Anorectal Physiology

Normal continence/defecation physiology, synthesized from ASCRS Ch. 3. Complements Colorectal Anatomy & Embryology (gross anatomy of the same structures, Ch. 1) and Anorectal Physiology Testing (the diagnostic toolkit that measures the mechanisms described here). For disorders of this physiology (fecal incontinence, defecatory dyssynergia, anorectal pain), see Fecal Incontinence. Textbook reference content, not primary literature.

Innervation of the anus and pelvic floor

Sympathetic fibers (L1–L3) join the preaortic plexus, extend as the hypogastric plexus, and join parasympathetic fibers (nervi erigentes, S2–S4) to form the pelvic plexus. The internal anal sphincter (IAS) receives both sympathetic (L5) and parasympathetic (S2–S4) motor innervation. The external anal sphincter (EAS) is innervated by the inferior rectal branch of the pudendal nerve (S2–S3) and the perineal branch of S4 — somatic, not autonomic. Notably, unilateral pudendal nerve transection does not impair EAS function, because of fiber crossover at the spinal cord level — a clinically important redundancy. The levator ani receives sacral roots S3/S4, the perineal branch, and the inferior rectal nerve; pudendal branches supply pubococcygeus/puborectalis while direct sacral nerves S3/S4 supply iliococcygeus (consistent with the split innervation pattern already described on Colorectal Anatomy & Embryology).

Upper anal canal sensation is both free and organized nerve endings: Meissner's corpuscles (touch), Krause's bulbs (temperature), Golgi-Mazzoni bodies (pressure), and genital corpuscles (friction) — concentrated in the transition zone, possibly contributing to sampling. The pudendal nerve's inferior rectal branch provides anal sensation and may help maintain continence and discriminate solid from gas.

Normal continence

Requires coordination between neuronal reflexes, sensory/motor pathways, the rectum, anal sphincters, and pelvic floor — despite this coordination being incompletely characterized even now.

Rectal sensation and compliance: baseline rectal pressure is low (~5 mmHg) vs. anal canal pressure (10–14× higher) — this differential allows stool deferment, forcing stool back into the sigmoid/rectum until defecation is initiated. The rectum lacks proprioceptive receptors; compliance is instead attributed to slowly adapting mechanoreceptors responding to tension/rapid distension, termed rectal intra-ganglionic laminar endings (rIGLEs). Defecation sensation itself is thought to occur at the level of the levators and anal canal rather than the rectum — consistent with preserved defecation sensation after proctectomy with ileoanal/coloanal anastomosis.

Anorectal reflexes: the rectoanal inhibitory reflex (RAIR) is the key intramural reflex — rectal distension relaxes the upper IAS, allowing rectal contents to contact specialized upper-anal- canal receptors that discriminate flatus from stool ("sampling"), while EAS/puborectalis contraction delays defecation. Occurs every 8–10 minutes, lasts <10 seconds. Absent in Hirschsprung's disease (no myenteric ganglia in the rectum — see Colorectal Anatomy & Embryology's embryology section) and may be injured/altered after rectal resection, with implications for postoperative functional outcome. Less-studied reflexes: cutaneous anal sphincter reflex (EAS contraction to touch/pain of perianal skin), bulbocavernosus reflex (EAS contraction on squeezing glans penis/clitoris — persists after urethral catheter removal), and cough-anal reflex (EAS contraction with coughing/sniffing, important during sudden intraabdominal pressure increases).

Internal and external anal sphincters: the IAS constitutes ~50–70% of resting anal tone, with hemorrhoid complexes contributing an additional ~15% (broadly consistent with — a more granular breakdown of — the "~80% from the internal sphincter" figure already on Colonic Physiology; not treated as a contradiction). Hemorrhoids (ASCRS Ch11) independently cites hemorrhoid cushions as contributing up to 20% of baseline continence — the same phenomenon described from the hemorrhoid- disease side, not a third conflicting figure. Resting tone is predominantly myogenic (slow, constant waves of smooth-muscle contraction), with additional excitatory sympathetic and inhibitory parasympathetic (nitric-oxide-mediated) input. IAS injury → passive incontinence/leakage; EAS injury → urge incontinence. The EAS's main contribution is voluntary/reflexive contraction in response to rectal distension or threatened incontinence (e.g., during increased intraabdominal pressure); after EAS contraction, urgency/tenesmus diminish over time as "rectal adaptation" occurs. Unlike the IAS, the EAS is fatigable — deferment of large stool volumes for only seconds to minutes despite normal rectal compliance.

Puborectalis and the pelvic floor: puborectalis forms a sling at the anorectal junction creating the anorectal angle (90–100° at rest), palpable as the top of the anorectal ring on DRE. Proposed mechanisms for its continence role: the "flap-valve theory" (pushes the anterior rectal wall against the upper anal canal during increased intraabdominal pressure) or a deeper-sphincter mechanism coordinated with the EAS.

Normal defecation

Sensory mechanisms allow the rectum to stretch/accommodate feces as it's sensed; the RAIR reflexively relaxes the IAS, allowing sampling and distinguishing solid/liquid/gas. If defecation isn't desired, the anal sphincters contract and the rectum continues to distend until the individual becomes aware — though the urge to defecate lasts only seconds and is controlled by continued (conscious) EAS contraction; sampling can continue even with a full rectum. During defecation: (1) puborectalis relaxes/lengthens, straightening the anorectal angle; (2) the conjoined longitudinal muscle contracts, shortening the anal canal; (3) the pelvic floor descends; and the anal sphincters relax as evacuation is initiated by rectosigmoid contractions, propelling feces through the anal canal. A squatting/hip- flexion position facilitates this by optimally straightening the anorectal angle and increasing intraabdominal pressure. Anal closure at the end of defecation ("closing reflex") is an exaggerated EAS contraction plus restoration of IAS resting tone.

Related pages

• Anorectal Physiology Testing — the diagnostic toolkit (manometry, PNTML, balloon insufflation/expulsion, defecography) that measures the mechanisms above; gained several new normal-value/mechanistic details from this chapter (added there directly).
• Fecal Incontinence — disorders of the continence/defecation mechanisms described here.
• Colorectal Anatomy & Embryology — gross anatomy underlying this physiology; the split levator innervation pattern here corroborates that page's account.
• Colonic Physiology — its brief RAIR mention has been trimmed to point here for the full mechanistic account, avoiding duplication.

Open items / gaps

• Continence mechanisms are explicitly described by the source as "incompletely understood" — not a wiki gap, an acknowledged open question in the field.