior mesenteric vein) and the middle and inferior hemorrhoidal veins draining into the caval system (by way of the internal iliac veins). Thus the anorectal region can provide a means of portal decompression when portal hypertension exists.

Lymphatic drainage of the rectum travels along the internal iliac vessels as well as the aorta. Lymphatic drainage of the anal canal can follow the internal iliac vessels but also may travel through channels in the inguinal region.

The nerve supply is complex. The external anal sphincter is innervated by the pudendal nerve (S2–S4), which leaves the pelvis via the lower part of the greater sciatic notch, where it passes under the pyriformis muscle. It then crosses the ischial spine and sacrospinous ligament to enter the ischiorectal fossa through the lesser sciatic notch or foramen via the pudendal (or Alcock’s) canal.

The pudendal nerve has two branches: the inferior rectal nerve, which supplies the external anal sphincter and sensation to the perianal skin; and the perineal nerve, which innervates the anterior perineal muscles together with the sphincter urethrae and forms the dorsal nerve of the clitoris (penis). Although the puborectalis receives its main innervation from a direct branch of the fourth sacral nerve root, it may derive some innervation via the pudendal nerve.

The autonomic supply to the anal canal and pelvic floor comes from two sources. The fifth lumbar nerve root sends sympathetic fibers to the superior and inferior hypogastric plexuses, and the parasympathetic supply is from the second to fourth sacral nerve roots via the nervi erigentes. Fibers of both systems pass obliquely across the lateral surface of the lower rectum to reach the region of the perineal body.

The internal anal sphincter has an intrinsic nerve supply from the myenteric plexus together with an additional supply from both the sympathetic and parasympathetic nervous systems. Sympathetic nervous activity is thought to enhance and parasympathetic activity to reduce internal sphincter contraction. Relaxation of the internal anal sphincter may be mediated via non-adrenergic, non-cholinergic nerve activity via the neural transmitter nitric oxide. The role of the interstitial cells of Cajal (ICC) is not elucidated yet. Animal studies suggest that intramuscular ICC in the IAS may serve as pacemaker cells rather than as mediators of neuromuscular transmission. A recent study in patients undergoing abdominoperineal resection or proctectomy suggested that the ICC modulate the tone and the spontaneous activity of the internal anal sphincter (Lorenzi et al. 2012).

Anorectal physiological studies alone cannot separate the different structures of the anal canal; instead, they provide measurements of the resting and squeeze pressures along the canal pudendal block demonstrated the basal pressure to be generated for 85 % by the internal and for 15 % by the external anal sphincter (Frenckner and von Euler 1975). Later, it was shown that the basal pressure is composed for 30 % of tonic external sphincter activity, for 45 % of nerve induced internal sphincter activity, for 10 % of pure myogenic internal sphincter activity, and for 15 % of expansion of the hemorroidal plexuses (Lestar et al. 1989). The resting pressure undergoes regular fluctuations. These consist of slow waves (amplitude 5–25 cm H₂O, frequency between 10/min and 20/min) and much larger amplitude, ultra slow waves (amplitude 30–100 cm H₂O, frequency <3/min) (Kerremans 1969). Ultra slow waves (Fig. 6.3) are associated with high resting pressures.

Fig. 6.3

Anal manometry recording of slow waves. Note the high basal pressure

The external anal sphincter and the puborectalis muscle generate the maximal squeeze pressure. Symptoms of passive anal leakage (where the patient is unaware that episodes are happening) are attributed to internal sphincter dysfunction, whereas urge symptoms and frank incontinence of feces are due to external sphincter problems.

Fecal continence is maintained by the complex interaction of many different variables. Stool must be delivered at a suitable rate from the colon into a compliant rectum of adequate volume. The consistency of this stool should be appropriate and accurately sensed by the sampling mechanism. Sphincters should be intact and able to contract adequately to produce pressures sufficient to prevent leakage of flatus, liquid and solid stool. For effective defecation there needs to be coordinated relaxation of the striated muscle components with an increase in intra-abdominal pressure to expel the rectal contents. The structure of the anorectal region should prevent herniation or prolapse of elements of the anal canal and rectum during defecation.

As a result of the complex interplay between the factors involved in continence and fecal evacuation, a wide range of investigations is needed for full assessment. A defect in any one element of the system in isolation is unlikely to have great functional significance and so in most clinical situations there is more than one contributing factor.

4 Physiology of Continence and Defecation

The function of rectum and anus is an integrated action and coordination of several structures.

Arrival of stool in the rectum causes rectal distension and induces a desire to defecate along with a decrease in anal resting pressure (the rectoanal inhibitory reflex) .

