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Enteric Nervous System
h
LM - Longitudinal muscle
MP
CM
SMP
NP
NE
SP
5-HT
AC
NO
NP
2 Colonic Physiology
35
Colonic Innervation
The gastrointestinal tract is densely innervated to provide
information on its luminal contents, processes regulating
digestion and absorption, and potential threats [20].
The enteric nervous system is the largest single division
of the autonomic nervous system (ANS), containing between
200 and 600 million enteric neurons throughout the GI tract
[21]. The colon and rectum are innervated by nerves of both
extrinsic and intrinsic origin. The extrinsic pathways originate from the central and autonomic (sympathetic and parasympathetic) nervous systems. Autonomic pathways run
along parasympathetic and sympathetic chains. Each of
these pathways include afferent (sensory) and efferent
(motor) innervation. The intrinsic innervation consists of the
enteric nervous system. Two major sets of ganglia are found
in the colon. The myenteric or Auerbach’s plexus is located
between the longitudinal and circular smooth muscle layers
and plays a crucial role in colonic smooth muscle function.
The submucosal or Meissner’s plexus regulates ion transport. The extreme importance of these two plexuses is clear
in children with Hirschsprung’s disease in which the ganglia
of the myenteric and submucosal plexuses are congenitally
absent. The aganglionic segments do not relax and peristalsis
is disturbed resulting in severe constipation [22].
Extrinsic innervation to the large intestine comes from
both parasympathetic and sympathetic branches of the
ANS.Colonic motility is modulated by sympathetic neurons
in prevertebral ganglia, which has potent effects on colonic
function (Fig.2.5). The proximal regions of the large intestine are sympathetically innervated by bers that originate
from the superior mesenteric ganglion. More distal regions
receive input from the inferior mesenteric ganglion. There is
evidence for ongoing tonic inhibition of colonic secretion,
since disrupting the pathway causes a substantial increase in
secretion. This is largely mediated by a strong inhibitory
drive to secretomotor neurons in submucosal ganglia, via
α-2-adrenergic receptors [23]. Sympathetic activation also
directly contracts sphincters via indirect effects (i.e., by
reducing acetylcholine release from cholinergic neurons)
and inhibits activation of enteric neurons. Both actions delay
GI and colonic transit. The distal rectum and anal canal are
innervated by sympathetic bers from the hypogastric
plexus.
There are two pathways of parasympathetic innervation.
The cecum and the ascending and transverse portions of the
colon are innervated by the vagus nerve, whereas the
descending and sigmoid areas of the colon and the rectum
are innervated by pelvic nerves from the sacral region of the
spinal cord. The pelvic nerves enter the colon near the rectosigmoid junction and project orally and aborally within the
plane of the myenteric plexus. The vagus and pelvic nerves
consist primarily of preganglionic efferent bers and many
afferent bers. The efferent bers synapse with the nerve cell
bodies of the myenteric and other intrinsic plexuses. The
external anal sphincter, a striated muscle, is innervated by
the somatic pudendal nerves. Sacral parasympathetic pathways to the colon primarily synapse onto myenteric neurons.
- Myenteric plexus
- Circular muscle
- Submucosal plexus
- Nerve plexus
- Nerve endings
- Substance P
- 5-hydorxytryptamine
h - Acetylcholine
- Nitric oxide
- Neuropeptide Y
Fig. 2.5 Schematic representation of the components of the enteric nervous system. (Courtesy of Robin Noel, used with permission)
LM
MP
CM
SMP
Serosa
Sensory
Fibers
NP
NP
Sympathetic
Postgangllonic
Fibers
SP
NP
5-HT
5-HT
NE
ACh
Parasympathetic
Postgangllonic
Fibers
NO
ACh
NE
ACh
NP
AC
36
G. T. Ault and J. S. Beaty
Excitatory pathways are important for colonic propulsive
activity, especially during defecation; damage to these pathways can cause severe constipation [24].
As in other regions of the gut, several diverse chemicals
serve as mediators at presynaptic and postsynaptic junctions
within the autonomic innervation to the large intestine.
