Figure 64-1. Layers of the colonic wall.
The transverse colon stretches from the hepatic flexure to the splenic flexure and is the longest segment of colon (between 30 cm and 60 cm). The transverse colon is suspended by the transverse mesocolon and is completely intraperitoneal. It is the most mobile portion of the colon and may descend to the level of the iliac crests or deep into the pelvis. The greater omentum descends from the greater curve of the stomach in front of the transverse colon and then ascends to attach to the transverse colon on its anterosuperior edge. To mobilize the transverse colon or enter the lesser sac, the fusion plane of the omentum to the transverse colon must be dissected. The splenic flexure is situated high in the left upper quadrant, more cephalad than the hepatic flexure, and lies anterior to the mid-left kidney and abuts the lower pole of the spleen. There are attachments from the colon to the diaphragm at the level of the 10th and 11th ribs and spleen (phrenocolic and splenocolic ligaments), and these must be carefully divided during mobilization of the splenic flexure to avoid splenic injury.
The descending colon is approximately 25 cm long and courses from the splenic flexure to its junction with the sigmoid colon at the pelvic brim. It lies anterior to the left kidney and, like the right colon, the anterior, lateral, and medial portions of the descending colon are covered by peritoneum.
The sigmoid colon extends from the pelvic brim to the sacral promontory, where it continues as the rectum and generally measures 15 to 50 cm in length. It is completely invested by peritoneum. The rectosigmoid junction is marked by the convergence of the colonic taenia. The sigmoid colon is extremely mobile and has a generous mesentery that extends along the pelvic brim from the iliac fossa across the sacroiliac joint to the second or third sacral segment. Because of its mobile mesentery, the sigmoid colon can twist and cause an obstruction, termed sigmoid volvulus. The left ureter runs in the intersigmoid fossa, which is at the base of the mesosigmoid. When a high ligation of the inferior mesenteric artery is performed during a cancer operation or the sigmoid colon is being mobilized along the white line of Toldt, the left ureter should be identified to avoid inadvertent injury. Preoperative placement of urinary stents can be useful for locating the ureter intraoperatively in complex, reoperative pelvic surgery.
muscle, where the three teniae splay. The rectum measures 12 to 15 cm in length. It proceeds posterior and caudal along the curvature of the sacrum and coccyx, passing through the levator ani muscles, at which point it turns abruptly caudal and posteriorly at the anorectal ring, becoming the anal canal. Anterior to the rectum are the uterine cervix and posterior vaginal wall in women, and the bladder and prostate in men. Posteriorly, the rectum occupies the sacral concavity where the median sacral vessels, presacral veins, and sacral nerves run, all of which are invested in the presacral fascia. The rectum is marked by three curves. The upper and lower curves are convex and to the right, while the middle is convex and to the left. Within the lumen, these correspond to the valves of Houston, which separate the lower third, middle third, and upper third of the rectum – important landmarks when the location of a rectal abnormality is established endoscopically (the lower rectal valve is at 7 to 8 cm from the anal verge, middle rectal valve at 9 to 11 cm, and upper rectal valve at 12 to 13 cm).4 The valves do not contain all layers of the bowel wall and thus biopsy at this location carries minimal risk of perforation. The middle valve of Houston is the internal landmark corresponding to the anterior peritoneal reflection. The anterior and lateral surfaces of the upper third of the rectum are intraperitoneal, whereas only the anterior surface of the middle third of the rectum is intraperitoneal in location. The lower third of the rectum is entirely extraperitoneal. The mesorectum is the term used to describe the areolar tissue surrounding the rectum that contains nerves, lymphatics, and terminal branches of the superior hemorrhoidal branch of the inferior mesenteric artery. Although it invests the rectum circumferentially, the mesorectum is most prominent posterior to the rectum. It is invested by the fascia propria of the rectum, a continuation of the parietal endopelvic fascia (Fig. 64-3). The fascia propria (investing fascia) includes the distal two-thirds of the posterior rectum and the distal one-third of the anterior rectum, where it is no longer intraperitoneal. A total mesorectal excision entails removal of the entire rectum without violating the fascia propria of the rectum. This is accomplished by mobilizing the rectum using the plane between the fascia propria of the rectum and the presacral fascia. Anterior to the investing fascia (fascia propria) is a delicate layer of connective tissue known as Denonvilliers fascia, which separates the rectum from its anterior structures. Waldeyer fascia (rectosacral fascia) is the presacral fascia that is an extension of the parietal pelvic fascia from the periosteum of sacral segment four to the posterior wall of the rectum. It contains branches of the sacral splanchnic nerves. Below Waldeyer fascia is the supralevator or retrorectal space.At the sacral promontory, the colon becomes the rectum. The outer layer of the rectal wall is composed of the longitudinal
Figure 64-2. General anatomic components of the colon.
