An anal fissure is an elliptical laceration or split in the epithelial lining of the anal canal inferior (distal) to the dentate line. The evacuation of stool causes severe anal pain and bleeding, the latter of which is characterized by small amounts of bright red blood on the stool or on tissue paper. The pain starts during, and continues after, defecation and is described as sharp or knifelike. In one study of over 15,000 consecutive outpatient proctology clinic visits, the prevalence of anal fissures was nearly 10 %, with men and women being equally affected. Children and geriatric patients are less likely to be affected than younger and middle-aged adults. Fissures are characterized into acute (up to 6 weeks in duration) or chronic. Many acute anal fissures are small and heal without medical assistance.

With respect to pathophysiology, fissures were traditionally thought to occur secondary to constipation, straining, and passage of hard stool (high-pressure fissure) or IBD/diarrheal conditions from overuse (low-pressure fissure). Recent studies, however, have demonstrated that fissures may develop due to reduced blood flow in the anal canal (especially in the posterior midline) and elevated anal canal pressures (of the internal anal sphincter (IAS) in particular). These events may cause localized ischemia, predisposing to ulcer formation that may tear with minimal trauma. Once a fissure develops, spasm of the IAS pulls the wound edges further apart, preventing or delaying healing.

Physical examination of the perianal region can be difficult in patients with fissures since the anal sphincter is often in spasm, and an internal rectal examination is impossible in some patients due to severe pain but may be mitigated in some by the use of a topical local anesthetic gel. However, a complete rectal examination, including anoscopy, often has to be performed in the setting of exam under anesthesia (EUA). The majority of fissures (90 %) develop in the posterior midline or the anterior midline especially in women; a skin tag (a “sentinel” tag or pile) is often seen at the inferior (distal) edge, while a hypertrophied papilla may be seen at the superior edge. Acute fissures characteristically have clean edges, while chronic fissures have indurated, heaped-up edges. Fissures located in the lateral position are unusual and typically associated with Crohn’s disease or other less common etiologies such as acquired immunodeficiency syndrome (AIDS) or tuberculosis (TB). Younger patients (<40 years of age) without warning signs (e.g., anemia, a family history of colorectal cancer, a family history of IBD) can be treated without any additional diagnostic testing. Patients >50 years of age should undergo a screening colonoscopy prior to treatment if not previously performed.

We recommend that chronic anal fissures be treated in a stepwise manner focusing on relaxing the internal sphincter, promoting atraumatic stool passage, and providing pain relief. First, patients should undergo lifestyle modification that assure adequate fiber in their diets (25–30 g/day) to avoid constipation and straining, as placebo-controlled studies have demonstrated that fiber improves fissure healing. Another key component of lifestyle modification is sitz baths which keep the perianal area clean and help relax the anal sphincter and which have been shown to increase local perfusion to speed healing. Medical therapy is the second line of treatment, and several options are available. Topical anesthetics (e.g., lidocaine) improve pain but do not improve healing; narcotics are contraindicated. Chemical sphincterotomy is the gold standard of medical therapy. A recent Cochrane meta-analysis reported that topical nitroglycerin (NTG, 0.2–0.3 % ointment applied twice daily for 4–6 weeks) improved healing in 48.6 % of patients, and other studies have reported healing rates as high as 88 %. Physiologically, topical nitrates are an excellent treatment choice, since nitrates relax smooth muscle, allow wound edges to closely appose, and improve blood flow to the anoderm. Unfortunately, headaches (in up to 70 % of patients), hypotension, and nausea are common side effects, thus limiting their use. Calcium channel blockers (CCBs, e.g., nifedipine and diltiazem, either topical or oral) relax the anal canal and promote healing of fissures in up to two-thirds of patients. Botulinum toxin A (Botox) injection improves wound healing in approximately 65 % of patients. The dose of Botox (60–100 U) used does not seem to affect healing rates. Side effects include transient incontinence in up to 3 % of patients. A recent meta-analysis noted that both Botox (described below) and topical NTG were slightly better at healing chronic fissures than CCB, although these differences were not significant. A second meta-analysis of three randomized controlled studies involving 180 patients found that Botox was as effective as NTG with fewer side effects. Both of these agents are less likely to cause side effects than NTG.

If medical therapy does not result in healing, surgery is the next step. Lateral internal sphincterotomy (LIS) is the gold standard, with healing rates of 90–95 %. Tailored division of the IAS allows the wound edges to appose and heal. The most significant complication is incontinence, which occurs in approximately 10 % of patients, although it usually involves only flatus and is minor in nature. A recent meta-analysis of four studies involving 279 patients found that LIS was more effective than Botox (relative ratio [RR] 1.31, p < 0.0001) for the treatment of the chronic anal fissures.

Pruritus ani, another benign condition which may cause anorectal pain, affects 1–5 % of the US population with a male to female ratio of nearly 4:1. Symptoms of intense perianal itching and burning are not relieved by having a bowel movement, and pruritus is not typically associated with bleeding. However, if there is associated excoriation, post-defecatory pain and bleeding may be present. Symptoms resolve spontaneously in some patients (acute pruritus ani), and the culprits in this group may be a medication side effect or dietary factors.

In terms of pathophysiology, symptoms of pruritus ani develop secondary to localized irritation. An inflammatory response then develops which may be limited to the superficial layers of the perianal skin or may extend deeper. For example, fecal soiling may lead to maceration of tissue that can then become infected with Candida, leading to chronic symptoms of itching and burning. Skin tags and fissures may interfere with proper hygiene, thus causing skin irritation, while excessive cleansing of the perianal area can further irritate the inflamed area. Regardless of the initiating event, irritation causes the patient to itch or scratch the affected area, resulting in trauma and excoriation/ulcer formation, further exacerbating the localized inflammatory response and symptoms.

The differential diagnosis for pruritus is shown in Table 20.2. A good history is essential in order to accurately diagnose the root cause of the pruritus ani. Examination of the perianal area reveals reddened, irritated skin in the acute setting. Linear or deep, punched out excoriations may be present. A careful examination should be performed, with the patient asked to strain to determine the presence of rectal prolapse or prolapsing hemorrhoids. Patients with chronic symptoms may develop thick, whitened skin in this area consistent with lichenification. Contrary to current popular opinion, pinworms (Enterobius vermicularis) are an unlikely cause of pruritus in the United States. In the absence of warning signs (unintentional weight loss, anemia, rectal bleeding, family history of colon cancer), no other evaluation is required during the initial visit, although anoscopy should be considered.