Acetylcholine (ACh) and tachykinins such as substance P
serve as major excitatory mediators, and nitric oxide (NO),
vasoactive intestinal peptide (VIP), and possibly adenosine
triphosphate (ATP) serve as major inhibitory mediators.
Transmission between the pudendal nerves and the external
anal sphincter is mediated by ACh [10].
Pain
The sensation of pain appears to be mediated by different
afferents depending on the location of the GI tract undergoing the noxious stimulus. Pain from the rectum primarily
involves pelvic pathways. Inammation (or inammatory
mediators) can change both the response properties of specic classes of sensory neurons and the involvement of specic ascending pathways, which is relevant in
post-inammatory hypersensitivity and postinfectious irritable bowel syndrome (IBS) [25].
Visceral sensory neurons activate reex pathways that
control gut function and give rise to important sensation,
such as fullness, bloating, nausea, discomfort, urgency,
and pain. Sensory neurons are organized into three central
nervous system pathways: vagal, thoracolumbar, and lumbosacral [22]. Experimental distension of the descending
or sigmoid colon is perceived as a sensation of cramping,
gas, or pressure in the lower abdomen, lower back, or
perineum [26].
Both central and peripheral mechanisms have been suggested to be involved in the development of pain symptoms.
Several studies have provided evidence that IBS is associated
with a dysregulation of the brain-gut axis, with peripheral
sensory alterations dominating in some patients and disturbed central processing dominating in others [27]. It is now
widely accepted that an altered visceral sensitivity through
abnormal endogenous pain processing plays an important
role in the pathogenesis of IBS [28]. IBS is associated with
decreased epithelial expression of the serotonin-selective
reuptake transporter (SERT) in many studies; however, it is
unknown if the disturbance is responsible for the symptoms
of IBS [29].
Colonic Motility
The motor function of the colon includes propulsion, accommodation, and rapid emptying of a variable portion of the
colon during defecation. In addition, the colon must be able
to store fecal material until socially acceptable to eliminate.
Colonic motility is mediated by the enteric nervous system
in association with autonomic parasympathetic and sympathetic input and with input from the extrinsic nervous system. Colonic motility is characterized by patterns of
contraction of longitudinal and circular muscle layers with
elimination of feces. Motility is integrated with colonic
secretion and absorption. Propulsion is achieved by numerous motor events including individual contractions, contractile bursts, high-amplitude propagated contractions
(HAPCs), and possibly changes in tone [22].
Accommodation, storage, and distribution of material
within the colon are mediated by colonic tone. Tone and
phasic activity in the colon show considerable diurnal variation, increasing slowly after a meal, reducing during sleep,
and increasing dramatically upon waking [30]. HAPCs
occur more frequently during the morning, during the postprandial period, and preceding defecation [30–32]. The
colonic motor response to eating consists of an increase in
phasic and tonic contractile activity that begins within several minutes of ingestion of a meal and continues for a
period of up to 3hours. This response is inuenced by both
the caloric content and composition of the meal with fat and
carbohydrate stimulating colonic motor activity, while
amino acids and protein inhibit motor activity [30].
A more prolonged state of contraction, referred to as tone,
is not regulated by slow waves and may be recognized clearly
in the colon (response to feeding), as well as in some sphincteric regions. Tone is regulated by actin-myosin interaction
mediated by cellular mechanisms that are modulated by neurogenic and mechanical stimuli. Phasic contractions, such as
those regulating lumen occlusion, may be superimposed on
tonic activity. Thus, tone can increase the efciency of phasic contractions by diminishing the diameter of the lumen.
Tone also modies wall tension in response to gut lling and
is therefore one determinant of perception of distension.
This motor input interacts with myogenic mechanisms to
create regional patterns of contraction and relaxation which
mix and propel content. It is likely that regular contractile
bursts – colonic motor complexes – do occur, each burst
occurring once or twice per hour and lasting approximately
6minutes [22]. Periodic or cyclic motor activity is evident
more clearly in the rectum, the so-called rectal motor complexes. They do not appear to be synchronized with the small
intestinal motor migrating complexes, and their precise function and regulation remain unclear [22].
The anorectum functions in defecation and continence.
Defecation is achieved through the integration of a series of
motor events and involves both striated and smooth muscle.
