Colonic Transit as 5 L of water and associated electrolytes can be absorbed in one day. Parasympathetic-mediated peristaltic contraction of colonic smooth muscle transfers fecal material to the rectum. A delay in stool transit at the rectosigmoid region of the colon allows for maximal absorption of water and sodium.
Storage As stool accumulates in the rectosigmoid, rectal distention triggers a transient decrease in the internal anal sphincter (IAS) tone and an increase in the external anal sphincter (EAS) tone, known as the rectoanal inhibitory reﬂex. Exposure of the anal canal to fecal matter facilitates sampling, whereby the anal canal and its abundant sensory nerves determine stool consistency (i.e., solid, liquid, or gas). Accommodation occurs as the normally compliant rectal vault relaxes in response to increased volume. This cycle, combined with increased rectal distention, stimulates an urge to defecate. This urge can be voluntarily suppressed through cortical control, resulting in further accommodation and activation of the continence mechanism.
Muscles The key muscles of the continence mechanism are the puborectalis, IAS, and EAS. The puborectalis muscle originates from the pubic rami at the level of the arcus tendineus levator ani and passes laterally to the vagina and rectum in a U-shaped configuration, creating a sling around the genital hiatus. Contraction of the puborectalis muscle narrows the genital hiatus, developing the near 90-degree anorectal angle. The resting tone of the puborectalis muscle serves as the primary continence mechanism for solid stool. The IAS and EAS are essential for continence of ﬂatus and liquid stool. The internal sphincter maintains most of the resting tone for the sphincter complex through autonomic reﬂex arcs and is essential for passive continence. Although the external sphincter also maintains constant resting tone, it is ultimately responsible for preventing fecal urgency and stress incontinence associated with sudden increases in intra-abdominal pressure. This function is under both voluntary and involuntary control. The anal cushions act as the final anatomic barrier. They fill with blood, causing occlusion of the anal canal.
Nerves Many pathologic states disrupt normal function through denervation. The IAS receives its sympathetic supply from L5, which passes through the pelvic plexus via the hypogastric plexus. The parasympathetic supply from S2-4 synapses at the pelvic plexus, where it joins the sympathetic nerves. In addition to the parasympathetic and sympathetic components, the autonomic nervous system of the gut has an enteric nervous system (ENS). The ENS provides local circuitry that can contract or relax the gut muscles, as well as impact absorption and secretion. The autonomic ganglia of the ENS, located in the gut, are interconnected to provide local integration and processing of information. The IAS acts through reﬂex arcs at the spinal cord without voluntary control. The puborectalis (levator ani) is innervated by branches of the S2-4 sacral roots and does not receive direct innervation from the pudendal nerve (1). The EAS is innervated bilaterally by the pudendal nerve (S2-4) via Alcock’s canal. The pudendal nerve fibers cross over at the level of the spinal cord, allowing preservation of EAS function in the event of unilateral damage. The rich sensory supply from the anal canal travels along the inferior rectal branch of the pudendal nerve.