An anal fissure is a tear of the squamous epithelial mucosa of the anal canal, between the anocutaneous junction and the dentate line.  They most commonly occur during passage of a firm stool. Anal fissures are common in infancy, and they represent the most common cause of bright rectal bleeding at any age.
An anal fissure, though ostensibly a minor problem, may lead to years of discomfort if diagnosis and treatment are not carried out in a timely fashion. If these small tears (and the occasionally associated superficial infection) are not promptly diagnosed and treated, they can cause severe anorectal pain during bowel movements and set in motion a cycle of stool negativism, constipation, and increasing pain with subsequent defecation.
Too often, this seemingly minor problem remains underappreciated or unnoticed by clinicians. However, when considered, the diagnosis is rather simple to make, and the treatment is usually quite effective.
The underlying pathophysiology of anal fissures is fairly complex. It is likely to be multifactorial and may involve anodermal ischemia, infection, chronic constipation, and hypertonicity of the smooth muscle of the internal anal sphincter and its elevated resting pressure.
Fissures have a predilection for the posterior midline (90%) but may also be located in the anterior midline or laterally. The explanation for this phenomenon is both anatomic and functional. The posterior commissure of the anoderm is less well perfused than other anodermal regions. Furthermore, before the branches of the inferior rectal artery reach the anoderm, they course perpendicularly through septa of the internal anal sphincter. Thus, flow through these arterioles is threatened by elevated intramuscular pressure of the internal anal sphincter.
Many studies have demonstrated that adult patients with anal fissures have significantly elevated anal canal pressures that exceed the intraluminal pressure of arterioles. Therefore, increased tone at the internal anal sphincter compromises perfusion of the anoderm, particularly at the posterior midline, by compressing arterioles of the inferior rectal artery. High canal pressures likely result in increased anodermal ischemia that prevents small mechanical tears from healing in a timely fashion; the tears then progress to clinically significant anal fissures.
A similar pathophysiology is speculated to be the etiology of anal fissures in infants and children.
The generally accepted proximate cause of the anal fissure is a mechanical tear resulting from the passage of hard stool. An unhealed fissure may become infected and develop into a chronic ulcer. A healed fissure may develop into a classic sentinel skin tag in the posterior midline.
Most fissures affecting the pediatric population manifest in children aged 6-24 months; however, the overall incidence of the problem is not well described.
In several small studies, chemical sphincterotomy using glyceryl-trinitrate (GTN) with adjunctive stool softeners was shown to be quite effective at relieving symptoms and promoting healing. However, most pediatric surgeons report equal success with open or closed lateral sphincterotomy for acute and chronic anal fissures.
Recurrence rates of open or closed lateral sphincterotomy have been reported to be 0-10%, with most of the recurrences occurring in adults and with chronic fissures. In contrast, anal dilatations have the highest rates of fistula recurrence (10-30%) and, for this reason, are not recommended in children.
Large prospective series describing outcome in patients following surgical intervention for chronic anal fissure also are lacking in the literature. However, most authors report that anal dilatation and lateral subcutaneous sphincterotomy are both effective therapeutic interventions for chronic anal fissures.
Patients and their families are educated about urinary retention, severe perianal pain, sepsis, bleeding, and transient fecal incontinence.