A sensation of rectal fullness is generated by rectal afferents
when colonic contents reach the rectum. Rectal lling also
induces the rectoanal inhibitory or rectosphincteric reex
2 Colonic Physiology
37
that leads to internal anal sphincter relaxation and external
sphincter contractions. At this stage, the individual can
decide to postpone or proceed with defecation. To facilitate
defecation, the puborectalis muscle and external anal sphincter relax, thereby straightening the rectoanal angle and opening the anal canal. The propulsive force enabling defecation
is generated by contractions of the rectosigmoid, diaphragm,
and the muscles of the abdominal wall to propel the rectal
contents through the open sphincter. The internal anal
sphincter is a continuation of the smooth muscle of the rectum, is under sympathetic control, and provides approximately 80% of normal resting anal tone. The external anal
sphincter and pelvic oor muscles are striated muscles innervated by sacral roots and the pudendal nerve.
Modulators ofColonic Motility
Muscarinic agonists (i.e., hyoscamine) and cholinesterase
inhibitors (i.e., neostigmine) increase colonic motility. The
α-2 adrenergic antagonist yohimbine also increases colonic
motility and promotes uid and electrolyte absorption, while
the α-2 agonist clonidine reduces motility. Clonidine reduces
colonic tone and phasic pressure activity, as well as the
colonic perception of distention which can increase colonic
compliance. Clonidine can be used to treat diarrhea predominant IBS.
Serotonin 5-HT receptors (5-HT3) antagonists such as
alosetron increase colonic compliance, reduce postprandial
rectal motor activity, improve stool consistency, delay colon
transit, and reduce rectal sensitivity in IBS. Alosetron was
approved for IBS-diarrhea predominant in women [33]. A
systematic review of published clinical trials through the
Food and Drug Administration (FDA) Adverse Events
Reporting System documented the risk of ischemic colitis
was higher with alosetron than placebo (0.15% vs. 0.0%)
[34], and it was subsequently withdrawn from the market.
A newer high selectivity afnity 5-HT4 receptor agonist,
prucalopride, has been approved by the FDA.Extensive cardiovascular assessment suggests it does not affect the Q-T
interval. For chronic constipation patients, prucalopride can
be used to accelerate intestinal and colonic transit [35, 36].
The GI tract contains three opioid receptors (δ, μ, κ), with
the gastrointestinal effects mediated primarily by μ receptors. Opioids reduce neuronal excitability and release of neurotransmitters. Morphine increases colonic phasic segmental
activity, reduces fasting colonic tone, and attenuates the gastrocolonic response. Opioids also increase uid absorption
partly by delaying transit and increasing mucosal contact
time. Opioid-induced constipation or opioid bowel dysfunction is common, affecting 41–81% of patients treated with
opioids [18].
Lubiprostone is a synthetic bicyclic fatty acid derived
from prostaglandin E1 that activates apical CIC-2 chloride
channels. Lubiprostone also activates prostaglandin EP
receptors and the apical cystic brosis transmembrane regulator (CFTR), causing intestinal uid secretion [37]. These
secretory effects likely explain why lubiprostone accelerates
small intestinal and colonic transit in healthy subjects.
Lubiprostone does not affect colonic motor activity in
healthy individuals [38] but is approved by the FDA for
treating chronic constipation and female constipation predominant IBS [18, 39].
Bile acids infused directly into the human sigmoid and
rectum at concentrations of 5 mmol/L stimulated colonic
phasic contractions; however, such concentrations are seldom achieved in the colon unless there has been an ileal
resection. Rectal infusion of chenodeoxycholic acid at physiological concentrations stimulates proximal colonic propagated contractions and increases rectal sensitivity. Hence,
chenodeoxycholic acid accelerates colonic transit in healthy
subjects. These effects have pathophysiological and therapeutic consequences. When enterohepatic circulation of bile
acids is disrupted by ileal disease (e.g., Crohn’s disease, surgical resection, or radiation ileitis) or idiopathic mechanisms
(idiopathic bile-acid malabsorption), bile acids spill into the
colon, causing diarrhea. Idiopathic bile-acid malabsorption
may explain diarrhea in some patients with IBS.From a therapeutic perspective, delayed-release chenodeoxycholic acid,
results in accelerated colonic transit and improved bowel
function in females with constipation-predominant IBS [18].
