Anal Fissures

Etiology

Anal fissures arise from various local and systemic factors. Common causes include constipation, chronic diarrhea, sexually transmitted infections (STIs), tuberculosis, inflammatory bowel disease (IBD), HIV, anal cancer, obstetric trauma, prior anorectal surgery, and anoreceptive intercourse. Most acute fissures result from the passage of hard stools, infectious proctitis, or direct trauma from anal penetration. Chronic fissures frequently stem from recurrences of acute episodes and develop when repeated mechanical trauma acts against elevated internal anal sphincter (IAS) tone, resulting in symptoms persisting beyond 6 weeks.

Physiologic studies consistently demonstrate (IAS) hypertonicity and hypertrophy in affected patients, leading to greater resting anal pressures and impaired anodermal perfusion. The resulting local ischemia contributes to poor healing and progression to chronicity. Atypical fissures, particularly those that are off-midline, multiple, or nonhealing, are often associated with normal or reduced IAS tone and may indicate systemic disease, including IBD, tuberculosis, HIV, malignancy, or consequences of prior anorectal surgery.[5] Approximately 40% of acute fissures progress to a chronic state.[6][7]

Epidemiology

Anal fissures can occur at any age but are most frequently diagnosed in younger and middle-aged individuals. Recurrent fissures in children should prompt evaluation for possible sexual abuse. Incidence is similar between sexes. In the U.S., an estimated 240,000 to 342,000 new cases are diagnosed annually, corresponding to an approximate 7.8% lifetime risk.[8]

Pathophysiology

The anoderm, the epithelial lining of the anal canal, lies immediately distal to the dentate line (see Image. Anal Canal). This delicate tissue is highly susceptible to microtrauma and tearing from repetitive mechanical stress or elevated intraluminal pressure. Increased pressure impairs local perfusion, delaying healing. In some cases, tears may extend sufficiently to expose the internal or external sphincter muscle. These lesions, combined with sphincter spasms, produce severe pain during defecation and occasional rectal bleeding.

Anal fissures predominantly occur at the posterior midline, where blood flow is less than half that of other regions of the anal canal. Perfusion within the anal canal inversely correlates with sphincter pressure. Fissures occurring in lateral or other atypical locations often suggest underlying pathology, such as HIV, tuberculosis, or IBD, although the precise mechanisms remain unclear. Anterior fissures are rare and frequently associated with external sphincter injury or dysfunction.

Histopathology

Acute anal fissures exhibit sharply demarcated mucosal edges, occasional granulation tissue at the base, and minimal fibrosis, reflecting recent trauma. Chronic fissures show indurated margins, absence of granulation tissue, exposed horizontal fibers of the IAS, and fibrosis, often accompanied by sentinel skin tags or hypertrophied papillae.[9][10] Primary fissures typically demonstrate nonspecific ulceration, acute and chronic inflammatory infiltrates, granulation tissue, and reactive epithelial changes. Secondary fissures display histologic features related to underlying pathology, including epithelioid granulomas in Crohn disease, tuberculosis, or fungal infections, and plasma cell-rich infiltrates in syphilis or lymphogranuloma venereum, aiding differentiation from idiopathic lesions. (Source: Rishi and Cornish, Last Updated 2025)

Routine histopathologic evaluation is not required for most fissures. However, this diagnostic modality becomes important when ruling out malignancy or systemic pathology.

History and Physical

Acute anal fissures present with severe anal pain, typically exacerbated during defecation, and minor bleeding that appears as streaks rather than overt hemorrhage. Pain often persists for hours following bowel movements. Misdiagnosis as hemorrhoids is common, underscoring the importance of careful clinical examination. Chronic fissures cause prolonged, recurrent painful defecation with intermittent rectal bleeding, often in the setting of constipation or passage of hard stools. Granulomatous conditions, such as Crohn disease, may produce intermittent, recurrent anal pain associated with defecation over extended periods.

