Representative manometric tracing showing an increase in the number of high-amplitude propagated contractions, spanning the colon and preceding the anal sphincter opening that leads to defecation. Abbreviations: T transverse colon, D descending colon, S sigmoid colon, AS anal sphincter
At rest, there is a state of continuous contraction by the external anal sphincter, the puborectalis muscle, and the levator ani; this state helps both to maintain continence and to support the weight of the pelvic viscera [3]. Concerning defecation, the puborectalis muscle probably has the most relevant role, since its traction maintains the anorectal angle at approximately 90°, helping in preservation of the continence. Of interest, its paradoxical contraction during straining is related to one of the main mechanisms of obstructed defecation, the so-called pelvic floor dyssynergia [12].
The first phase of defecation is characterized, as recalled above, by the defecatory urge, and it is preceded by a progressive increase in frequency and amplitude of HAPC [11] (Fig. 2.1). It is currently thought that this sensation is primarily originated in the rectum [3], as demonstrated by the fact that progressive rectal distension causes a graded sensory response that starts with an awareness of filling [13]. Continuing the distension, there is the onset of a constant sensation (often described as the desire to pass flatus) progressively replaced by an urge to defecate when the maximum tolerable volume is reached [14, 15]. However, the urge sensation may also originate extra-rectally, from the stimulation of nerve endings and stretch receptors of the pelvic floor muscles (including the puborectalis muscle) and from structures adjacent to the rectum [16].
The rectum fills during the predefecatory phase. In normal conditions, the rectal ampulla accommodates to increased volumes with a small change in pressure (adaptive relaxation) [17], allowing it to temporarily store the contents until defecation is socially convenient. A reduced perception of the call to stool and constipation are frequently associated with an impaired perception of rectal distension (rectal hyposensitivity) [17]; this can lead to overflow incontinence [14]. On the other hand, an increased perception of distension (i.e., rectal hypersensitivity) is found in patients with urgency, with or without fecal incontinence [18]. An appropriate response to the call to stool, needing intact neurophysiological and biomechanical activity, is of a paramount importance for a correct evacuation, and it may be attenuated by the habitual suppression of the defecatory stimulus. This may ultimately result in fecal impaction up to the development of a secondary megarectum when the stimulus suppression is repeated in the time course [19].
It is still uncertain whether the anal canal contributes to the generation of the defecatory urge, since the distension of a balloon in the anal canal elicits a sensation of “stool escape” from the anus rather than an urge to defecate [20]. The anal canal chiefly provides a tight seal throughout the day, except when the subject decides to pass winds or wants to defecate; the major contribution to this sealing is due to the internal anal sphincter (IAS) [3, 21], and its intact sensation is essential for the sampling reflex [22].
Termination of defecation starts semi-voluntarily with the sense of complete rectal emptying, followed by the contraction of the external anal sphincter and the pelvic floor; their contraction allows the closure of the anal canal and re-directs the pressure gradient towards the rectum [3]. Finally, the “closing reflex” (a transient pressure increase following the passage of stools) of the external sphincter provides time to the internal sphincter to recover its tone [25]. After the individual terminates to strain, intra-abdominal pressure decreases and the postural reflex of the pelvic floor is reactivated [26], with the increased traction of the puborectalis muscle on the anorectal junction that causes to re-establish the basal state of the angle. The concomitant elongation of the anal canal also causes the passive distention of the anal cushions, thus resulting in the complete closure of the anal canal [3].