Laxatives work either via osmotic effects (e.g., polyethylene glycol-based solutions, magnesium citrate-based products, sodium phosphate-based products, and nonabsorbable
carbohydrates [lactulose, sorbitol]) or by stimulating colonic
propulsive activity [18]. Osmotic agents, which are hypertonic, pull uid into the intestinal lumen, causing diarrhea.
Stimulant laxatives (e.g., bisacodyl, sodium picosulfate,
and glycerol) stimulate HAPC wave sequences, thereby
leading to mass movements; bisacodyl and sodium picosulfate also have anti-absorptive plus secretory effects [18, 40,
41]. Bisacodyl exerts its motor effect through mucosal affer-
ent nerve bers, because the response can be blocked by
topical mucosal application of lidocaine [18].
While sacral nerve stimulation is approved by the FDA to
treat fecal incontinence, its role for treating constipation is
unclear [42]. Sacral nerve stimulation modulates the extrinsic nerves innervating the pelvic oor and colon. In addition, stimulation of the S3 root also induces propulsive
activity throughout the entire colon and has been shown to
increase stool frequency in patients with slow transit constipation [43]. In Kamm’s study, colonic transit was assessed
in 27 of 45 patients with medically refractory chronic constipation who proceeded to permanent sacral nerve stimula-
38
G. T. Ault and J. S. Beaty
tion [42]. Of these 27 patients, 20 had delayed colonic
transit before but only 9 had delayed transit after sacral
nerve stimulation.
Microbiome
A normally functioning GI tract has healthy, well-established
colonizing microbiota in its mucosa and lumen, which are
major contributors to the maintenance of whole-body
homeostasis. It is well established that the species composition and relative abundance of the gut microbiota are
impacted by the diet, lifestyle, and overall health of an individual. Humans have developed a commensalistic relationship with the gut microbiome. Over time, this relationship
has evolved to become a mutual and interdependent one, in
which the physiologic activity of the microbiota has a signicant impact on the host and the activity of the host impacts
the genera comprising the microbiota. In support of life, gut
microbial metabolism supplies the host with short-chain
fatty acids and essential vitamins (vitamins B and K) and
contributes to the synthesis and absorption of essential amino
acids.
The adult human intestine contains approximately 110
trillion bacteria. Gas chromatography-mass spectrometry
analysis detected more than 700 volatile organic compounds
from human feces [44]. Our microbiota is established in the
period after birth and although it can be modulated by factors, such as diet, illness, and antibiotic treatment, is relatively resistant to change in later life. The microbial
composition changes along the length of the gut, in response
to changes in the luminal environment including presence of
nutrients, acidity, and oxygen content. Microbial diversity
has been used as an index of a “healthy” microbiota, but this
is probably a simplistic notion as some benecial plant foods
will decrease diversity yet produce a benecial host response.
There is considerable variability that likely depends predominantly on diet and lifestyle [45].
The role the human microbiome plays in health and disease is actively under investigation. The composition of feces
is altered in diseases such as IBS [46], IBD, colorectal cancer [47], and autism [48], implicating that the pathogenesis
of these diseases is associated with dysbiosis. Several studies
demonstrate alterations in the fecal and colonic mucosal
microbiome in constipation and diarrhea. Absent interventional trials, it is unclear whether these associations reect
cause and effect. However, even after adjusting for demographic features, diet, and colonic transit, the microbiome
discriminated between health and constipation with an accuracy of 92% [18].
Patients with IBD have altered microbiota, and they may
have changes in their gut microbiota that precede a diagnosis. IBD is thought to be an aberrant immune response to
luminal content including the microbiota. A shift in the delicate balance (dysbiosis) of “good” bacteria and “bad” proinammatory bacteria may be important for the development
and maintenance of IBD.For example, Roseburia spp. are
decreased in those already diagnosed with IBD, and as such,
the manipulation of the microbiota using antibiotics, probiotics, and prebiotics might be useful in treating IBD [49, 50].
