**1. Introduction**

Since the publications of Park and Eisenhammer in the 1960s to 1970s, we have gained better understanding on the pathogenesis of cryptoglandular infection leading to perianal abscesses and eventually fistula in ano. With this knowledge, we have moved in strides in producing numerous classifications and treatment options, ranging from minimally invasive techniques to surgical procedures that produces significant disruption to the anorectal anatomy.

Anorectal fistulous abscesses and chronic fistula-in-ano are the same disease. This view has been shared by both Parks and Eisenhammer [1, 2]. We tend to separate both topics and discuss the management separately. However, recent views suggest we should treat it as a same disease, both at different spectrum.

We have yet to achieve a gold standard as recurrence rates and success rates still varies widely across continent. I believe the reasons are:

• Lack of comprehensive classification of fistula-in-ano due to a lack of understanding of the natural pattern and progression of the disease.

• Lack of unified surgical approach to address different types of fistula-in-ano. Understanding and practices of surgical techniques varies according to institutions and regions.

Chapter Outline:


#### **2. Revisiting the pathogenesis of cryptoglandular infection**

In 1961, Park reported his study of 44 specimens of normal anorectal anatomy, and 30 resected specimens from fistula-in-ano surgery. Anal glands were racemose structure of widely ramifying ducts, opening internally via the anal crypts (at dentate line), and extended deep into internal sphincters or ends in the longitudinal layer. They never extend into external sphincter muscles. He concluded that, anal glands provided free channels for infection to pass from the anal lumen deep into the internal sphincter muscles [1]. This observation was echoed by Eisenhammer in 1966, who added that main concentration of large crypts was situated posteriorly, followed by the anterior commissure and last, laterally. Internal orifice of a fistula was always found at the crypt entrance in the pectinate line, at approximately the midlevel of the anal canal [2]. Another study in 1994 by Seow found that 1% of anal glands in fact do penetrate the external sphincter [3]. However, infection arising from external sphincter was never reported.

The term fistulous abscess was used by Eisenhammer; the acute stage represents the abscess, and the chronic stage represents the fistula [2]. Acute abscess progress to a recurrent acute abscess or a chronic infection within the anal glands [1]. Fistula is a granulation tissue tract, develops after abscesses spontaneously rupture or are surgically drainage, where it continues to discharge materials from infected anal gland/ducts. It is kept open by chronic granulomatous inflammation [1, 2].

Pyogenic infections constituting 90% of all cases [1, 2]. Parks noted that 73% of infections occurred at either anterior or posterior midline [1]. Eisenhammer postulated that this intermuscular infection is due to obstructive suppurative adenitis, where causative organism were intestinal bacilli, streptococcus or anaerobes [2].

The cryptoglandular infection pathogenesis remains relevant till present day. From the evidence of early studies, we can conclude that:

1.Anorectal abscess and fistula are essentially the same disease, both at different end of a spectrum, and therefore should always be treated as a single disease entity.


Why does complex fistula occur?

Of course, secondary causes of complex fistula-in-ano are not uncommon. It can be due to tuberculosis, Crohn's disease, perforated colonic diverticular disease or any form of pelvic sepsis [5, 6]. These are beyond the scope of this chapter.

Eisenhammer believes both spectrums of this disease have a pre-determined pattern and is predictable. He wrote: 'When faulty surgery is performed, natural anatomic barriers become disrupted, new planes of infections opened, leading to complex and complicated conditions' [6]. Recently, this concept is highlighted again. The pattern of spread should be predictable. Infection of the anorectal region should track in between the anogenital muscular and fascia layers rather than penetrating them, forming abscesses in various anorectal spaces. Anorectal musculature, fascias and spaces are constant. Therefore, the natural patterns of anal fistula should also follow a constant pattern [7].

To understand how cryptoglandular disease manifest as simple or complex disease, we should first discuss the natural patterns of cryptoglandular anorectal abscesses and fistulas.