Examination should be performed with the patient in a position that minimizes discomfort. The prone jackknife position, with hips flexed, optimizes exposure and is preferred in procedure rooms. In outpatient or acute care settings, bending over an examination table or assuming the lateral decubitus position provides adequate visualization. Manipulation should be minimized, and digital rectal examination or instrumentation, including anoscopy, is generally avoided to reduce pain.

An acute anal fissure appears as a superficial, longitudinal laceration extending proximally from the anal verge. Bleeding may be absent or minimal, and both the fissure and the sphincter are typically exquisitely tender to palpation. Visualization is generally straightforward in lean individuals. In patients with obesity, gentle pressure over the anterior or posterior sphincter that reproduces pain can assist in localization. Chronic fissures present as larger, deeper defects, sometimes with exposed IAS fibers. Repeated injury and healing result in indurated margins and thickened distal tissue, forming a sentinel pile. Granulation tissue may be variably present, depending on the chronicity and reparative stage.

Evaluation

Examination under anesthesia is often indicated for chronic, recurrent anal fissures to facilitate accurate diagnosis and, in some cases, provide definitive treatment. The initial evaluation should determine whether the lesion is primary or secondary. Primary (typical) fissures occur at the posterior or anterior midline. In contrast, secondary fissures are located in atypical, nonmidline positions and warrant investigation for underlying conditions such as Crohn disease, infection, or malignancy. Importantly, individuals with systemic disorders such as Crohn disease may still develop fissures in typical locations. Chronic fissures frequently demonstrate the classic triad of sentinel tag, fissure, and hypertrophied anal papillae.[11]

Treatment / Management

Nonoperative Management

Initial management of anal fissures typically involves a 6-week trial of conservative measures. Recommended strategies include frequent sitz baths, analgesics, stool softeners, and a high-fiber diet to facilitate healing and reduce recurrence. Adequate hydration is also advised to minimize the risk of recurrent fissures. Maintenance fiber supplementation (eg, psyllium) after healing reduces recurrence. No single fiber type is superior.[12](A1)

Pharmacologic options are considered if conservative measures, including dietary modification and laxatives, fail. Topical treatments include lidocaine jelly (2%), topical nifedipine (0.2%-0.5%), topical nitroglycerin (0.2%-0.4%), or compounded combinations.[13][14] Lidocaine jelly is primarily for pain control and not a standalone fissure therapy. Topical nifedipine reduces IAS tone, increases local blood flow, and promotes healing. Nitroglycerin acts as a vasodilator to enhance perfusion and fissure recovery.(A1)

Topical nifedipine is generally preferred due to higher healing rates and fewer adverse effects. Nitroglycerin may induce headaches and hypotension. Patients are advised to apply nitroglycerin while seated and avoid rapid standing. Concurrent use with phosphodiesterase inhibitors, including sildenafil, tadalafil, and vardenafil, is contraindicated.[15][16][17](A1)

Chronic anal fissures (CAFs) are often more challenging to manage due to their tendency to recur. When conservative measures fail, botulinum toxin injections provide an alternative by producing a reversible chemical sphincterotomy lasting up to 3 months. Healing rates with botulinum toxin are comparable to topical therapies but are lower than those achieved with surgical intervention. However, treatment with this neurotoxin offers the advantage of a reduced risk of fecal incontinence. Dosing and injection protocols vary widely, with some evidence suggesting lower doses may yield fewer adverse events without compromising efficacy. Botulinum toxin is a reasonable 1st-line alternative to topical agents or a 2nd-line after failure of topical therapy. Recurrent CAFs frequently require surgical management when nonoperative treatments prove insufficient.

Surgery

The gold standard surgical approach is lateral internal sphincterotomy (LIS), which relieves fissures by reducing IAS hypertonia. Studies report that approximately 96% of patients achieve complete resolution within 3 weeks following LIS. The procedure may be performed via open or closed techniques under local or general anesthesia, though local anesthesia is associated with higher recurrence rates. In the open technique, an incision is made along the intersphincteric groove, the IAS is dissected from the mucosa, and the muscle is divided with scissors. The closed technique involves a small incision at the intersphincteric groove, insertion of a scalpel parallel to the sphincter, and rotation to divide the IAS. Healing rates are similar for both methods.

