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2 Anorectal Anatomy Related to Anal Fistula and Abscess 21
Fig. 5 Coronal section of the anal canal and sphincter complex, showing details of anal glands,
dentate line, anal cushions
consequently determine which fistulas are potentially safe to lay open (fistulotomy,
the most effective cure for anal fistulas since first described by Hippocrates in
460 BC) in terms of how much of the anal sphincter complex would be left intact
should all the tissue enclosed by the fistula be divided.
The spread of sepsis from the infected intersphincteric anal gland may occur in
the vertical, horizontal, or circumferential planes.
Caudal spread in the vertical plane is the commonest way by which infection
disseminates and presents as a perianal fistulous abscess arising at the anal verge.
This can result in a chronic intersphincteric fistula. They are usually uncomplicated
consisting of a single track; however, some fistulous abscesses may travel cranially
or have a secondary track that passes in a cranial direction to end in a supralevator
pararectal blind sinus or open directly into the rectum.
Horizontal spread of sepsis will cross the external anal sphincter to enter the
ischioanal fossa. Caudal spread in this plane will lead to an ischioanal abscess
terminating at the skin of the buttock. If the acute track fails to heal following
spontaneous or surgical drainage, it will lead to a transsphincteric fistula, which may
be subdivided into “high” or “low” dependent on where the track crosses the external
sphincter – above (“high”) or at the level of or below the dentate line (“low”). The
fistula will often pass through the sphincter complex in an oblique fashion, which
may significantly have an impact on the amount of sphincter divided depending on
the orientation of the track, in the event of a fistulotomy being performed. Upward
spread of infection in the ischioanal space, through the levator ani muscle, can lead
to a secondary extension in the supralevator pararectal space.
Cranial spread in the intersphincteric space can lead to the relatively rare suprasphincteric fistula. They pass beyond the anorectal junction, curl over the external
anal sphincter, and traverse the levator ani muscles to enter the ischioanal fossa to
reach the skin.
22 K. R. Cattle and T. M. Hammond
45%
Type 1
20%
Type 3
30%
Type 2
5%
Type 4
Fig. 6 Park’s classification of fistula-in-ano
Extrasphincteric fistulas are not related to intersphincteric anal gland sepsis. They
run without relation to sphincters and are classified according to their pathogenesis.
Circumferential spread of infection may occur in any of the intersphincteric,
ischioanal, or supralevator pararectal planes, in a horseshoe configuration.
10 Conclusion
Knowledge of the anatomy of the anal canal, the anal sphincter complex supported
by the pelvic floor, and their associated spaces in relation to potential pathways for
the spread of infection from the intersphincteric anal gland is key to understanding
how to clinically assess, guide, and treat patients with an anal fistula. However,
equally as important is taking the time to assess the function of the sphincter
complex and the impact of the fistula on the patient’s lifestyle thereby allowing
them to make an informed decision on the management options.
2 Anorectal Anatomy Related to Anal Fistula and Abscess 23
11 Cross-References
▶ Classification of Anal Fistula and Abscess
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25–36. https://doi.org/10.1159/000145103
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study of the anal sphincter musculature. J Neurol Sci 42(1):111–127. http://www.ncbi.nlm.nih.
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61. https://doi.org/10.1111/j.1445-2197.1956.tb06374.x
Hill MR, Shryock EH, ReBell FG (1943) Role of the anal glands in the pathogenesis of ano-rectal
disease. J Am Med Assoc 121(10):742–746. http://jama.jamanetwork.com/
Kumar L, Emmanuel A (2017) Internal anal sphincter: clinical perspective. Surgeon 15(4):211–226.