Figure 64-3. Fascial relationships of the pelvis.
The surgical anal canal begins at the anorectal ring or levator ani muscles and extends to the anal verge. It measures 2 to 4 cm and is usually longer in men than in women. The internal anal sphincter (continuation of the circular smooth muscle of the rectum) and the external anal sphincter (continuation of the puborectalis muscle) encircle the anal canal and control fecal continence. The internal anal sphincter relies on autonomic innervation, while the external anal sphincter uses somatic innervation. The median length and thickness of the female anterior external sphincter is 11 and 13 mm and thus a small tear sustained during vaginal delivery may cause fecal incontinence.5 There are three layers of the external sphincter – subcutaneous (traversed by the conjoined longitudinal muscle with some fiber attachments to the skin), superficial (connective tissue attaches posteriorly, forming the anococcygeal ligament), and deep (continues with the puborectalis muscle). Between the internal and external anal sphincters, the longitudinal muscle of the rectum joins fibers of the levator ani and puborectalis muscles to form the conjoined longitudinal muscle. The dentate line marks the transition between the columnar epithelium of the intestine and the squamous epithelium of the anal canal. The transition between these two epithelia is called the anal transitional zone. The Columns of Morgagni are the 6 to 14 longitudinal folds located at the dentate line. Small pockets between these columns called anal crypts contain anal glands, which may become obstructed with foreign material to cause an infection. Below the dentate line is the anoderm, which extends to the anal verge and does not contain accessory skin structures, such as hair, sebaceous and sweat glands. The autonomic nervous system innervates proximal to the dentate line and the somatic nervous system supplies the anoderm and distally.
The perineal body is the tendinous insertion of the external anal sphincter, bulbocavernosus, and superficial and deep transverse perineal muscles. It supports the perineum and separates the vagina from the anus.
Three striated muscles that attach to the pubic bone make up the pelvic floor or levator ani muscles: iliococcygeus, pubococcygeus, and puborectalis. The pelvic floor muscles are supplied by branches from the third sacral nerve, while the external anal sphincter is supplied by nerve fibers traveling with the pudendal nerve on the levators undersurface.
The puborectalis originates from the back of the symphysis pubis and forms a U-shaped sling as it joins the opposite muscle posteriorly. The iliococygeus muscle arises from the ischial spine and posterior part of the obturator fascia and travels inferiorly, posteriorly, and medially to insert into the last two segments for the sacrum and coccyx. The pubococcygeus muscle arises from the anterior half of the obturator fascia and the posterior pubis. Its fibers are directed backward, downward, and medially, where they decussate with fibers of the opposite side. The decussation is called the anococcygeal raphe.