Crohn’s disease (CD) is associated with lower overall microbial diversity when compared to healthy controls. The abundance of both the Proteobacteria and Bacteroidetes was
signicantly higher in CD when compared to healthy controls and those with ulcerative colitis (UC). Low numbers
and the absence of Faecalibacterium prausnitzii, a common
member of the healthy gut microbial community, have been
associated with UC.Antibiotics have been used to treat IBD
with the goal of decreasing concentrations of bacteria in the
lumen and altering the community composition.
These observations and many others have been the motivating force for the National Institutes of Health (NIH)
Human Microbiome Project (NIH HMP) [51]. The NIH
HMP is a roadmap for biomedical research and has three
main goals: (1) utilize new high-throughput screening technology to characterize the microbiome more completely by
studying multiple body sites from 250 “normal” individuals;
(2) determine if there are associations between changes in
the microbiome and health and disease; and (3) standardize
data resources and new technologies for the wider scientic
community [52, 53]. Phase II of this project has begun, and
it aims to examine changes in three microbiome-associated
conditions: (1) preterm birth, (2) IBD, and (3) type 2 diabetes [54–57].
The indigenous human microbiome is dominated by two
bacterial phyla: Firmicutes and Bacteroidetes. In many stud-
ies, the Firmicutes and Bacteroidetes account for greater
than 98% of the bacteria present in the human gut. It has long
been appreciated that different classes of antibiotics affect
the human gut microbial community, both targeted and offtarget [58, 59]. The use of antibiotics can open niches that
were otherwise occupied and allow for new species (good or
bad) to take up residency [60].
For example, changes in human gut microbiome community structure after exposure to the uoroquinolone antibiotic, ciprooxacin, have shown that much of the community
is altered [61]. Dethlefsen etal. reported that all aspects of
the gut microbiome community, that is, diversity, richness,
and evenness, were decreased and the abundance of approximately one-third of the species present was changed [61].
The loss of diversity may cause acute human disease by
impacting the role of the microbiome on nutrition, metabolism, and pathogen resistance. After antibiotic treatment was
stopped, many of the communities rebounded and closely
resembled the original community. In some cases, it took
nearly 6 months for the microbiome to rebound. It has been
2 Colonic Physiology
39
suggested that broad-spectrum antibiotics, especially those
with activity against anaerobes, might cause longer-lasting
changes in the gut microbial community [62].
Conclusion
The colorectum is a complex organ with multiple roles in
homeostasis. By increasing understanding of its anatomy
and complex physiology, the colorectal surgeon can gain a
better understanding of the etiology of derangements in
pathophysiologic conditions. In addition, a thorough understanding of colorectal physiology allows an opportunity to
develop new therapies based on its known functions. These
examples are demonstrated with much greater detail throughout other chapters of the text.
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Anorectal Physiology
PasithornA.Suwanabol andScottE.Regenbogen
3
Key Concepts
• Maintenance of fecal continence and defecation are complex processes requiring both voluntary and involuntary
reexes that have yet to be fully characterized.
• Normal continence is dependent on coordination between
neuronal reexes, sensory and motor pathways, the rectum, anal sphincters, and pelvic oor and requires adequate rectal compliance and competence of the anal
sphincter.
• During defecation, sensory mechanisms allow the rectum
to stretch to accommodate feces, the pelvic oor muscles
relax, and intraabdominal pressure increases.
Simultaneously, the puborectalis relaxes and straightens
the anorectal angle, the anal canal shortens, and the pelvic
oor descends. Finally, the anal sphincters relax and evacuation is initiated.
• Anatomy and physiology of the rectum and anus are
intrinsically related, allowing physiologic testing to be
exceedingly useful for diagnosis and management of anorectal pathologies.
• Disorders of continence can derive from decits of mental, anatomic, and physiologic functions, including
reexes, sensory and motor nerves, and the muscles of the
rectum, sphincters, and pelvic oor.
• Functional defecatory disorders frequently coexist with
urogynecologic conditions likely due to the shared musculature of the pelvic oor and urogenital diaphragm, as
well as from the overlap in peripheral innervation and spinal nerve roots.
