Colon and pelvic floor anatomy and physiology

Chapter 8

Colon and pelvic floor anatomy and physiology Askin Erdogana, Yeong Yeh Leeb a

Alanya Alaaddin Keykubat University, Alanya, Turkey, bUniversiti Sains Malaysia, Gelugor, Penang, Malaysia

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The motility function of colon and pelvic floor is to propel, store and remove bowel contents and this coordinated function requires intact gut–brain interactions and regulation by the enteric nervous system. Neuromechanical loop and colonic migrating motor complex are two important factors that affect colonic motility. Colonic contractions can be propagating (low-amplitude and high-amplitude contractions) and non-propagating, whereas periodic rectal motor activity provides the braking mechanism. The act of defecation and maintaining continence is largely dependent on intact anal sphincters and levator ani in the pelvic floor. Also intact recto-anal reflexes, sensation of rectal content and intact lumbo-anorectal and sacro-anorectal nerves are needed.

Anatomy and physiology of colon Colon anatomy Embryologically, it originates from midgut (from ascending colon to proximal transverse colon) and hindgut (from distal transverse colon to sigmoid colon). The length of colon is approximately 150 cm long, starting with the caecum and ends with anal verge. Colon has four segments; caecum and appendix vermiformis, colon segments (ascending, transverse and descending colon), sigmoid colon and anal canal. Different segments have different diameters; caecum being the widest (7.5 cm) and sigmoid colon being the narrowest (2.5 cm). Fig. 1 shows the anatomy of colon. There are several important features that distinguishes colon from small intestine. Colon is wider and is mostly fixed except for the transverse colon. Longitudinal muscles, that run outside and along the colon, form into three bands of muscles (taenia liberis, taenia omentalis and taenia mesocolica), that are located 120° from each other, and cover caecum to proximal rectum. Taenia omentalis is attached to greater omentum, taenia mesocolica is attached to mesocolic taenia and taenia liberis is boundless. At the rectosigmoid junction, taenia expands to cover the rectum. Taenia causes shortening of colon and together with semilunar folds and haustra that are located between these taenia cause a sacculated view of the colon. Although transverse and sigmoid colon are fully covered with mesentery, other colon parts only have mesentery on the anterior part. Caecum is located at the right iliac fossa and is fixed with mesocecum. Due to its large diameter, tumors can grow to a large size without any signs of obstruction. Ileocecal (IC) valve is located on the posteromedial wall of caecum and has two elliptical folds forming the orifice. Appendix vermiformis, attached to caecum, is blind-ended and is located inferiorly. Ascending colon is fully covered with peritoneum and therefore lies in the retroperitoneum. Ascending colon extends approximately 12–20 cm vertically from caecum and when reached to posterior lobe of liver makes a right-angled turn (hepatic flexure or right colic flexure) to connect transverse colon. Transverse colon is an intraperitoneal portion of colon and after making a medial and anterior turn, travels approximately 40–50 cm from hepatic flexure across the abdomen and anterior stomach until it reaches the spleen. Transverse colon is tied to the diaphragm by the phreno-colic ligament and is the most mobile portion of colon that may extend and drop into the pelvis. At the spleen, transverse colon makes a right-angled turn to point downward, known as the splenic flexure (left colic flexure).

Clinical and Basic Neurogastroenterology and Motility. https://doi.org/10.1016/B978-0-12-813037-7.00008-X © 2020 Elsevier Inc. All rights reserved.

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FIG. 1  Anatomy of (A) colon and (B & C) pelvic floor. Barium defecography (D) showing (a) pubococcygeal line, (b) perineal descent, (c) anorectal angle. ((A)–(C) Modified from Raizada V, Mittal RK. Pelvic floor anatomy and applied physiology. Gastroenterol Clin N Am 2008;37:493–509, vii; Drake RL, Vogl AW, Mitchell AWM, Gray's atlas of anatomy, Elsevier; 2008. (D) Modified from Chang J, Chung SS. An analysis of factors associated with increased perineal descent in women. J Korean Soc Coloproctol 2012;28(4):195–200.)

Descending colon is the retroperitoneal part of colon that travels inferiorly after the splenic flexure and is 25–45 cm in length. Descending colon continues into the left iliac fossa becoming the sigmoid colon, a S-shaped, and redundant portion of the colon that extends until at the level of S3 vertebra. Sigmoid colon is the narrowest portion and therefore obstructive symptoms tend to occur early with sigmoid tumors. Sigmoid colon is attached to the pelvis with sigmoid mesocolon. Due to its long length and tortuosity, sigmoid colon is at increased risk of volvulus and often the most difficult part during colonoscopy due to its looping potential. Sigmoid colon continues into rectum. Paracolic gutters are located lateral to ascending and descending colon allowing fluids to drip into the pelvic cavity. Rectum begins at the level of S3 and is approximately 12–15 cm in length. Rectum lacks taenia coli, sacculation, haustra, and omental appendices. The proximal one-third of rectum is covered with peritoneum anteriorly and laterally, middlepart is covered anteriorly only and distal third is not covered at all. Peritoneum forms different pouches in female and male. In female, peritoneum forms rectouterine pouch (pouch of Douglas) between rectum and posterior vagina and cervix but in male it forms the rectovesical pouch between rectum and posterior bladder wall. Rectum follows the anteriorly concave curves of the sacrum and coccyx (sacral flexure) and continues with an anteriorly convex curve (anorectal flexure) before it connects to the ampulla. Anorectal flexure (anorectal ring) is formed by the puborectalis muscle that maintains fecal ­continence mostly. Apart from two major anorectal and sacral flexures, there are three lateral flexures (plica transversalis recti superior, intermediate and inferior) known as the Valves of Houston. Ampulla ends with the anal canal.