LIS is highly effective but carries potential complications. Fecal incontinence, including uncontrolled flatus, mild soiling, and gross stool leakage, is the most significant, affecting approximately 45% of patients immediately postoperatively, with a higher incidence in female patients (50% versus 30% in male patients). Incontinence is generally transient, with rates declining to less than 10% at 5 years post-LIS and gross stool incontinence occurring in under 1% of cases. The recurrence rate of CAFs after LIS is approximately 5%, compared with a 25% failure rate for conservative therapy.

Other acute complications include excessive bleeding, more common with the open technique and occasionally requiring suture ligation, and perianal abscess formation in about 1% of closed LIS cases, typically due to dead space created by mucosal separation. Rare long-term complications include keyhole deformity, predominantly following posterior fissure repair. In a cohort of over 600 patients, only 15 developed keyhole deformities, which were asymptomatic and did not result in incontinence, although surgical repair was performed.

For patients at higher risk of fecal incontinence, sphincter-preserving options such as anocutaneous advancement flap surgery (eg, dermal V-Y or house flaps) are recommended. These procedures have high healing rates (81%-100%), low rates of minor fecal incontinence (0%-6%), and, in comparative studies, lower risk of fecal incontinence than LIS (2% vs. 17%) while maintaining similar healing outcomes. When combined with botulinum toxin or LIS, flaps may reduce postoperative pain, accelerate healing, and further minimize fecal incontinence, with recurrence rates of 2% to 7%.

Management of Secondary Anal Fissures

General management of secondary anal fissures focuses on identifying and treating the underlying systemic, infectious, traumatic, or neoplastic causes. An interprofessional approach involving gastroenterologists, surgeons, infectious disease specialists, and other relevant clinicians is recommended. Initial management often includes conservative measures while addressing disease-specific therapy (eg, immunomodulators for Crohn disease or antibiotics for infections). Surgical intervention is reserved for refractory cases with controlled underlying disease to minimize complications, particularly preserving sphincter integrity to reduce incontinence risk. Monitoring and treating coexisting conditions is essential to improve healing and prevent recurrence.

Differential Diagnosis

Anal fissure is primarily a clinical diagnosis made on physical examination, which also aids in excluding other causes of rectal pain. Hemorrhoids are the most common alternative finding. However, pain is typically limited to external hemorrhoids, particularly when thrombosed. Perianal abscesses are another source of pain, often exacerbated during defecation, and may be accompanied by bleeding. These abscesses can progress to anal fistulas, which may present with bleeding or purulent discharge. Additional considerations include perianal ulcerations associated with STIs, IBD, and tuberculosis. Solitary rectal ulcer syndrome, a rare disorder of uncertain etiology, may also mimic fissure-related symptoms and is generally identified several centimeters proximal to the anal verge on sigmoidoscopy.

Prognosis

Acute anal fissures in otherwise low-risk patients generally respond to conservative therapy, with resolution occurring within several days to weeks. However, a subset of patients experience progression to CAF, necessitating pharmacologic intervention or surgical management. Surgical treatment achieves durable healing in more than 90% of cases, with complete resolution typically observed within 3 to 4 weeks postoperatively.[18]

Complications

Complications of anal fissures include bleeding, pain, secondary infection, and varying degrees of fecal incontinence. Fistula formation is the most serious complication, often necessitating surgical intervention.

Complications from anal fissure treatment may include transient fecal incontinence, most commonly flatus incontinence, following LIS. Other risks include bleeding, perianal abscess formation, and, rarely, keyhole deformity. Topical nitroglycerin may cause headaches or hypotension, while botulinum toxin injection carries a small risk of transient sphincter weakness.