internal anal sphincter

**Anatomy** - Smooth muscle, a distal thickening of the inner circular layer of the rectum. It extends from the anorectal junction to the intersphincteric groove (near the dentate/pectinate line, about 3–4 cm long). - It lies inside the external anal sphincter (EAS, skeletal muscle). The longitudinal muscle layer lies between them in the intersphincteric space. - It is involuntary, unlike the EAS and puborectalis, which are voluntary.

**Innervation** - Sympathetic (L5 via the hypogastric nerves/inferior hypogastric plexus): contraction, which maintains tone. - Parasympathetic (S2–S4 pelvic splanchnic nerves): relaxation, mediated by inhibitory enteric neurons releasing NO and VIP. - By contrast, the EAS is supplied by the inferior rectal branch of the pudendal nerve (S2–S4, somatic).

**Physiology** - Tonically contracted, it provides about 70–85% of resting anal canal pressure. The EAS provides about 10–25% and the anal cushions about 15%. The EAS and puborectalis account for most of the squeeze (voluntary) pressure. - Rectoanal inhibitory reflex (RAIR): rectal distension causes transient IAS relaxation and a reflex EAS contraction. This lets the rectal contents "sample" the anal canal, and continence is maintained by voluntary EAS contraction. Defecation occurs when voluntary relaxation of the EAS and puborectalis follows.

**Clinical correlations** - **Hirschsprung disease**: absent ganglion cells (Meissner and Auerbach plexuses; RET mutation) lead to a tonically contracted aganglionic segment. The IAS fails to relax, so the RAIR is absent on anorectal manometry. Diagnosis is confirmed by rectal suction biopsy, which shows absent ganglion cells and hypertrophic nerve trunks with increased acetylcholinesterase staining. Presents with delayed meconium passage (>48 h), a transition zone, and a "squirt sign" on rectal exam. Complications include enterocolitis and megacolon. - **Chronic anal fissure**: IAS hypertonia and spasm reduce posterior midline blood flow, causing ischemia and poor healing. Treatments are topical nitroglycerin or calcium channel blockers (diltiazem, nifedipine) and botulinum toxin. Lateral internal sphincterotomy is the surgical option. - **Fecal incontinence**: IAS damage, for example after obstetric injury, hemorrhoidectomy, or fistula surgery, causes passive incontinence or soiling. EAS damage causes urge incontinence. Passive incontinence suggests IAS dysfunction. - **Hemorrhoids**: internal hemorrhoids are above the dentate line (visceral innervation, painless, bleed). External hemorrhoids are below it (somatic innervation via the inferior rectal nerve, painful when thrombosed). - **Anal canal landmarks**: the dentate (pectinate) line marks the embryologic junction of endoderm and ectoderm. Above it, the arterial supply is the superior rectal artery, venous drainage is via the portal system, and lymph drains to the internal iliac nodes. Below it, the supply is the inferior rectal artery, venous drainage is systemic via the caval system, and lymph drains to the superficial inguinal nodes. - **Scleroderma**: IAS smooth muscle atrophy and fibrosis cause fecal incontinence. - **Pharmacology**: nitrates and CCBs (NO donors) relax the IAS. Botulinum toxin blocks ACh release. Sympathomimetics increase tone.

**High-yield pearls** - IAS = smooth muscle, involuntary. EAS = skeletal muscle, voluntary. - Absent RAIR on manometry = Hirschsprung disease. - Anal fissure: IAS hypertonia, treated with nitrates, CCBs, or botulinum toxin. - The IAS is the major contributor to resting tone.