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Anal canal is 4–5 cm in length, travels in the inferior–posterior direction and ends with anus (anal verge). Anal canal is completely located extra-peritoneally. One-third of the anal canal is located below the dentate line (pectinate line) and two-third is located above the dentate line. Although anal canal from anal verge to dentate line is covered by pigmented and keratinized skin, it does not have skin appendages like hair, sweat glands and sebaceous glands unlike perianal skin. At the dentate line, anal canal has a transitional zone called anal pecten (zona alba) and is 1–2 cm long. Above the transitional zone, anal canal is covered by columnar epithelium. Distally to the rectum and at the upper parts of anal canal, there are 6–12 longitudinal folds called the Morgagni columns that end in the anal papilla and merge together to form anal valves at the dentate line. Anal glands and anal papillae open into these valves to secrete mucus. Some of these columns form cushions that include parts of hemorrhoidal (superior rectal) artery and veins that also help to maintain fecal continence. There are several perianal spaces around the anal canal such as subcutaneous, submucosal, inter-sphincteric, ischio-anal (rectal) and pelvi-rectal. Anteriorly, the anal canal is in close relationship with seminal vesicles, prostate, and urethra in males and cervix, perineal body and vagina in females. Posteriorly, the lower part of sacrum and tip of the coccyx, are connected to anal canal by the anococcygeal ligament. Rectovesical fascia is located anteriorly and presacral endopelvic fascia is located posteriorly. The anorectal junction, also known as anorectal ring, is located within the pelvic diaphragm, and is made-up of levator ani, coccygeus, and puborectalis muscles. Internal anal sphincter (IAS) is formed by the circular muscle layer of the rectum that becomes thicker at the anal canal level with septa between muscles. External anal sphincter (EAS) is made up of longitudinal muscles of rectum. Since Santorini's first reported observation [1], EAS is known to have three muscle parts; subcutaneous, superficial, and deep layers [2, 3]. Subcutaneous part is located below the IAS and superficial part is located around the distal part of IAS. Lately, the new MRI and three-dimensional (3-D) ultrasound (US) images in combination with high-definition manometry mapping studies have observed that the deep part of EAS is likely a part of or indeed the puborectalis muscle itself [4]. Furthermore, although EAS has been thought to be “donut-shaped,” recent data using novel techniques such as 3-D trans-perineal ultrasound imaging, MRI, diffusion tensor imaging and muscle fiber tracking suggests that the EAS had a “purse-string” morphology [5] (Fig. 2). According to this study, EAS muscles cross contralaterally from the perineal body to the contralateral transverse perineal and bulbospongiosus muscles, and posteriorly to the coccyx by the anococcygeal raphae. In its craniocaudal extend, the posterior wall of EAS is longer than the anterior wall. On the other hand, IAS is an involuntary sphincter with nerve supplies from autonomic, sympathetic (spinal nerves) and sacral parasympathetic (pelvic plexus nerves) (Table 1) [6]. Sympathetic nerves start from the lower thoracic ganglia and after joining branches of aortic plexus, then form superior hypogastric plexus (presacral nerve) and divide into the right and left hypogastric nerves. The parasympathetic (pelvic splanchnic) nerves start from S2–S4 sacral nerves and join with fibers of superior hypogastric plexus to form the inferior hypogastric plexus. The inferior hypogastric plexus divides into the uterovaginal plexus, vesical plexus and middle rectal plexus. Superior and inferior rectal nerves (derived from pudendal nerve) and middle rectal nerve supply rectum and anal canal and merge with postganglionic neurons in the myenteric plexus. The α-adrenergic receptors of sympathetic nerve mediate contraction, whereas β1, 2, 3-adrenergic receptors mediate relaxation of the IAS. Parasympathetic nerve stimulation causes relaxation of IAS mediated mainly by nitric oxide containing neurons in myenteric neurons. Vasoactive intestinal polypeptide (VIP) and carbon monoxide probably have only limited effects on parasympathetic nerves [7]. Other than relaxation, myenteric nerves also have excitatory motor neurons acting via acetylcholine and substance P. Recently it has been shown that intramuscular interstitial cells of Cajal (ICC–IM), the predominant cells in ICC [8] play a major role on maintaining tone activity of IAS being the pacemaker cells [9]. The EAS is a voluntary muscle and is innervated by inferior rectal branches of right and left pudendal nerves. There is controversy regarding the origin of pudendal nerve. Some authors describe that pudendal nerve originates from the sacral spinal cord at S2–S4 (Onuf's nucleus motor neurons) [2], while others state that the pudendal nerve originates from S1 [10]. Arterial blood supply of caecum, ascending colon and two thirds of transverse colon is derived from the superior mesenteric artery (SMA) through right and middle colic branches. The inferior mesenteric artery (IMA) supplies arterial supply of one-third of transverse colon, descending and sigmoid colon and rectum through the left colic and sigmoid branches. Along the mesenteric border of the colon runs an anastomosis of proximal and distal arteries called the marginal artery of Drummond. The intersection of SMA and IMA is an area with less blood supply that is susceptible to ischemia. The venous blood is drained via superior mesenteric vein (SMV) and inferior mesenteric vein (IMV). Lymph fluids drain into epicolic, pericolic, intermediate and mesocolic lymph nodes. Anal canal has different arterial and venous supplies at different levels. Above the pectinate line, the arterial supply comes from the terminal branch of superior rectal (hemorrhoidal) artery that is the terminal branch of inferior mesenteric artery. Whereas below the pectinate line, arterial supply derives from the middle rectal artery, a branch of the internal iliac artery (hypogastric artery) and the inferior rectal artery that is a branch of the internal pudendal artery. Anal canal has a strong portosystemic venous connection. Above the pectinate line, venous blood is drained by internal hemorrhoidal plexus,