P. A. Suwanabol · S. E. Regenbogen (*)
University of Michigan, Division of Colorectal Surgery,
Department of Surgery, Ann Arbor, MI, USA
e-mail: pasuwan@med.umich.edu; sregenbo@med.umich.edu
Introduction
Recognition and appropriate management of anorectal
pathology require an understanding of both anatomy and
physiology of the rectum, anus, and pelvic oor. The purpose
of this chapter is to review the anatomy and innervation of
the rectum and anus, characterize normal continence and
defecation, and provide an overview of physiologic testing
relevant to anorectal physiology and pathophysiology. In
addition, we will briey review the pathophysiology of functional disorders of the anus and rectum.
In general, defecation and maintenance of fecal continence are complex processes requiring both voluntary and
involuntary reexes that have yet to be fully characterized.
Much of what is known is based on an understanding of
pathologic disorders and functional studies among healthy
subjects or animals. Despite our incomplete understanding
of anorectal physiology, it is critical to gain as much knowledge of normal and abnormal physiology as possible as it
will enable the surgeon to advise and intervene when needed.
Anatomy
For detailed discussion of the anatomy and physiology of the
rectum and anus, please refer to Chap. 1.
The rectum serves as a reservoir for feces, measuring
approximately 12–15cm in length, yet its proximal and distal margins continue to be debated– particularly in light of
differences in treatment approaches for lower gastrointestinal cancers [1]. The rectum, which is identied in the abdomen by the lack of haustra, taeniae, or epiploica, is located
along the curve of the sacrum and coccyx and becomes the
anal canal as it passes through the levators [2]. The rectal
wall contains a layer of longitudinal smooth muscle and a
layer of circular smooth muscle that are in continuity with
the gastrointestinal tract [3]. The rectum encompasses three
folds, known as the valves of Houston, which do not contain
all the muscle wall layers and are not believed to serve any
© Springer Nature Switzerland AG 2022
S. R. Steele et al. (eds.), The ASCRS Textbook of Colon and Rectal Surgery, https://doi.org/10.1007/978-3-030-66049-9_3
41
42
Female pelvis (from below)
urethral or
e
P. A. Suwanabol and S. E. Regenbogen
specic function. The middle valve corresponds to the anterior peritoneal reection and is the most consistent with
regard to location and its presence [2].
Like the rectum, the denition of the anus or anal canal is
controversial and is distinguished by embryologic origin and
mucosal histology or by its function. The embryologic anal
canal, which does not incorporate anal function, is dened as
the area from the anal verge to the dentate line [2]. First
described by Milligan and Morgan in 1934in order to guide
anorectal surgery, the functional or surgical anal canal begins
where the rectum enters the pelvic hiatus and passes through
the puborectalis. It encompasses the area from the anal verge
to the anorectal ring and is surrounded by the anal sphincters
and the puborectalis [4]. On average, the functional or surgical anal canal measures approximately 2.5–5cm in length
and is shorter in females [5]. The anal canal is characterized
by columnar mucosa above the dentate line and squamous
epithelia below, which are important as they represent two
separate inputs, supplied by different aspects of the arterialvenous, lymphatic, and nervous systems [6]. Above the dentate line, the anal canal is supplied and drained by the
hypogastric vessels and innervated by the sympathetic and
parasympathetic nervous systems. Below the dentate line,
the anal canal is supplied by the inferior hemorrhoidal vessels and innervated by the somatic nervous system [2] The
1–2cm area between these two regions is known as the transition or cloacogenic zone, which is composed of columnar,
transitional, and stratied squamous epithelium [6].
The anal sphincter complex consists of the internal anal
sphincter (IAS), the conjoined longitudinal muscle (CLM),
and the external anal sphincter (EAS). The IAS is a 2–3mm
thick circular band composed of the distal inner circular
smooth muscle layer of the rectum, which is always maximally contracted to prevent involuntary loss of stool and atus [3]. The IAS is encompassed proximally by the levator
ani and distally by the supercial external sphincter muscle
and subcutaneous external straited anal sphincter muscle [7,
8]. The CLM, located between the IAS and the EAS, is com-
posed of the bers of the outer layer of the rectum at the level
of the anorectal ring and runs distally to the puborectalis
muscle [9]. The CLM’s functions are unclear, but it may contribute minimally to maintaining continence and defecation
[10, 11]. More importantly, the CLM may act as a scaffolding for the entire anal sphincter complex [12]. The EAS
comprises striated muscle as a continuation of the puborectalis muscle and is attached anteriorly to the perineal body and
posteriorly to the anococcygeal ligament. The EAS is in constant state of tonic contractile activity, even at rest, and voluntarily contracts during any threat of incontinence [13].