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Lawson J (1974a) Pelvic anatomy I. Pelvic floor muscles. Ann R College Surg Engl 54:244–252
Lawson J (1974b) Pelvic anatomy II. Anal canal and associated sphincters. Ann R College Surg
Engl 54(6):288–300
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79(9):882–884. https://doi.org/10.1002/bjs.1800790908
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operative treatment of haemorrhoids. Lancet 230(5959):1119–1124
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doi.org/10.1007/BF02588867
Seow-Choen F, Ho JMS (1994) Histoanatomy of anal glands. Dis Colon Rectum 37:1215–1218
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clinical practice, 41st edn. Elsevier Ltd., pp 1136–1159
Standring S (2016b) True pelvis, pelvic floor and perineum. In: Standring S (ed) Gray’s anatomy.
The anatomical basis of clinical practice, 41st edn. Elsevier Ltd., pp 1221–1236
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doi.org/10.1016/s0889-8545(05)70037-1
Sultan AH, Kamm MA, Hudson CN, Nicholls JR, Bartram CI (1994) Endosonography of the anal
sphincters: normal anatomy and comparison with manometry. Clin Radiol 49(6):368–374.
https://doi.org/10.1016/S0009-9260(05)81819-7
Wendell Smith CP, Wilson PM (1970) The vulva, vaginal and urethra and the musculature of the
pelvic floor. In: Philipp E, Setchell M (eds) Scientific foundations of obstetrics and gynaecology,
4th edn. Butterworth Heinemann, pp 84–100
Zoulamoglou M, Kaklamanos I, Zarokosta M, Flessas I, Bonatsos V, Piperos T, Theodoropoulos P,
Barla G, Stathopoulou I, Mariolis-Sapsakos T (2017) The ligament of Parks as a key anatomical
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24(April):31–33. https://doi.org/10.1016/j.amsu.2017.10.004
Anorectal Physiology Related to Anal Fistula and Abscess
P. G. Vaughan-Shaw and Y. Maeda
Contents
1 Principal Aspects of Anorectal Physiology .................................................. 26
1.1 Secretory Function of the Anorectum and the Cryptoglandular Hypothesis .......... 26
1.2 Histology and Cellular Physiology of the Anorectum and Fistula .................... 27
1.3 Microbiology and Fistula . . ............................................................. 28
1.4 Host Factors Relevant to Abscess and Fistula . . ..... . . . . . ..... . . . . . . ..... . . . . . . ... . . . . 28
1.5 Anal Continence ..... ................................................................... 29
1.6 Defecation . . ..... . . . . . . ..... . . . . . . ..... . . . . . . ..... . . . . . . ..... . . . . . . ..... . . . . . . ..... . . . . . 31
1.7 Anorectal Physiology Testing in the Context of Fistula . . .... . . . . . ..... . . . . . ..... . . . . . 32
2 Conclusion ................................... ................................................. 33
References .................... ................................ ................................ .... 34
Abstract
3
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
P. G. Vaughan-Shaw · Y. Maeda (*)
Department of Colorectal Surgery, University of Edinburgh, Western General Hospital,
Edinburgh, UK
e-mail: peter.vaughan-shaw@igmm.ed.ac.uk; yasuko.maeda@ed.ac.uk
© Springer Nature Switzerland AG 2022
C. Ratto et al. (eds.), Anal Fistula and Abscess, Coloproctology,
https://doi.org/10.1007/978-3-030-76670-2_3
25
26 P. G. Vaughan-Shaw and Y. Maeda
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 speci fic 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.