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FIG. 2  (A) Upper: Magnetic resonance imaging (MRI) sagittal view of pelvis showing cranial elevation of the anorectal angle with squeeze (from 44° to 62°), and Lower: Sagittal image of high definition manometry (HDM) demonstrating the similar cranial elevation of anorectal angle observed in MRI with squeeze, where both external anal sphincter (EAS) and puborectalis (PRM) contributed. (B) Based on findings of MRI and HDM in (A), EAS was hypothesized as being part of PRM (B1). Findings of proton density MRI (B2, right) and 3-dimensional reconstruction (B2, left) of the EAS concurred with the above hypothesis and this was further supported by fiber tracking using tensor images (B3, right). Based on the above imaging findings, the EAS complex can be concluded to have a “purse-string” morphology (B3, left). (Modified from Raizada V, Bhargava V, Karsten A, Mittal RK. Functional morphology of anal sphincter complex unveiled by high definition anal manometery and three-dimensional ultrasound imaging. Neurogastroenterol Motil 2011;23:1013–1019, e1460; Mittal RK, Bhargava V, Sheean G, Ledgerwood M, Sinha S. Purse-string morphology of external anal sphincter revealed by novel imaging techniques. Am J Physiol Gastrointest Liver Physiol 2014;306:G505–514.)

the superior rectal veins, the inferior mesenteric vein and then by the portal vein respectively. Below the pectinate line, venous blood is drained by external hemorrhoidal plexus, the middle rectal and pudendal veins and the internal iliac vein, and then by the systemic circulation respectively. Lymph of upper rectum drains into the inferior mesenteric nodes and lower rectum drains into the internal iliac nodes. Above the pectinate line, anal canal lymph is drained into systemic drainage system, whereas below the line drains into superficial inguinal lymph nodes.

Colon physiology Innervation of colon and rectum Most of the sympathetic innervation of the colon arises from the L2–L5 roots and most without interruptions, merge into the inferior mesenteric plexus (Table 1). Proximal part of the colon (caecum to left colic flexure) also receives sympathetic supply from celiac ganglia and superior mesenteric plexus. Distally to the left colic flexure, the inferior mesenteric plexus provides the nerve supply until the rectum. Sympathetic nerves supply the submucosal blood vessels, ENS, Meissner's plexus, and cause inhibitory effects on blood flow, secretion and colonic motor activity. Parasympathetic innervation is supplied by both the vagus nerve and sacral spinal cord (S2–S4). Parasympathetic innervation of caecum, ascending colon and the transverse colon is through the superior hypogastric plexus formed by branches of the vagus nerve. Descending and sigmoid colon innervations are through the pelvic splanchnic nerves that are derived from sacral parasympathetic nerves through the pelvic nerves either directly into the bowel wall or into the pelvic plexus.

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TABLE 1  A summary of the nerve supply and its regulation of colon, anal sphincters and pelvic floor function

Nerve supply

Function

Colon

Internal anal sphincter

External anal sphincter

Pelvic floor

Sympathetic innervation: L2–L5 roots, inferior and superior mesenteric plexus and celiac ganglia

Autonomic

Right and left pudendal nerves (52–54)

Central, somatic and visceral pathways

Parasympathetic innervation: The vagus nerve and sacral spinal cord (S2–S4)

Sympathetic nerves (spinal nerves): The right and left hypogastric nerves

Enteric nervous system

Sacral parasympathetic nerves (pelvic plexus nerves): S2–S4 sacral nerves

Parasympathetic nerves triggers propagating complexes in the ascending and transverse colon and increases propulsive activity of the distal colon

Passive continence Resing and sphincter tone

Levator ani: Pudendal, inferior rectal, perineal, and S2–S4 nerves (The puborectalis: pudental nerve, The pubococcygeous: S3–S5, The ileococcygeous: Aponeurotic) The coccygeous: S3–S5

Active continence Squeeze and sphincter tone

Provide support for the viscera of the abdominopelvic cavity Support continence mechanisms of the anal, urethral and vaginal orifices Assist defecation process

PRMA, periodic rectal motor activity.