The pelvic oor muscles include the levator ani, which
consists of the pubococcygeus, puborectalis, and iliococcygeus (Fig.3.1). These muscles function to support the viscera
of the pelvic cavity and play a key role in defecation [7]. The
pubococcygeus arises from the posterior pubis, travels alongside the anorectal junction, and inserts into the anococcygeus
ligament and the coccyx. The puborectalis is a U-shaped
Fig. 3.1 Muscles of the
pelvic oor. (Illustration
created by H.R.Fischer,
MFA)
Clitoris
External
ifice
Ischiopubic
ramus
Vagina
Perineal body
Anus
Anococcygeal
ligament
Ishciocavernous muscle
Bulbospongiosus
muscle
Perineal membrane
Superficial transvers
perineal muscle
External anal
sphincter musctes:
Deep
Superficial
Subcutaneous
Levator ani muscles:
Pubococcygeus
Puborectalis
lliococcygeus
Gluteus maximus
muscle
3 Anorectal Physiology
43
muscle that slings the anorectal junction to the posterior pubis
to pull the rectum anteriorly and forms the anorectal angle. It
is palpable on digital rectal exam as the top of the anorectal
ring [3]. The iliococcygeus arises from the ischial spine and
obturator fascia, travels inferiorly and medially, and inserts
into the anococcygeal raphe and coccyx [2].
Physiology
Innervation oftheAnus andPelvic Floor
Sympathetic nerves derived from L1, L2, and L3 join the
preaortic plexus, which then extend to form the hypogastric
plexus below the aorta. These then join parasympathetic
bers called nervi erigentes (S2, S3, and S4) to form the pelvic plexus (Fig.3.2) [14]. Motor innervation of the IAS is
supplied by the sympathetic (L5) and parasympathetic
nerves (S2, S3, and S4) from the autonomic nervous system.
In contrast, the EAS is supplied by the inferior rectal branch
of the pudendal nerve (S2 and S3) and by the perineal branch
of S4 from the somatic nervous system. Unilateral transection of the pudendal nerve does not impact EAS function due
to ber crossover at the spinal cord level [15]. The sacral
roots of S3 and S4, the perineal branch, and the inferior rectal nerve of the pudendal nerve innervate the levator ani [16].
The pudendal nerve branches supply the pubococcygeus and
puborectalis, whereas direct sacral nerves S3 and S4 innervate the iliococcygeus [17].
Upper anal canal sensory innervation is supplied by both
free and organized sensory nerve endings, including
Meissner’s corpuscles (touch), Krause’s bulbs (temperature),
Golgi-Mazzoni bodies (pressure), and genital corpuscles
(friction) [18, 19]. Within the transition zone of the anal
canal, these organized nerve endings may play a role in sampling [20]. The inferior rectal branch of the pudendal nerve
provides anal sensation and may provide some maintenance
of fecal continence [2, 21, 22]. In addition, it may play a
smaller role in discriminating between solid and gas [23].
Normal Continence
Normal continence requires adequate rectal compliance to
accommodate fecal contents and competence of the anal
sphincter to resist propulsive forces of the distal gastrointestinal tract, assess its contents, and release them under voluntary control [7, 24]. Although normal continence is
incompletely understood, it is known to be dependent on
complex coordination between neuronal reexes, sensory
and motor pathways, the rectum, anal sphincters, and pelvic
oor [25, 26].
