In an adult male with an anal fissure, is the internal anal sphincter (IAS) or the external anal sphincter (EAS) responsible for the painful spasm?

Internal Anal Sphincter (IAS) Hypertonia Drives Anal Fissure Spasm

The internal anal sphincter (IAS), not the external anal sphincter (EAS), is responsible for the painful spasm and elevated resting anal pressure in patients with anal fissures. 1, 2

Pathophysiologic Mechanism

The IAS is a smooth muscle structure that maintains basal anal canal tone at rest. 1 In anal fissure patients, IAS hypertonia creates a pathologic cycle:

• Elevated IAS tone reduces anodermal blood flow, creating local ischemia that prevents fissure healing 1, 2
• The pain-spasm-ischemia cycle perpetuates chronicity: anal trauma → pain → reflex IAS spasm → ischemia → delayed healing 1, 2
• Resting anal pressures in fissure patients (114 ± 17 cmH₂O) significantly exceed normal values (73 ± 27 cmH₂O), even when measured with minimal instrumentation 3

Evidence Supporting IAS as the Primary Culprit

All effective pharmacologic treatments target the IAS specifically:

• Calcium channel blockers (nifedipine 0.3% with lidocaine 1.5%) achieve 95% healing by blocking L-type calcium channels in IAS smooth muscle, reducing sphincter tone and increasing local blood flow 1, 2, 4
• Nitric oxide donors (nitroglycerin) cause IAS smooth muscle relaxation, though with lower efficacy (25–50% healing) and significant headache side effects 1, 2
• Lateral internal sphincterotomy (LIS)—the gold standard surgical treatment with >95% healing rates—divides the IAS, not the EAS, confirming that IAS hypertonia is the therapeutic target 1, 2

The therapeutic success of these IAS-directed interventions provides strong indirect evidence that IAS hypertonia drives the pathophysiology. 1, 5

Addressing the Controversial Hypothesis

One 2016 hypothesis proposed that the EAS might be responsible for elevated basal pressure through overreaction of the anal-external sphincter continence reflex. 6 However, this hypothesis contradicts established guideline-based treatment and lacks supporting clinical evidence:

• The EAS is a striated (voluntary) muscle that contributes to squeeze pressure during voluntary contraction, not resting tone 3
• Manometry studies show that maximum voluntary contraction pressures (reflecting EAS function) are normal in fissure patients, while resting pressures (reflecting IAS function) are consistently elevated 3
• The observation that basal pressure remained elevated after LIS when anesthesia wore off 6 may reflect incomplete sphincterotomy, residual IAS tone, or EAS compensation—but does not negate decades of evidence supporting IAS as the primary driver

Clinical Implications

Treatment algorithms universally target IAS relaxation:

1. First-line: Fiber (25–30 g/day), hydration, warm sitz baths, and topical 0.3% nifedipine/1.5% lidocaine TID for 6–8 weeks 1, 2, 4
2. Second-line: Botulinum toxin injection into the IAS (75–95% cure rates) 1, 2
3. Surgical: LIS after failed medical therapy (>95% healing, 1–3% recurrence) 1, 2

Critical pitfall: Manual anal dilatation is absolutely contraindicated due to 10–30% permanent incontinence risk from uncontrolled IAS and EAS injury. 1, 2, 4

The consistent therapeutic success of IAS-targeted interventions—and the failure of treatments that do not address IAS tone—confirms that IAS hypertonia is the mechanistic driver of anal fissure spasm and chronicity. 1, 2, 5, 3