Sacral nerves make synapses with the ENS. This cholinergic activation of parasympathetic nerves both triggers propagating complexes in the ascending and transverse colon and increases the propulsive activity of the distal colon before defecation.

Enteric nervous system There is a bidirectional gut–brain communication between the ENS and central nervous system (CNS). This communication is performed by the vagus, pelvic and sympathetic nerves. ENS incorporates two plexuses. The myenteric plexus (Auerbach's plexus) is located between longitudinal and circular muscles of the muscularis externa. Submucosal plexus has two components; Meissner's plexus and Schabadasch's plexus. ENS mediates muscle contraction, mucosal fluid secretion, effects local blood flow through their effects on muscles, mucosal crypts and epithelium and through mediators such as acetylcholine (Ach) and nitric oxide (NO) as well as cytokines and purines.

Interstitial cells of Cajal (ICC) ICC is not neuronal in its nature and originates from smooth muscle cells. ICC has three sub types based on their location; ICCMY is located at myenteric plexus, ICCSM is located near the submucosa and ICCIM is located between the circular and longitudinal muscle layers of the colon. Some ICCs act as pacemaker and some provide transmission from neurons to the smooth muscle. ICCMY and ICCSM form connections between themselves and smooth muscle cells through gap junctions. ICCMY is believed to be the pacemaker cells of colon that causes rapid (12–20/min) and small myenteric potential oscillations (MPOs) of the circular and longitudinal muscle layers. ICCSM gives rise to large-amplitude slow waves (2–4/min) in the submucosal plexus that causes contraction. When activated by Ach, NO and other neurotransmitters stimulation spreads through smooth muscles. Platelet-derived growth factor receptor alpha-positive cells (PDGFRα+-cells), previously known as “fibroblast-like cells” or “ICC-like” cells, has been identified lately in the colon [11]. PDGFRα+-cells together with ICCs and smooth muscle cells (SMC) form a network in the myenteric plexus and longitudinal and smooth muscle layers called the SIP syncytin that generates slow waves [12].

Colon physiology and motility Colon functions include storage, fermentation, absorption, secretion and motility. Colonic motility has a circadian rhythm. During night-time, rectosigmoid region is more active, colonic motility is inhibited and periodic rectal motor activity

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(PRMA), which is an intense retrograde activity, is activated ensuring continence (Table 1). When gas and stools come to the rectum, PRMA acts as a break mechanism [13]. Transverse and descending colon show more activity during waking hours and promote absorption, mixing, propulsion of contents, as well as formation and storage of stool. Waking are the major stimulants of colonic motility and fatty meals have stronger influence than carbohydrates meals [14]. Waking and meal induces threefold and twofold increase in colonic motor activity, also termed gastro-colonic response. Gastro-colonic motor response to meal is dual, i.e., with gastric and cerebral involvement [15]. Neurohormonal mechanisms, CNS and ENS are probably responsible for these responses [16]. During defecation, both propagating and non-propagating contractions increase along the whole colon. Bampton et al. showed there are two components of defecation [17]. Firstly, an unperceived component starts 60 min before defecation and a set of antegrade propagating contractions occur in the proximal colon and sites of origin then move distally carrying colonic contents into the distal colon. This stimulates distal colonic afferents and in turn leads to the second component that starts 15 min before defecation. This second component is characterized by antegrade propagating contractions originating in the distal colon with sites of origin moving more proximally. This is associated with sensation of urge and with at least one high-amplitude propagated contraction (HAPC) (described below) leading to voluntary phase of defecation that can be delayed. Normally rectal distention inhibits proximal colonic activity protecting rectum from further filling and possible stool leakage (termed colo-colonic reflex). Myogenic and ENS mechanisms located in the gut wall act together to ensure a well-coordinated colonic motility. External neural and hormonal factors also have effects on colonic motility. Any damage to spinal cord or extrinsic nerves can cause altered gut motility [18]. When activated by gut distension, mechanosensory enteric neurons located in the myenteric plexus with mechanosensitive nerve endings in circular muscle cause proximal contraction and anal relaxation. The “neuromechanical loop” hypothesis was proposed stating that shape, consistency and size of luminal content affect the speed of motility and that increased fluidity increases the speed of motility [19]. To verify this hypothesis, it has been shown experimentally that solid contents moved slower than fluid contents [20]. Neural-dependent colonic migrating motor complex (CMMC) is less dependent on the luminal content and can migrate in either direction and can occur simultaneously. In guinea pig it was shown that myenteric plexus is responsible for CMMCs and submucosa (including enterochromaffin cells (ECs)) is not needed for initiation or propagation of the stimulus [21]. Mechanical and electrical stimulation of the mucosa by the mucosal nerve endings of sensory neurons can modulate the motility. It is not known whether and how the byproducts of diet and microbiota modulate motility [18]. Interestingly, there are data to indicate that microbiota can either directly or indirectly modulate motility through the modulation of luminal short-chain fatty acids or bile salt metabolism as well as through fermented gases such as methane [22, 23]. Most probably, the neuromechanical loop and CMMCs are the major factors responsible for propulsion of motility. Myogenic motor activity also affects colonic motility. Colon has spontaneous oscillatory electrical activity generated by pacemaker ICCs. In most mammalian species studied, three types of activity have been described. Slow waves, faster oscillations (30min−1) called myenteric potential oscillations (MPOs) and slow phasic contractions (occurring at intervals of 1min or more). Slow waves, derived from circular muscle, move at short distances up and down and when they cross each other from opposite sites, they mix the luminal contents. MPOs are faster oscillations (30 min−1) generated by pacemaker cells located near the myenteric plexus and slow phasic contractions occur at intervals of 1 min or more. Although needed, myogenic activity is not enough if solely for propulsion of the colonic content [18]. Spatio-temporal mapping of colonic activity is made possible using colonic manometry with multiple sensors spaced closely apart (Fig. 3A and B). The increased spatial resolution of intraluminal colonic pressure sensing from high resolution manometry (HRM) provides even more accurate motility patterns and therefore better understanding of human colon motility [24]. Bassotti et al. had proposed two main types of colonic contractile patterns according to manometric findings. Firstly; non-propagating/segmental contractions and secondly; propagating contractions that can be divided into low-amplitude propagated contractions (LAPC) and high-amplitude propagated contractions (HAPC) (Fig. 3C) [25]. Characteristics of these normal contractions and their physiological responses to stimuli including food, awakening and pharmacological agents are given in Table 2. Non-propagating/segmental contractions cover most of the colonic motility and have amplitude that ranged from 5 to 50 mmHg, but infrequently they may have higher amplitudes. This may be single or grouped (bursts). Bursts are usually arrhythmic and rarely may be rhythmic (<6%/d). Rhythmic bursts mostly occur in distal colon segments with a frequency of 3cycle/min and move the luminal content distally helping to absorb water, short chain fatty acids and electrolytes [26]. LAPCs have amplitude <50 mmHg and daily frequency of 100 events/d. They may move antegrade (aboral) or retrograde (orad), retrograde being dominant. LAPCs mainly transport water to the distal colon, and usually occur after meal and upon awakening. They are also associated with passage of flatus [27]. PRMA is the “gatekeeping/braking mechanism” that arises at the rectosigmoid colon and mostly occurs at night. PRMA is not related to meals or to anal motor activity, lasts ≥3 min and occurs with a frequency of 3 waves/min [13]. During defecation, PRMAs are inhibited but emotions such as stress and anger can affect sigmoid activity [28].