This allows the rectal contents to come into contact with the sensitive anoderm, and based on the amount and nature of fecal material “sampled,” solid, liquid, or gas, an urge to defecate is induced that can only be resisted by vigorous contractions of the EAS and puborectalis muscle. If social conditions are favorable, the subject sits or squats, holds breath, contracts the diaphragm, abdominal, and rectal muscles, and simultaneously relaxes the EAS and puborectalis muscle. These maneuvers open the anus and move stool. Thus, sensory perception and coordinated movement of stool are important physiologic variables that affect anorectal function.

4.1 Anal Resting Pressure

The resting pressure prevents leaking from fecal material and fluid from the rectum and anus. This can be disturbed by direct damage to the internal sphincter by trauma like forceful dilatation (Speakman et al. 1991; Felt-Bersma et al. 1995), in grade 3c sphincter rupture during childbirth (Visscher et al. 2014), surgery (Felt-Bersma et al. 1995; Johannsson et al. 2013; Hirano et al. 2011; Lindsey et al. 2004), radiation (Canda et al. 2010) as well as scleroderma (Thoua et al. 2012), neuropathy due to autonomic dysfunction like diabetes (Pinna Pintor et al. 1994; Rogers et al. 1988), multiple sclerosis (MS) (Nusrat et al. 2012), Parkinson’s disease (Kim et al. 2011; Stocchi et al. 2000), or idiopathic (Ricciardi et al. 2006; Felt-Bersma et al. 1992). Isolated insufficiency of the internal sphincter will rather lead to fecal soiling than overt fecal incontinence, since the pelvic floor and external anal sphincter can compensate.

Anal resting pressure can be established with digital palpation, which correlates well with anal manometry (Orkin et al. 2010; Felt-Bersma et al. 1988) (see Chap. 19, “Anorectal Manometry”). With high resolution anal manometry (HRAM), a more detailed image can be obtained throughout the sphincter (Fig. 6.4).

Fig. 6.4

Normal 3D HRAM with anal resting pressure, increase during squeeze and relaxation during strain

4.2 Rectoanal Inhibitory Reflex

Increasing rectal distension is associated with transient reflex relaxation of the internal anal sphincter and contraction of the external anal sphincter, known as the rectoanal inhibitory or distention reflex. This can be demonstrated with anorectal manometry and was originally described by Schuster (Schuster et al. 1965). With (high resolution) anal manometry (HRAM), it can be shown that the more air is inflated in the balloon, the more profound the anal pressure drops. Furthermore, the level of the largest drop is in the middle of the anal canal, where the internal sphincter is at its maximum, can be seen (Fig. 6.5). This correlates very well with the anatomical image, which can be seen with anal ultrasound (Fig. 6.6)

Fig. 6.5

(a) Conventional and (b) 3D-HR anal manometry. Inhibition reflex. A fast drop in resting pressure, followed by a slow recovery. Increasing the volume of distention from 10 to 40 ml gives a pore profound relaxation

Fig. 6.6

3D anal ultrasound of the anal sphincter, frontal view. The external anal sphincter (EAS) is longer and runs more distal then the internal anal sphincter (IAS)

The exact neurological pathway for this reflex is unknown, although it may be mediated via intrinsic nerves of the myenteric plexus and stretch receptors in the pelvic floor. Its existence depends on intramural autonomic ganglions and its modulation on the integrity of the autonomic nervous system. Patients with rectal hyposensitivity have higher thresholds for rectoanal inhibitory reflex; it is absent in patients with Hirschsprung’s disease, progressive systemic sclerosis, Chagas’ disease, and initially absent after a coloanal anastomosis, although it often recovers. When anal pressures are low, the reflex can also not be elucidated.

4.3 Contraction of the External Anal Sphincter and Pelvic Floor

Fecal continence is maintained by an adequate basic tone of the pelvic floor and anal sphincter. When this is insufficient, pressure of the stool in the rectum can easily overcome the pressures generated by the internal and external anal sphincter. Causes for external anal sphincter dysfunction can be both muscular and neurological. Trauma of the anal sphincters during childbirth, even unnoticed, can be an important reason. Anorectal surgery, especially surgery for perianal fistula, is a notorious cause (Visscher et al. 2014). The most frequent (peripheral) neurological cause is stretch damage of the pudendal nerve resulting in atrophy of the external sphincter and to a lesser extend of the puborectal muscle. This can occur during chronic straining with childbirth (Snooks et al. 1986) and chronic constipation (Snooks et al. 1985), as was demonstrated in the eighties of the previous century. Another cause of peripheral neuropathy is diabetes (Pinna Pintor et al. 1994; Rogers et al. 1988).

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