Keywords
Anorectal physiology · Continence · Cryptoglandular
1 Principal Aspects of Anorectal Physiology
1.1 Secretory Function of the Anorectum and the Cryptoglandular Hypothesis
The whole length of the gastrointestinal tract has a secretory function, providing
lubrication as well as the enzyme, hormone, and antibody release. Within the anal
canal, the submucosal anal glands primarily provide lubrication to the passage of stool
through the anus in humans, while in animals scented secretions fulfill important
functions in marking territory and sexual stimulation. These glands were described in
humans in the nineteenth century by French anatomists Hermann and Desfosses (1880)
and bear direct relevance to fistula given Park’s cryptoglandular hypothesis of abscess
and fistula pathogenesis, which is now generally accepted (Parks 1961). Longitudinal
folds of mucosa run parallel to the length of the anal canal and have at their lower end
small anal crypts of Morgagni which lead into up to 10 distal anal submucosal glands. It
is known that these glands can traverse the internal anal sphincter and into
intersphincteric muscle fibers, and histological staining methods have demonstrated
the presence of mucous secreting cells and intraluminal secretions in these glands
(Gosselink et al. 2015). It is thought that around 80% of the anal glands are purely
submucosal, with the remaining 20% extending into the muscular layers of the anal
canal and beyond (Seow-choen 2003). The intramuscular glands are found in 60% of
patients and extend into the intersphincteric space in 12% and the external anal sphincter
in 6%. Park’s hypothesis postulates that the abscess-fistula sequence starts with obstruc-
tion of the anal glands by fecal material or trauma, blocking the outlet ducts, and
resulting in stasis and subsequent infection. Those glands that traverse the sphincter
constitute an “open canal between the lumen of the gut and the connective tissue of the
3 Anorectal Physiology Related to Anal Fistula and Abscess 27
sphincter muscles” and as such may not discharge into the anal canal but instead into the
sphincter or intersphincteric space, and thereafter pus will track along muscle fibers into
the ischioanal fossa. Despite the theory being synonymous with Parks, it was first
conceived by Hermann and Desfosses who suggested that infection of the anal submucosal glands might cause fistula-in-ano. Further reports in the early twenty-first century
supported this concept before Parks popularized it. It is the presence of anal gland
epithelium in the track that supports anal glands as central to the abscess-fistula
sequence. In 1929, Lockhart-Mammary described causes of perianal abscess as congenital cysts, foreign bodies, fissures or ulcers, suppuration of the intramuscular glands,
ortubercleandinregardtoanalglandsstatedthat“these glands, communicating as they
do with the bowel lumen, afford a path for infective organisms to reach the connective
tissue of the ischio-rectal fossa and so set up an abscess in this region” (LockhartMummery 1929). Support increased in the following years, including from Gordon
Watson ( 1935)andEisenhammer(1956), and in his study of 30 completely excised
perianal fistula tracts, Parks reported histological evidence of anal gland epithelium in
most specimens and concluded that fistula-in-ano was caused by infected anal glands in
over 90% of these cases. Subsequent studies have provided some resistance to Park’s
cryptoglandular hypothesis, with Goligher (Goligher et al. 1967) finding a communication between perianal abscess and crypt in the minority of cases studied and thus
concluding that although glandular infection may be implicated in the etiology of some
perianal abscesses, other causal mechanisms must exist. More recently, Mitalas et al.,
detected no mucin-producing cells in the fistula tracts of 53 specimens, with epithelialization of the distal and intersphincteric fistula tract observed in only 25 and 22% of
fistulas (Mitalas et al. 2012). Therefore, it is reasonable to assume that the variable
susceptibility to anorectal sepsis of cryptoglandular origin, and the conflicting findings
upon histological examination of fistula tracts may reflect the known variation in
number, depth, and shape of anal glands (Seow-choen 2003).
1.2 Histology and Cellular Physiology of the Anorectum and Fistula
There are three primary histologic linings in the anal canal: glandular or columnar
epithelium, transitional or intermed iate, and squamous epithelium. Glandular
mucosa is seen most proximally, extending down to the dentate line, transitional
epithelium, which contains crypts and anal glands within the anal transitional zone,
and non-keratinizing squamous epithelium from the dentate line, down to the
mucocutaneous junction where keratinizing squamous epithelium of the perianal
skin begins. At a cellular level, one feature of importance is the presence of tight
junctions. Anal glands might constitute an “open canal between the lumen of the
gut” that permits extraluminal migration of enteric bacteria or stool, yet a failure of
the normal physiological barrier in the gut would also facilitate this. In health, tight
junctions form an intestinal barrier along the whole gastrointestinal tract that regulates the permeability of ions, water, and nutrients. Junctional adhesion molecules
such as claudin, occludin, and zonulin are central components of this barrier, and
28 P. G. Vaughan-Shaw and Y. Maeda
evidence from the study of Crohn’s fistulae suggests that these may be disrupted,
allowing a fistula tract to form. Meanwhile, histopathological examination of fistula
tracts has demonstrated evidence of epithelial to mesenchymal transition (Ratto et al.