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FIG. 3  (A) Colonic manometry assembly, (B) abdominal x-ray showing typical location of sensors after placement of manometer and (C) typical colonic manometric patterns in a normal healthy volunteer showing non-propagating contractions before meal and propagating high and low amplitude contractions after meals. (Modified from Lee YY, Erdogan A, Rao SS. How to perform and assess colonic manometry and barostat study in chronic constipation. J Neurogastroenterol Motil 2014;20:547–52.)

HAPCs, with an amplitude up to 200 mmHg and occur 6–20 times/day, were first described by Narducci et al. [29]. HAPCs mostly occur after awakening, late postprandial period [30], and especially after high caloric diet [31] and before an urge to defecate [17]. Some of the HAPCs do not propagate farther than mid-colon and <5% reach the rectum. This suggests a regulatory mechanism in the rectosigmoid region. HAPCs can carry colonic content for long distances before defecation occurs. Stimulation of HAPCs with awakening may suggest that central or peripheral “clock genes,” a group of genes that govern 24-h, circadian rhythms, might be involved. The clock genes play a role in the transcriptional regulation of two genes that are rhythmically expressed in the distal colon; i.e., vasoactive intestinal peptide (VIP) and neuronal nitric oxide synthase (nNOS), and were found to modulate colonic motility [32]. Whether there are diurnal variations for HAPCs and colonic motor activity is not known. HAPCs are absent in empty, prepared bowel [33] and are stimulated by meals suggesting that they need extrinsic autonomic stimulation and parasympathetic involvement [34]. Most HAPCs form at the caecum and ascending colon and propagate long distances than the ones that form more distally. These contractions have a velocity of 1–2 cm/s in the right colon and the speed increases as they move distally and may be followed with defecation [34]. HAPCs cause an early anal relaxation even before HAPCs arrive mainly left colon and even as proximal as the hepatic flexure. This may be a result of colo-anal reflex during mass movements of the colon. This was found to be different from rectoanal inhibitory reflex (RAIR), again suggesting a neurally-mediated intra-colonic descending inhibitory reflex [35, 36].