Rectal Sensation andCompliance
Rectal sensation encompasses the feeling of both rectal lling and anal reexes, which is distinct from the rest of the
lower gastrointestinal tract where distension evokes pain
[27, 28]. The rectum’s function is to store feces, which
requires the ability to accommodate volumes of feces without substantially altering rectal pressures. Accommodation
is reliant on both the content and the contractile state of the
rectum [3, 29]. Baseline rectal pressure is low (approximately 5mmHg) compared to anal canal pressures, which
measure approximately 10–14 times that of the rectum. This
pressure differential may allow for stool deferment, forcing
stool back into the sigmoid and rectum, until defecation is
initiated [19]. Although the rectum does not have proprioceptive receptors, rectal compliance may be due to unique,
slowly adapting mechanoreceptors that respond to tension
and rapid distension, termed rectal intra-ganglionic laminar
endings (rIGLEs) [30]. This idea is consistent with the
observation that rectal lling sensations coincide with
increased rectal pressure during rectal distension [27].
Instead, defecation is sensed at the level of the levators and
the anal canal, which may underlie the preserved sense of
defecation among patients after proctectomy with ileoanal
or coloanal anastomoses [31, 32].
Anorectal Reexes
The rectoanal inhibitory reex (RAIR) is an intrinsic intramural reex critical to normal continence. It occurs in
response to distension of the rectum, relaxing the upper IAS
to allow fecal material or atus to interact with specialized
receptors in the upper anal canal. This sampling enables atus to pass without fecal incontinence as the lower IAS resting pressure, the contraction of the EAS, and puborectalis
push feces to the upper rectum and delays defecation [3, 33,
34]. The RAIR occurs every 8–10minutes and lasts less than
10 seconds [35, 36]. The RAIR is absent in those with
Hirschsprung’s disease due to the absence of myenteric ganglia in the rectum [37]. Furthermore, injury or alteration to
the RAIR may play a role in patients with poor functional
outcome or incontinence after rectal resection [38–41].
Less studied anorectal reexes include the cutaneous anal
sphincter reex, the bulbocavernosus reex, and the coughanal reex. The cutaneous anal sphincter reex is dened as
contractions of the EAS with touch or pain of the anal skin,
while the bulbocavernosus reex is characterized by contractions of the EAS when squeezing the glans penis or clitoris.
The bulbocavernosus reex can also occur when a urethral
catheter is removed. Finally, the cough-anal reex is
described as contractions of the EAS when coughing or
snifng. The cough-anal reex is important in maintaining
continence during sudden increases of intraabdominal pressures, such as coughing, sneezing, or laughing [42].
44
ight sacral
h
P. A. Suwanabol and S. E. Regenbogen
Fig. 3.2 Innervation of the
anus and pelvic oor.
(Illustration created by
H.R.Fischer, MFA)
Female pelvis
(lateral below)
Abdominal aorta
Inferior vena cava
splanchnic
Superior
ypogastric
plexus
Right hypogastric
Internal iliac plexus
Inferior hypogastric
(pelvic plexus)
Sympathetic trunk
and L2 ganglion
Lumbar
nerves
Left and r
sympathetic trunks
and ganglia
nerve
Pelvic
parasympathetic
nerves
Sacral splanchnic
nerves (sympathetic)
Pudendal nerve
Rectal plexus
Rectum (retracted)
Internal andExternal Anal Sphincters
The IAS constitutes approximately 50–70% of resting tone
or pressure and is maximally contracted at rest, with the
hemorrhoid complexes accounting for an additional 15% of
resting tone or pressure [2, 43–46]. Hemorrhoid complexes
contribute to continence by expanding to create a seal proximal to the anal opening [46]. Due to the intrinsic function of
smooth muscle, most of the resting tone is due to myogenic
tone, which is characterized by slow, constant waves of contraction [42, 47]. The IAS receives additional excitatory
sympathetic input and inhibitory parasympathetic input,
which are mediated by nitric oxide [3, 48–50]. Injury to the
IAS leads to passive fecal incontinence or leakage, whereas
injury to the EAS is associated with urge fecal incontinence
[3, 51]. Whereas the EAS plays a smaller role in resting tone,
its primary contribution to continence involves voluntary or
reexive contraction in response to rectal distention and
threat of incontinence, for example, during increases in
intraabdominal pressure [3, 52]. Similarly, defecation may
be deferred by contraction of the EAS to oppose increased
rectal pressure. After EAS contraction, the sensation of
urgency and tenesmus will diminish over a period of time
Uterus, fallopian tube
and ovary (retracted)