2016). This process allows cells to assume a mesenchymal phenotype, including
increased capacity for migration and invasion and resistance to apoptosis. The
process is important in health and disease. It is central to embryogenesis and organ
development but also a hallmark of inflammatory and neoplastic processes (Kalluri
and Weinberg 2009). The pathogenesis of fistula is considered further below but is
thought to also involve the overexpressi on of the pro-inflammatory cytokines IL-1
beta and IL-8 (Ratto et al. 2016) and some contribution from matrix metalloproteinases which are capable of degrading extracellular matrix proteins and
thus may help break down the epithelial barrier and facilitate fistula formation
(Sugrue et al. 2017). It is clear that the cellular physiology and molecular biology
in relation to fistula formation remain incompletely understood. Histological and
molecular factors are likely to play a role, yet further mechanistic investigation to
increase understanding and help define targeted molecular therapies is required.
1.3 Microbiology and Fistula
The infective process of abscess formation is central to Park’s cryptoglandular
hypothesis of fistula formation. If the anal submucosal glands do indeed act as an
“open canal between the lumen of the gut and the connective tissue of the sphincter
muscles,” then enteric flora would be expected in association with abscess and
fistula. Findings from several studies support this concept with E. coli and other
gut-derived microorganisms seen more frequently in perianal abscesses associated
with fistula-in-ano (Eykyn and Grace 1986; Toyonaga et al. 2007). However, it may
be argued that the presence of enteric flora in such abscesses is purely a marker of a
connection with the gut, namely, a fistula, rather than evidence for causative etiology. Furthermore, more recent studies of the fistula tract microbiome, through
culture and rRNA sequencing, have failed to show a strong predisposition towards
bowel flora (van Onkelen et al. 2013; Tozer et al. 2015). It is clear that the study of
the gut microbiome in relation to health and disease is a fast-developing area of
translational science. The advent of next-generation sequencing such as 16S rRNA
gene sequencing that allows a comprehensive characterization of the gut microbiome
will facilitate a much deeper and more detailed study of microbiological factors
relevant to fistula formation, persistence, and management.
1.4 Host Factors Relevant to Abscess and Fistula
Perianal abscesses occur at a mean age of 40 years and are twice as common in men
than in women (Sainio 1984; Read and Abcarian 1979). It is known that the
functional anal canal length is markedly shorter in women, compared to men,
while men also have higher canal pressures, which may contribute to the observed
3 Anorectal Physiology Related to Anal Fistula and Abscess 29
higher incidence of fistulae in men (Sainio 1984). Higher BMI is associated with
increased risk (Adamo et al. 2016), yet there is no evidence that a sedentary lifestyle
or poor personal hygiene impacts abscess risk (Read and Abcarian 1979). However,
Crohn’s disease is a very potent risk factor for both abscess and fistula-in-ano, while
factors impacting on the body ’s natural immune system also increase abscess risk,
e.g., HIV, smoking, and diabetes (Wei et al. 2013 ). Rarely, abscess an d fistula may
develop from abdominal or pelvic infections (e.g., appendix or diverticular abscess),
tuberculosis (Gupta 2005), or actinomyces (Fry et al. 1965). Local trauma may
initiate fistula formation, e.g., rectovaginal fistula following obstetric injury
(Debeche-Adams and Bohl 2010). Abscess and fistula are also very prevalent in
patients with neutropenia secondary to hematological disease (Solmaz et al. 2016),
while any cause of immunosuppression can also increase the risk of delayed healing
and recurrence following abscess surgery (Bakhtawar and Usman 2019).