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TABLE 2  Characteristics of colonic motility and physiological significance Contractions

Normal findings

Phasic contractions High amplitude propagating contractions (HAPCs)

Amplitude >50–100 mmHg, 4–10/day, mostly after meal and awakening, propagate over 3 or more sites, duration ≥14 s, arise proximally, velocity 1.5 cm/s right and left side of colon, antegrade or retrograde

Low amplitude propagating contractions (LAPCs)

Amplitude <50 mmHg with mean of 20 mmHg, 60/day, more frequent after meal and upon awakening, actual physiology not clear, possible mixing

Periodic rectal motor activity (PRMA)

Retrograde, propagating or non-propagating, arise at rectosigmoid colon, more common at night, lasts ≥3 min, frequency 3 waves/min, possible brake

Physiological responses Gastro-colonic response to food

Twofold increase in contractions in the first 2 h vs. 1 h before food

Upon awakening

Threefold increase in contractions in the first hour vs 1-h pre-wake

Endoluminal instillation of bisacodyl (10–20 mg) and intravenous neostigmine (1.5 mg)

Activate myenteric plexus to produce propagating contractions in normal individuals

Response of colonic tone and compliance to food

Increase tone more in transverse colon than in sigmoid colon (mean 24% vs. 13% increase in 90 min)

 

HAPCs not only occur spontaneously and after colonic distension but also as a response to pharmacological agents [35, 36]. Neostigmine, bile acids (chenodeoxycholic acid) and bisacodyl when administered in physiological concentrations (10–20 mg) produce propagating contractions originating from the left colon indicating a neural activity [34, 37].

Anatomy and physiology of pelvic floor The major roles of pelvic floor muscles are to provide support for the viscera of the abdominopelvic cavity and support continence mechanisms of the anal, urethral and vaginal orifices, as well as assist defecation process (Table 1). The bony pelvis is constituted from pubis, ischium, ileum anteriorly and laterally, sacrum and coccyx posteriorly. Pelvis accommodates lower GI, urinary and internal reproduction organs. Pelvic brim divides the pelvis into two parts. The first part is the “false pelvis” located above the pelvic brim and second part is the “true pelvis,” located below the pelvic brim. True pelvis has an inlet, outlet and a cavity. Pelvic brim (inlet) is made up of sacral promontory, anterior ala of the sacrum, arcuate line of the ilium, pectineal line of the pubis and pubic crest that ends with symphysis pubis. It is tied to symphysis pubis anteriorly, ileopectineal line laterally and sacral promontory posteriorly. Pelvic outlet is tied to the pubic arch anteriorly, to the ischial tuberosities laterally and to the coccyx posteriorly. The pelvic cavity is a short-curved canal lied between pelvic brim above and pelvic diaphragm (inferior pelvic wall-pelvic floor) below. The pelvic cavity has a shallow anterior wall and a deep posterior wall. The pelvic diaphragm is a wide but thin strap that is composed of muscles, ligaments and endopelvic fascia that extends between lateral sidewalls and from symphysis pubis to the coccyx with connections to urethra, anal sphincters and vagina in women. Pelvic floor is a complex set of muscles and has superficial and deep muscle layers (Fig. 1). From top to bottom is the endopelvic fascia, levator plate of muscles (pelvic diaphragm), perineal membrane (urogenital diaphragm) and superficial layer of muscles. Bulbospongiosus, ischiocavernosus and superficial and deep transverse perineii are superficial layer of muscles. Deep layer of muscles of pelvic floor is made up of coccygeus and levator ani that is composed of puborectalis, pubococcygeus and iliococcygeus muscles. A study where nulliparas were evaluated by magnetic resonance imaging showed anatomic size and configuration variations of levator ani and endopelvic fascia [38]. The perineal body is positioned between vagina and anus providing support to the pelvic floor. Pelvic floor has innervations from central, somatic and visceral pathways. Innervation of levator ani is supplied from pudendal, inferior rectal, perineal, and S3 and S4 nerves (Table 1) [39]. The puborectalis originates from symphysis pubis and forms a U-shaped sling around the anorectal junction with no posterior attachment. With novel techniques it is now known that the puborectalis forms the deep muscle layer of external anal sphincter [4, 40]. The puborectalis is innervated



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by the pudendal nerve [41]. The pubococcygeous originates anteriorly from posterior pubic bone and arcus tendineus and inserts posteriorly into the anococcygeal raphe and coccyx. Pubococcygeous has direct innervations from S3–S5. The ileococcygeous originates from ischial spine and arcus tendineus, travels posteriorly to insert into anococcygeal raphe and coccyx. It is also the posterior part of levator ani. The ileococcygeous from both sides integrate and extend to the anorectal junction. The ileococcygeous is a flat thin layer and mostly aponeurotic. The ischiococcygeous (coccygeous) muscle was first believed to also a part of levator ani. The coccygeous originates from posterior surface of the ischial spine and attaches into the lower sacral bone and upper coccyx. It is innervated by the anterior rami of S3–S5, has a triangular shape and continues with sacrospinous ligament. Endopelvic fascia has visceral and parietal linings and supports the pelvic floor. Visceral endopelvic fascia is extraperitoneal and parietal endopelvic fascia covers the pelvic diaphragm with attachments to arcus tendineus levator ani and the arcus tendineus fascia pelvis.

Pelvic floor physiology Main functions of the pelvic floor are to support the pelvic organs, maintain continence and aid defecation (Table 1). These functions need intact and coordinated pelvic floor muscles that work with the nervous system in a synchronized fashion.

