**2. History**

The first description of anal sphincterotomy in the world literature is found in Alexis Boyer's 11-volume Traite des Maladies Chirurgicales published between 1818 and 1826 (DeMoulin, 1977). His descriptions of the condition are dramatic, detailing the severe suffering patients endured. Louis Lemmonier, in 1869, gave the world the first anatomic description of an anal fissure. Boyer established the relationship between anal sphincter spasm and no healing of anal fissures, as well as the association between constipation and anal fissure. He was the first to divide the sphincter to cure the problem. This procedure, routine and quite safe today, caused deaths and pelvic abscesses in four patients, as reported by Velpeau in 1832. During the 1950s, fissure excision, anal sphincter stretching, injection therapy (local anesthetic and sclerotherapy) and sphincterotomy were performed for chronic anal fissures. Later, in the late 1960s and early 1970s, cutaneous island advancement flaps were added to this group (Ruiz-Moreno, 1968; Samson & Stewart, 1970). The modern reintroduction of sphincterotomy for anal fissure can be attributed to Eisenhammer (1951). In 1953, Inburg published his technique of partial internal sphincterotomy, cutting the sphincter through the bed of the fissure. It was not until the mid to late 1970s that lateral internal sphincterotomy became accepted as the standard of care to treat anal fissures surgically (J. Nelson, 2006).

Nifedipine Gel with Lidocaine in the Treatment

immunodeficiency virus (HIV), or tuberculosis.

**6. Pathophysiology** 

Schouten & Blankensteijn, 1992).

**8. Differential diagnosis** 

diseases, neoplasm, and sexual abuse.

**7. Classification** 

of Anal Fissure in Children: A Pilot Study and Review of the Literature 55

anal fissures is still unknown. Constipation and passage of hard stool were traditionally blamed and believed to be the causative factor of anal fissure, but a history of constipation is elicited in only approximately 20% of the patients (McCallion & Gardiner, 2001). Trauma, usually because of passage of a large or hard stool, is believed to be a common initiating factor. Ball suggested that passage of hard stool tore down the anal valve, leaving the coiledup skin at the anal verge as the "sentinel pile" (Lund & Scholefield, 1996). The remaining fissures are associated with chronic diarrhea, food allergy, Crohn's disease, syphilis, human

The pathophysiology is fairly complex and multifactorial, with anodermal ischemia, infection, chronic constipation, hypertonicity of the smooth muscle of the internal anal sphincter (IAS) and elevated maximal anal resting pressure (MARP) being involved (Gillet & Padias, 2006; Schouten et al., 1996). The exact mechanism surrounding the pathophysiology of anal fissures has not been clearly established, but current theories involve the tonicity of the anal sphincter and anal blood flow. A relative lack of nitrate oxide synthase, as found in other spasmodic states of the gastrointestinal tract, has been suggested as a possible mechanism for IAS hypertonia (Lund, 2006). As fissures are most commonly seen in the posterior midline, inadequate blood flow to this region has been hypothesized to play a role in the development of fissures. End arterioles from the inferior rectal artery pierce both sphincters to reach the submucosa of the anal canal and travel cephalad in this plane. Klosterhalfen et al. (1989) suggested that hypertonic sphincter decreases blood flow in these terminal vessels as they pass through the IAS fibers. Recognized features common to most chronic anal fissures are a high resting anal canal pressure due to hypertonicity of the internal anal sphincter, reduced vascular perfusion index at the site of the fissure, and the presence of "ultraslow" pressure wave activity in the internal anal sphincter (Hancok, 1977,

Anal fissures may be classified as acute or chronic and typical or atypical. Acute fissures cause bright red bleeding with bowel movements and anal pain or spasm that can last for hours after the bowel movement. They have the appearance of a simple tear, superficial or deep in the anoderm. Chronic anal fissures present with induration at the edges, a sentinel pile, visible fibers of the internal anal sphincter, chronic granulation tissue in the base of the fissure and a hypertrophied anal papilla. They are acute fissures that fail to heal following 6 to 8 weeks of intensive treatment. Typical fissures are usually in the posterior or anterior midline, and are not associated with other diseases. Atypical fissures can occur anywhere in

Pruritus ani, inflammatory bowel disease (mostly Crohn's disease), tuberculosis, immune system diseases, acquired immunodeficiency syndrome (AIDS), Chlamydia, venereal

the anal canal, and tend to be associated with other diseases.