1.5 Anal Continence
Continence is a complex process which prevents the involuntary passage of stool
through the anus, thereby allowing voluntary defecation. Distension of the normal
rectum produce s the call to stool, which results in a coordinated interaction between
many different neuronal pathways, the pelvic floor, and perineal musculature to
maintain continence. This section describes the physiology of normal continence.
The complexity of the neuronal pathways and interaction with both voluntary and
involuntary stimuli mean that the process of continence is not fully understood.
Fistula and abscess, like other local or systemic diseases, add further complexity,
with sphincter integrity, stool consistency, and emotional factors all impacting
continence (Mavrantonis and Wexner 1998). Investigations of anal function continue to develop the understanding of continence, with anorectal manometry, electromyography, defecography, nerve stimulation testing, and radiological studies
utilized (Barleben and Mills 2010) and discussed later in this chapter.
1.5.1 The Rectum
The primary function of the rectum is the storage and controlled evacuation (i.e.,
defecation) of stool. As stool passes into the rectum, its walls distend (as measured
by rectal compliance) to accommodate fecal content and delay defecation. The
compliance of the rectum facilitates a low constant pressure in the face of increasing
volume but may be reduced by certain rectal pathology, with both decreased
compliance and increased smooth muscle tone in the rectum seen in patients with
fecal incontinence after fistulotomy (Awad et al. 2015 ). Investigation of rectal
compliance is most simply performed using a rectal balloon that is inflated while
recording rectal pressure, yet does not always correlate well with patients’ symptoms, with low tolerated volumes observed in patients with seemingly normal
compliance and sensation. As such, compliance should be seen as more than just
the physical properties of the rectal wall but an interplay between rectal wall
contractility and rectal sensation. The study of rectal sensation is complex, with
30 P. G. Vaughan-Shaw and Y. Maeda
less understanding about rectal sensory nerve physiology than those of the anal
canal. Rectal intraganglionic laminar endings which are tension mechanoreceptors
have been identified in animal studies and found to be more sensitive than those in
the colon, resulting in the sensation of filling, rather than pain, and stimulating anal
reflexes involved in maintaining continence (Barleben and Mills 2010). Another
important consequence of rectal filling is the recto-anal inhibitory reflex. This is the
transient relaxation of the internal anal sphincter and concurrent contraction of the
external anal sphincter in response to rectal distension. The relaxation of the internal
anal sphincter is mediated by the myenteric plexus and facilitates “sampling” of
rectal content by the transition zone anal mucosa and differentiation between solid
and liquid stool or flatus, thus ensuring continence of flatus and stool. The impact of
adult anal fistula or abscess on the recto-anal inhibitory reflex is not known, although
it is commonly absent in patients with congenital perineal fistula and other anorectal
malformations (Kyrklund et al. 2017).
1.5.2 The Musculature of the Pelvic Floor and Sphincter Complex
The anatomy of the pelvic floor musculature is discussed in the previous chapter. In
brief, the pelvic floor consists of a sheet of striated muscles, mostly the levator ani,
(innervated by the second, third, and fourth sacral nerves) through which the pelvic
viscera pass. The paired levator ani, which surround the rectum, vagina (in women)/
prostate (in men), and urethra, are thought to comprise the ileococcygeal,
ischiococcygeal, and pubococcygeal (including puborectalis) muscles and are primarily involved in defecation. Nevertheless, contraction of the muscles of the pelvic floor
provides resistance to the involuntary passage of stool, particularly during periods of
rest or deep sleep (Karulf 2011), while voluntary contraction of the puborectalis
supports the external anal sphincter in closing the anal canal and deferring defecation
during coughing and straining. Puborectalis provides an additional important contribution to continence through maintenance of the anorectal angle, the angle between
the longitudinal axis of the anal canal, and the posterior rectal line, created by the
anterior pull of puborectalis. Parks postulated that the result of the anorectal angle is
that any increase in intra-abdominal pressure results in rectal mucosa being forced
against the upper anal canal, as a “flap-valve” thus contributing to continence (Parks
1975). Indeed, puborectalis can maintain some degree of continence even in the
absence of an intact sphincter complex, e.g., after obstetric trauma. High, extrasphincteric fistula-in-ano runs through the levator ani muscle and may impact upon
the contribution of puborectalis to continence. Such fistulae commonly originate in the
abdomen secondary to appendix, diverticular, or Crohn’sabscess.