Supporting the pelvic organs With increase in abdominal pressure, the pelvic floor contracts and the coccyx moves ventrally toward the pubic bone lifting the pelvic visceral organs and changing the pelvic floor shape from a “basin” shape to a “dome” shape [42]. Pelvic floor supports and compresses the distal parts of urethra, vagina, and rectum pulling them toward pubic bones that they originate. Therefore, the levator ani muscle works as a sphincter for the vagina, urethral and anal canal. Weaknesses of pelvic muscles can cause perineal descent, and the amount of descent can be measured through magnetic resonance imaging (MRI) or defecography by determining the site of anorectal angle relative to the pubococcygeus line (Fig. 1). The pubococcygeus line is an imaginary line between the tip the coccyx and the lower edge of symphysis pubis [43]. Normally, anorectal angle and pubococcygeus line is located very closely. The puborectalis muscle is a major contributor of the anorectal angle. With perineal descent, the anorectal angle falls below this pubococcygeus line [44]. Rectocele, cystocele, rectal intussusception, and prolapse are the other possible disorders linked to pelvic floor dysfunction.

Physiology of anal continence Continence involves rectal sensation, rectal compliance, local reflexes, anal sphincter and pelvic floor function, colonic motility and stool consistency. Stool consistency and volume are also important factors of continence. When continence mechanisms are intact, person can be continent even with a liquid stool however may be incontinent when this mechanism is not intact. Structural elements play important roles in continence. Houston valves of the rectum as well as anal vascular cushions help to maintain continence. Vascular cushions contribute 10–20% of the resting pressure [45]. It is without doubts that IAS, EAS and levator ani muscles are the main contributors of anal continence. IAS is mainly a slow-twitch, fatigueresistant smooth muscle that generates mechanical activity with a frequency of 15–35 cycles/min and ultraslow waves at 1.5–3 cycles/min [46, 47]. IAS is responsible for 70–85% of the resting anal pressure. After rapid rectal distention, IAS contributes only 40% but 65% with steady rectal distension. Any damage to the IAS causes passive incontinence or fecal seepage. With the tonic activity of IAS, anal sphincter is closed at rest and EAS further maintains the closure with squeeze [47]. Underlying factors that cause EAS dysfunction may include damage to the muscle, myopathy, neuropathy or altered corticospinal function. The puborectalis forms a U-shaped sling around the rectum and forms an anorectal angle. At rest, the angle is 90° and during squeeze, the puborectalis pulls the rectum anteriorly to form an acute angle of 70° and further enhances continence. Obstetric trauma and episiotomy are the most common reasons of anal sphincter damage (20–35%) [48]. Hemorrhoidectomy, anal dilatation, fistulas, fissures and lateral sphincterotomy are the other underlying reasons. Anatomical defects of one or more of these muscles create a composite effect of damage known as “multi-hit hypothesis” [49]. Therefore, the severity of incontinence depends on the rate of damage to the muscles. Sensation or perception of the rectal content is also important for continence. Consequently, rectal hyposensitivity and increased rectal compliance contributes to fecal incontinence. Rectal hyposensitivity is found in approximately 10% of incontinent patients [50]. In patients with rectal hyposensitivity, stools enter the anal canal and leakage may occur before the EAS contracts [51]. Other mechanisms that rectal hyposensitivity may cause incontinence are through fecal impaction and pelvic floor dyssynergia [51–53]. Decreased sensation and increased compliance reduce the frequency of urge and

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d­ efecation, allowing stools to accumulate in the rectum. This may also diminish rectal sensation either by modifying afferent pathways or viscoelastic properties of the rectum [54]. Pudendal nerve, arising from S2–S4 sacral nerves, has both sensory and motor function and this dual action applies to lower third of the rectum and EAS [55]. Although perianal and genital skin sensation as well as the rectoanal contractile reflexes (RACR) are lost, and anal sphincter muscle is weakened after pudendal nerve blockage or damage, the rectal sensation is not affected [56]. It is likely that sensation of rectal distension is mediated through S2–S4 parasympathetic nerves independent of pudendal nerve [47]. Any interruption to the afferent pathway at any levels from rectum to cortex leads to impaired perception and rectal hyposensitivity. This nerve damage may be due to childbirth, chronic straining or pelvic surgery [57, 58]. Rectal compliance allows rectal content to be stored and defecation is deferred until social conditions are appropriate. Conditions such as inflammation, surgery, tumor infiltration and spinal cord injury may cause loss of compliance [59–61]. Rectal hyposensitivity with normal compliance may be due to afferent nerve dysfunction, however when increased compliance is present, then rectal wall problems are the most probable underlying mechanism [62]. Rectal hypersensitivity that may be associated with reduced rectal compliance may also contribute to fecal incontinence [63]. Autonomic neuropathy is another contributor to impaired continence. Pelvic nerves help to relax the rectum and accommodate gas and stool in rectum. Damage to the pelvic nerves cause impaired accommodation and rapid rectosigmoid transit and incontinence [47, 64]. Proximal to the pelvic and anal nerves there may be cauda equina nerve injury. In these patients the pudendal nerve terminal motor latency (PNTML) is normal but with prolonged nerve conduction [65]. Recto-anal reflexes are also important for continence. Recto-anal inhibitory reflex (RAIR), defined as loss of anal canal pressure during rectal balloon distension on anorectal manometry, is a transient relaxation of the proximal part of IAS that allow sampling and discrimination of rectal contents such as gas and stool, and passing of flatus [66]. This reflex helps to defer defecation if not socially desired by active contraction of lower part of IAS, EAS and puborectalis [67]. RAIR is mediated through myenteric plexus, pudendal nerve and its relaxation mediated mainly by nitric oxide (NO) [68]. Sampling was found to be altered and diminished in patients with fecal incontinence [54]. Recto-anal anal contractile response (RACR) is another reflex that is important for continence. RACR is a subconscious reflex mediated by the pelvic splanchnic and pudendal nerves and prevents unintended discharge of rectal contents like flatus by the contraction of EAS and puborectalis muscle [69]. More recently, the sensorimotor response (SMR) has been described, and this is a reproducible anal contraction in response to desire to defecate during rectal balloon distension [70]. Unlike RAIR and RACR which are independent from rectal sensation, SMR is associated with conscious rectal sensation. Constipated patients with rectal hyposensitivity were found to induce abnormal SMR, suggesting that disruption of gut–brain pathway may be a pathogenesis of rectal hyposensitivity [71] (Fig. 4). Other than RAIR and RACR, there may be a reflex increase in anal sphincter pressure after unexpected increase in intra-abdominal pressure due to coughing and laughing [72]. This may be mediated by

