What is the nerve supply to the anal sphincter in a patient with a history of diabetes, Parkinson's disease, or previous pelvic surgery?

Nerve Supply to the Anal Sphincter

Primary Innervation Anatomy

The external anal sphincter (EAS) receives its primary motor innervation from the inferior rectal branches of the pudendal nerve (S2-S4), with approximately 31% of individuals having additional direct supply from the S4 sacral nerve root 1.

The internal anal sphincter (IAS) has a distinctly different nerve supply pattern:

• The IAS receives autonomic innervation primarily from the inferior rectal branches of the pelvic plexus (IRB-PX), which originate from the posterolateral corner of the prostate in males or the lower paracolpium in females 2, 3.
• These nerves descend along the internal aspect of the levator ani muscle and enter the anal canal on the anterolateral side 2, 3.
• The IAS contains predominantly sympathetic (tyrosine hydroxylase-positive) nerve fibers with fewer parasympathetic-nitrergic (neuronal nitric oxide synthase-positive) fibers, in contrast to the distal rectum which has primarily parasympathetic innervation 2, 3, 4.
• The major autonomic input to the IAS does NOT originate from the distal rectal myenteric plexus but rather from the IRB-PX running along the conjoint longitudinal muscle coat 3.

Sensory Innervation and Coordination

A sensory-motor regulation loop exists for both sphincters, with afferent sensory fibers traveling from the urinary and anal sphincters through the anterior and posterior branches of the inferior hypogastric plexus respectively 5.

• The external layer of the urethral and anal sphincters demonstrates highly positive nitrergic (anti-NOS1) and sensory (anti-CGRP) labeling, indicating rich sensory innervation 5.
• This sensory feedback mechanism coordinates the function of internal (smooth muscle) and external (striated muscle) sphincter layers 5.

Critical Clinical Implications in High-Risk Populations

Diabetes and Parkinson's Disease

Patients with diabetes mellitus, Parkinson's disease, and other generalized neurological disorders commonly develop secondary visceral neuropathy affecting both parasympathetic and sympathetic nerves that innervate the gut and anal sphincters 6.

• Diabetes is the most common cause of autonomic neuropathy affecting anal sphincter function 6.
• Parkinson's disease can cause basal ganglia calcification and leukoencephalopathy that affects gut motility and sphincter coordination 6.
• These conditions may cause a lymphocytic leiomyositis and myenteric ganglionitis affecting the enteric nervous system 6.

Previous Pelvic Surgery

Surgeons must exercise extreme caution when operating in the lower pelvis, as multiple surgical approaches can damage the nerves supplying the anal sphincters 1, 2, 3:

• Debridement of lower sacral segments (below S3/S4) during pelvic osteomyelitis treatment can damage the S2-S4 nerve roots innervating the EAS, resulting in permanent fecal incontinence in non-paraplegic patients 1.
• Intersphincteric dissections for low rectal cancer will most likely damage the IRB-PX because of its intersphincteric course, leading to loss of innervation to the major part of the IAS 1, 2, 3.
• Radical prostatectomy can sacrifice or damage the IRB-PX at the posterolateral corner of the prostate 2.
• Tension-free vaginal tape insertion can damage the IRB-PX in the lower paracolpium 2.
• Fistula surgery involving the intersphincteric space places the inferior rectal branches at risk 1.

Diagnostic Approach for Suspected Nerve Damage

Begin with anorectal manometry to quantify sphincter pressures and rectal sensation, followed by 3D anal ultrasonography or MRI to identify structural defects, atrophy, or sphincter tears 7.

• Anorectal manometry serves as both a diagnostic tool and therapeutic component for biofeedback therapy 8.
• 3D anal ultrasonography is superior for visualizing IAS defects, while MRI better demonstrates EAS tears, atrophy, and patulous anal canal 7.
• Digital rectal examination should evaluate resting tone (IAS function) and squeeze augmentation (EAS and puborectalis function), with observation of perineal descent during simulated defecation 6.

Management Algorithm for Neurogenic Sphincter Dysfunction

Step 1: Conservative Management (Always First-Line)

All patients must receive an optimal trial of conservative therapy before considering surgical intervention 7:

• Fiber supplementation (25-30g daily) with adequate fluid intake to optimize stool consistency 7.
• Loperamide 2mg starting 30 minutes before breakfast, titrated up to 16mg daily for diarrhea-associated incontinence 7.
• Pelvic floor biofeedback therapy is essential for patients with concurrent dyssynergic defecation or evacuation disorders, with success rates exceeding 70% 8, 7.

Step 2: Device-Based Interventions (After Conservative Failure)

Dextranomer microspheres in hyaluronic acid (NASHA Dx) is the only FDA-approved bulking agent for fecal incontinence, with 52% of patients achieving ≥50% reduction in incontinence episodes at 6 months 7.

Sacral nerve stimulation (SNS) should be considered for patients who fail conservative therapy and bulking agents, with initial test stimulation for 2-3 weeks 7.

• SNS is particularly relevant given that it targets the S2-S4 nerve roots that supply the EAS 1.
• However, SNS should not be used for managing defecatory disorders based on limited evidence 6.

Step 3: Surgical Repair (For Structural Defects)

Overlapping sphincteroplasty is indicated for patients with documented structural sphincter defects on imaging who have failed conservative measures 7.

• Sphincteroplasty should be considered in postpartum women with fecal incontinence and in patients with recent sphincter injuries 6.
• In patients presenting later with symptoms unresponsive to conservative and biofeedback therapy with evidence of sphincter damage, sphincteroplasty may be considered when perianal bulking injection and SNS are not available or unsuccessful 6.

Critical Pitfall to Avoid

Never perform manual anal dilatation, as it causes permanent incontinence in 10-30% of patients and is absolutely contraindicated 7.

Special Considerations for Complex Sphincter Dysfunction

Evaluation of sphincteric function after surgery is difficult because of the complex control mechanism that operates somewhat independently of nerve supply 2.

• The IAS maintains resting tone through intrinsic myogenic properties and autonomic modulation, but paradoxically relaxes during moments of greatest need through the rectoanal inhibitory reflex 9.
• The EAS can only maintain full contraction for seconds before fatiguing, requiring coordination with the IAS and puborectalis for sustained continence 9.
• This complex interplay explains why isolated nerve damage may not always correlate with clinical symptoms 2, 9.