**6. Pathophysiology**

54 Complementary Pediatrics

An anal fissure is a linear, longitudinal split in the lining of the distal anal canal, extending from below the dentate line to the anal verge. They are usually very painful because of their somatic innervations, the pain resulting from spasm of the anal sphincter in response to stretching and tearing during passage of stool. A well developed anal fissure rests directly over the internal sphincter and the circular fibers of this sphincter are visible on the floor of

ANAL FISSURE - ANATOMY

Anal fissures presents mostly in children aged 6-24 months. The overall incidence in children is not well described. Anal fissures are located in the posterior midline in 90% of the cases, although 10-20% in women and 1-10% in men are located in the anterior midline (Notaras, 1988). The posterior commissure of the anoderm is less well perfused than other anodermal regions (Schouten et al., 1994). Pressure over the branches of the inferior rectal artery (increased tone at the internal sphincter and high canal pressures) causes relative ischemia (Klosterhalfen et al., 1989). First described as a disease entity in 1934, the cause of

**3. Definition** 

**4. Anatomy** 

the fissure on naked eye inspection.

Fig. 1. Anal fissure anatomy.

**5. Incidence and etiology** 

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, Schouten & Blankensteijn, 1992).