FIG. 4  (A) Recto-anal reflexes including recto-anal inhibitory reflex (RAIR), recto-anal contractile reflex (RACR) and sensorimotor response (SMR) in response to rectal balloon distension. SMR, not RAIR or RACR, occurs in association with rectal sensation. (B) Types of abnormal SMRs in patients with constipation and rectal hyposensitivity. (Modified from De Ocampo S, Remes-Troche JM, Miller MJ, Rao SS. Rectoanal sensorimotor response in humans during rectal distension. Dis Colon Rectum 2007;50:1639–46; Remes-Troche JM, De-Ocampo S, Valestin J, Rao SS. Rectoanal reflexes and sensorimotor response in rectal hyposensitivity. Dis Colon Rectum 2010;53:1047–54.)

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complex mechanisms including reflex contraction of the puborectalis [73]. As a summary, fecal incontinence is a complex disorder that incorporates multiple underlying mechanisms.

Physiology of defecation Defecation needs a coordinated complex interaction between nerves, muscles and CNS. Defecation involves increase in intraabdominal and rectal pressure with contraction of abdominal muscles and diaphragm together with a coordinated relaxation of the pelvic floor and anal sphincter muscles (Fig. 5). During defecation, pelvic floor relaxation causes pelvic floor descent and anorectal angle to fall below the pubococcygeal line and anorectal angle becomes obtuse. This makes the pelvic floor hiatus wider allowing discharge of stool. When this coordination is impaired such as in patients with functional defecation disorders (dyssynergic defecation), it results in chronic constipation [74]. In this concept, either there is defect in creating adequate rectal pressure or the patient is not able to completely relax anal sphincter or both. This condition is generally acquired. Rectal hyposensitivity is a result of either through afferent nerve pathway dysfunction or due to rectal wall dysfunction, subsequently leading to inadequate rectal wall contraction and a diminished urge to defecate causing fecal accumulation and impaction [50]. Colonic motility may also be delayed in one third of patients with rectal hyposensitivity either due to accumulation of stool or directly due to colonic dysmotility [75].

Conclusions Luminal contents from the small bowel are eventually removed from the body through coordinated actions of propulsion, storage and defecation by the colon and pelvic floor. Coordination requires intact gut–brain interactions mediated largely by neural and myogenic mechanisms within the bowels. Colonic motility is affected by luminal-dependent neuromechanical loop and neural-dependent colonic motor-migrating complex. Colonic contractions can be propagating (high-amplitude and low-amplitude) and non-propagating whereas periodic rectal motor activity provides the braking or gate-keeping mechanism. Pelvic floor supports the bowels and is required for the act of continence. Both anal sphincters and levator ani are the main effectors of continence. However, for a coordinated defecatory process, an intact recto-anal reflexes and sensing of rectal contents are also needed.

PR

IAS EAS

Normal defecation

Normal stool perception Normal rectal compliance Relaxation of EAS and PR

Fecal incontinence

Altered stool perception Reduced rectal compliance Low EAS and IAS pressure Weak PR Neuropathy

Dyssynergic defecation

Rectal hyposensitivity Abnormal rectal compliance Paradoxical anal contraction Poor rectal propulsive force

FIG. 5  An illustration of normal defecatory process and the pathophysiological changes that underlie two common conditions that affect defecation, i.e., fecal incontinence and dyssynergic defecation. (Modified from Lee YY. What's new in the toolbox for constipation and fecal incontinence? Front Med (Lausanne) 2014;1:5.)

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Acknowledgment The following grants have supported author, Yeong Yeh Lee, in his clinical studies related to current chapter: Fundamental Research Grant Scheme (FRGS) of Ministry of Higher Education of Malaysia (Reference: 203.PPSP.6171192) and Research University Individual (RUI) grant of Universiti Sains Malaysia (Reference: 1001/PPSP/812151).

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Further reading [76] Drake RL, Vogl AW, Mitchell AWM. Gray's atlas of anatomy. Elsevier; 2008. [77] Chang J, Chung SS. An analysis of factors associated with increased perineal descent in women. J Korean Soc Coloproctol 2012;28(4):195–200.