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An anal fissure is a linear tear in the lining of the anal canal that usually becomes symptomatic because it exposes the internal anal sphincter and causes painful spasms in that muscle. An anal fissure is a common condition that significantly disturbs the quality of life of persons who experience it.
Most fissures are benign, primary, and idiopathic—that is, they are typical anal fissures. Atypical fissures are much less common and occur as a result of other conditions such as Crohn disease, immunosuppression (including human immunodeficiency virus), malignancy, syphilis, or tuberculosis, or they are drug induced (e.g., through the use of nicorandil). An atypical fissure is painless, not situated in the midline, multiple, or associated with a mass or a fistula-in-ano. Management of atypical fissures involves treating the underlying condition and is beyond the scope of this chapter.
Typical fissures can be arbitrarily classified into acute and chronic on the basis of duration of symptoms: chronic fissures have been present for more than 6 weeks. However, certain features are associated with chronic fissures, and the presence of one or more of these features is possibly a more accurate indicator of chronicity than the duration of symptoms alone.
Acute fissures are managed with a high-fiber diet, stool softeners, and topical local anesthetic ointment. They will not be discussed further. This chapter will focus on the clinical assessment, pathophysiologic features, and management of typical chronic anal fissures (CAFs).
The diagnosis of CAF can be suspected based on the patient’s history and confirmed with clinical examination. The patient usually reports having severe, sharp pain at defecation that persists for several minutes to hours afterward and then slowly subsides, with minimal discomfort experienced at other times of the day. CAF is often associated with a small amount of bright red blood on the toilet tissue. The patient often has a history of constipation and straining to defecate.
Upon examination, the following features of a CAF are observed:
A linear ulcer with a fibrotic rolled edge; the circular muscle fibers of the internal anal sphincter are visible at the base of the ulcer, and minimal granulation tissue is present.
A sentinel skin tag at the caudal (external) apex of the fissure.
A hypertrophied anal papilla at the internal apex.
CAF occurs in the midline and is usually posterior but may be anterior. Fissures away from the midline are atypical.
The caudal end of the fissure often can be seen upon gentle separation of the buttocks. Digital examination and proctoscopy will confirm the diagnosis but are unlikely to be tolerated because of anal spasm and pain. An anal block will allow anoscopy, but with the combination of a typical history and a “shy” anus, it is reasonable to begin empiric management and perform an examination at a later date when symptoms have improved. However, if the history is atypical, examination should be undertaken with use of an anesthetic.
Endoanal ultrasonography and manometry are not necessary in the initial workup but may be useful prior to considering more invasive treatment options if first-line conservative treatment fails.
Shearing forces created by passage of hard stool, childbirth, instrumentation of the anus, or anal intercourse leads to the development of a split in the anal canal mucosa. If this split exposes the internal anal sphincter, an acute fissure is present. There are probably two different mechanisms by which an acute fissure may progress to CAF.
Although the exact pathophysiology of CAF remains obscure, a baseline hypertonia of the internal anal sphincter appears to be the most important factor, particularly in posterior CAF. Patients with posterior CAF have been shown to have higher mean resting anal pressures than do control subjects. Whether the hypertonia is the cause of the CAF or a secondary phenomenon caused by pain is not clear. Nevertheless, treatment of internal sphincter hypertonia remains the focus of management and therefore must at least be central to the persistence of CAF. Sphincter hypertonia leads to reduced perfusion pressure of the anal canal, which is more pronounced posteriorly as a result of a relative paucity of small arterioles supplying the posterior anal canal. This phenomenon has been shown in anatomic studies of normal subjects. Reduction of anal pressure by either medical or surgical means is aimed at improving mucocutaneous blood flow, resulting in healing of the fissure.
Manometric studies have shown that up to 50% of patients with CAF do not have increased anal pressures. These patients are typically women with anterior midline CAF, which, in small studies, has been associated with vaginal delivery, external sphincter injury/dysfunction, rectocele, and rectoanal intussusception.
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