The anal sphincter complex comprises the internal and external anal sphincters.
The internal anal sphincter is formed from the continuation of the inner smooth
circular muscle of the rectum, while the external anal sphincter extends upwards to
meet the levator ani muscles. Innervated by S2, S3, and S4 via the pudendal and
perineal nerves, the striated external anal sphincter provides a small but continuous
contribution to resting anal tone at rest and even whilst sleeping, through the
monosynaptic spinal reflex stimulating “slow-twitch” fibers. As such, is it unlike
other striated muscles which are typically electrically silent at rest. Increases in
3 Anorectal Physiology Related to Anal Fistula and Abscess 31
resting tone are seen with changes in posture, sneezing, and coughing, while a
transient involuntary contraction of the external anal sphincter is also observed in
the recto-anal inhibitory reflex as descri bed above. Meanwhile, the external anal
sphincter provides a greater contribution to voluntary contraction of the sphincter
complex and the conscious effort to defer the passage of stool. This is achieved via
the phasic contraction of “fast-twitch” fibers, which is maintained for ~40–60 s
before fatigue.
The internal anal sphincter is the major contributor to resting anal pressure
through an intrinsic, “slow-wave” activity. It is thought to contribute up to 85% of
resting tone, with the remaining contribution from the hemorrhoidal plexus and
external anal sphin cter. As such, weakness or defects in the internal anal sphincter
result in passive fecal incontinence. The primary excitatory sympathetic innervation
to the internal anal sphincter is supplied via the lumbar splanchnic nerves and
hypogastric nerves. Conversely, parasympathetic innervation from S2, S3, and S4
ganglia via pelvic nerves results in relaxation of the internal anal sphincter. Aberrations in internal anal sphincter tone with increased incidence of ultraslow waves and
increased pressure within the anal canal are associated with hemorrhoid disease and
fissure-in-ano and may logically contribute to the persistence of the fistula tract.
Meanwhile, the presence of a fistula or its surgical management has been shown to
have a significant effect on maximal resting pressure and maximum squeeze pressures achieved by the sphincter complex within the anal canal (Roig et al. 2009). As
such, preoperative evaluation of the sphincter complex with manometry and anal
endosonography may be helpful in planning operative management of fistula,
especially in those who are at risk of incontinence, e.g., the elderly, previous history
of incontinence, fistulotomy, or obstetric trauma.
1.6 Defecation
Defecation is a chain of events that results in the passage of stool through the anus.
Once the threshold volume of rectal filling is reached, sensory signals are transmitted
superior frontal gyrus and anterior cingulate gyrus. Rectal compliance, stool consistency, and emotional and social factors may all impact the threshold at which this
process is initiated. Once socially appropriate, the subje ct will squat or sit, thus
straightening the anorectal angle. The subject performs a Valsalva maneuver by
contracting the diaphragm and abdominal muscles against a closed glottis, which
overcomes the actions of the external sphincter. Puborectalis relaxes, with resultant
straightening of the anorectal angle and the pelvic floor, descend. As stool moves
down into the lower rectum, spontaneous rectosigmoid contractions push stool
through the anal canal, enabled by the complete inhibition and relaxation of the
external anal sphincter. As the last bolus of stool is passed, the stretching of the
external anal sphincter ceases (Porter 1962), stimulating the closing reflex comprising the contraction of the sphincter complex and ascent of the pelvic floor.
Abnormal defecation may result from anatomical abnormalities such as enterocele
or rectocele, rather than fistula or abscess. However, obstructive defecation has been