Introduction
Anal fissure is a common and debilitating condition that is usually seen in young and
otherwise healthy patients. It causes significant pain, discomfort and disability far
exceeding that which might be expected from the size of the lesion. Pathologically
anal fissure develops following a linear tear in the squamous epithelium of the
cutaneous anal canal located distal to the muco-cutaneous junction and usually in the
posterior midline of distal anal canal.
Classically it had been thought that acute anal fissure develops following the passage
of a large hard faecal mass or recurrent bouts of diarrhea [1]. Under these
circumstances, the tear results in pain and spasm of the underlying anal sphincters.
This causes anal hypertonia. Anal hypertonia then in turn results in a decreased anodermal
blood flow. The decreased ano-dermal blood flow results in non-healing and
chronicity of the anal fissure. Therefore anal sphincter spasm had been shown to
influence blood flow to the mid-line of the anal verge and hence resulting in
chronicity of the fissure [2,3]. Nonetheless, it does not quite explain how the fissure is
caused in the first place. Studying the physical structure of the anal canal had led us
to believe that during the act of defaecation, whilst the puborectalis is lax, there is a
general lack of support to the perineum (Fig1). The exiting faecal bolus therefore
extends the length of the anal canal and stretches the lip of the anal verge (Fig 1).
This action initiates the tear as well as perpetuates the chronicity of the fissure [3]. In our initial experience with the perineal support device [4], we have found that usage
of the device facilitates defaecation as well as enabling the healing of anal fissures.
This tearing of the anoderm causing significant acute pain and spasm of the internal
anal sphincter (IAS). The IAS tone starts to elevate and overtime it remains
persistently elevated as demonstrated by anal manometric studies showing a high
resting anal canal pressure [5,6].