Anorectal Physiology Related to Anal Fistula and Abscess

Abstract

The secretory function of the anorectum and in particular the anal glands are central to Parks’ cryptoglandular hypothesis, which describes the abscess fistula sequence which starts with obstruction of the anal glands by fecal material or trauma, blocking the outlet ducts, and resulting in stasis and subsequent infection. As these glands are known to traverse the sphincter complex, pus can thereafter track along muscle fibers into the ischioanal fossa and thereafter a potential fistula.

Emerging data in relation to the molecular aberrations which may help break down the epithelial barrier and facilitate fistula formation support the role of pro-inflammatory cytokines IL-1 beta and IL-8 with contribution from matrix metalloproteinases and transition towards an epithelial-mesenchymal phenotype. The importance of the immune system in abscess and fistula formation is also demonstrated in the high incidence in patients with a weakened immune system (e.g., HIV infection, diabetes). Meanwhile, findings from microbiological investigation have found E. coli and other gut-derived microorganisms more frequently in perianal abscesses associated with fistula-in-ano supporting the cryptoglandular hypothesis.

It is known that continence is a complex process which prevents the involuntary passage of stool through the anus, thereby allowing voluntary defecation. There is complex interplay involving specific aspects of the anatomy and physiology of the rectum, anal canal, pelvic floor, and sphincter complex to facilitate both continence and normal defecation. The disease process of perianal fistula formation or consequence of fistula treatment often cause profound disturbance to the mechanism of continence.

This chapter briefly considers normal anorectal physiology relevant to abscess and fistula etiology and thereafter its relevance to the selection of treatment to avoid disturbance to continence mechanism.