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© Borgis - New Medicine 1/2005, s. 2-4
Łukasz Ulatowski, Grzegorz Krasowski
Anal fissure
Departament of Surgery, Wolski Hospital,Warsaw, Poland
Head: Marek Kruk MD, PhD
Anal fissure is a benign condition of the anus, most commonly found in the posterior commissure, causing severe rectal pain and bleeding. In the present paper the authors review the available literature and describe the pathogenesis, manifestations as well as currently employed treatment methods with respect to the division into acute and chronic anal fissures.
Anal fissure is one of the most frequent benign conditions of the anus. Due to its symptoms related to defecation (severe pain, bleeding, pruritus), the fact that it tends to become chronic and troublesome for the patient, as well as a long-term and difficult treatment, the condition still raises a vital concern in modern proctology. The term anal fissure refers to a longitudinal tear in the mucosa of the anoderm and the anal canal, extending from the external anal orifice to the pectinate line. Anal fissure is frequent in young active professional adults; its peak incidence is in the third and fourth decades of life. The general prevalence rate in men and women is similar, however, more men than women are affected in the group under the age of 20 years; in women, the condition is more common at a later age. Anal fissure may also occur in infants; some authors have reported the condition in about 80% of one-year old infants, which, with adequate hygiene, heals spontaneously. Anal fissure does not only produce symptoms, but it may also be an aetiological factor in chronic constipation.
The current approach shows that the condition is caused by an impaired anorectal motor function manifested by, e.g., an exaggerated resting sphincter spasm, a paradoxical sphincter spasm on defecation. This assumption has been confirmed by manometry which shows an increased pressure in the anal canal up to 120mm Hg (reference value approx. 70 mmHg). The abnormality results in an inadequate blood supply to the distal portion of the anal canal with resulting tissue anaemia and susceptibility to trauma. This has been confirmed by an increased blood flow in the anal mucosa after an effective treatment [1]. The theory presented by Gibbons and Read assumes that the fissure formation is mainly due to an impaired motor function of the sphincters. An inflammatory aspect is also worth considering – it accounts for an increased prevalence of anal fissure in patients with persistent diarrhoea. During degradation, perianal and cryptal faecal residue releases irritant substances, which leads to inflammation.
Severe colicky pain on defaecation, which may persist after the passage of stool, is the main symptom in anal fissure. The pain is due to a strong involuntary spasm of the internal anal sphincter. This may be subsequently followed by difficult defaecation and bleeding from the anus. Mucous and faecal discharge may appear in the course of the disease. The patient experiences a ”wet anus”; occasionally, pruritus may develop. In view of their duration and severity of symptoms, anal fissures are divided into acute and chronic. Diagnosis is not difficult: inspection of the anus reveals a linear tear in the anal mucosa which is most frequently found (75%) at the posterior commissure, in the midline. Anterior anal fissures occur more frequently in women; concomitant posterior and anterior anal fissures are rare. Chronic anal fissures have a typical appearance: a hypertrophied papilla in the dentate line (a sentinel pile) at the lower end, and pale fibres of the internal sphincter, a hypertrophied marginal fold, known as Brodie´s pile, at the upper end. A chronic, painless anal fissure in a lateral location, makes it imperative for the clinician to search for an underlying pathology, e.g., Crohn´s disease or AIDS. In some cases fissure-like lesions are accompanied by a macerated anal verge. Since it is painful, rectal examination and instrumental diagnostic procedures are contraindicated in patients with anal fissure. A thorough proctological examination is performed when the acute stage of the disease has subsided.

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New Medicine 1/2005
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