The perianal space surrounds the anal canal superficially and contains the external hemorrhoidal plexus. The ischioanal space extends laterally and goes superiorly to the levator ani from the skin on the perineum. The levator ani and external sphincter muscles form the medial boundary, while the lateral wall is formed by the obturator fascia. The superficial postanal space connects the perianal spaces with each other posteriorly below the anococcygeal ligament, while the deep postanal space lies above the anococcygeal ligament. The ischioanal and perianal spaces make the ischioanal fossa. The deep postanal and ischiorectal spaces form a horseshoe configuration that may be involved in a horseshoe abscess. Below the perianal space between the sphincter muscles is the intersphincteric space. The submucosal space contains the internal hemorrhoidal plexus and lies between the internal anal sphincter and the mucosa distal to the dentate line. Proximally, it becomes the submucosa of the rectum. Above the levator complex is the supralevator space, which extends superiorly to the peritoneum at the rectosacral fascia. The retrorectal space extends above the rectosacral fascia and lies between the upper two-thirds of the rectum and sacrum.
Arterial Blood Supply
Fig. 64-4). In addition to supplying the small bowel through jejunal and ileal branches, the superior mesenteric artery gives rise to the ileocolic, right colic, and middle colic branches that supply the cecum, ascending colon, and proximal transverse colon. The right colic arterial anatomy is particularly variable and can be absent or arise from the ileocolic or the superior mesenteric artery. The middle colic artery has a right branch that supplies the hepatic flexure and the right portion of the transverse colon, while the left branch supplies the left portion of the transverse colon. The inferior mesenteric artery arises from the anterior surface of the aorta, typically 3 to 4 cm above the aortic bifurcation, and supplies the distal transverse colon, descending colon, sigmoid colon, and upper rectum. The inferior mesenteric artery gives rise to the left colic artery and sigmoidal branches, then continues in the sigmoid mesentery, and after crossing the left iliac vessels, is renamed the superior rectal/hemorrhoidal artery. The inferior mesenteric artery may also function as an important collateral vessel to the lower extremities during instances of distal aortic occlusion. The superior hemorrhoidal artery descends behind the rectum and splits into right and left branches in the mesorectum. It is the main blood supply of the rectum. The middle and inferior rectal/hemorrhoidal arteries arise from either the internal pudendal arteries or the hypogastric arteries and supply the distal two-thirds of the rectum. The presence of the middle rectal artery, in particular, can be variable. A series of arterial arcades along the mesenteric border of the entire colon, known as the marginal artery of Drummond, connect the superior mesenteric and inferior mesenteric arterial systems. The marginal artery may be attenuated or absent at the distal transverse colon/splenic flexure, the delineation between the midgut and hindgut, and thus ischemic colitis most commonly affects this region. The arc of Riolan (“meandering mesenteric artery”) is a short loop connecting the left branch of the middle colic artery and the trunk of the inferior mesenteric artery. The inferior rectal/hemorrhoidal arteries traverse the ischioanal fossa and supply the anal canal and external anal sphincter muscles.The arterial blood supply to the colon, rectum, and anus is highly variable. The following summarizes the general courses of the arterial blood supply. The superior mesenteric artery arises from the aorta, runs posterior to the pancreas, and passes anterior to the third portion of the duodenum (
Figure 64-5. Venous drainage of the colon by the portal vein.
The veins that drain the large intestine bear the same terminology and follow a course similar to that of their corresponding arteries (Fig. 64-5). The veins from the right colon and transverse colon, along with the veins draining the small intestine, drain into the superior mesenteric vein. The superior mesenteric vein runs slightly anterior to and to the right of the superior mesenteric artery. The superior mesenteric vein courses beneath the neck of the pancreas, where it joins with the splenic vein to form the portal vein. The inferior mesenteric vein is a continuation of the superior rectal vein and drains blood from the left colon, sigmoid colon, rectum, and superior anal canal. The inferior mesenteric vein follows a course of its own, starting at the left colic artery, and ascends over the psoas muscle in a retroperitoneal plane. The vein courses under the body of the pancreas to drain into the splenic vein. During an anterior resection of the rectum, division of the inferior mesenteric vein at the inferior border of the pancreas can provide additional mobility of the left colon to facilitate a coloanal anastomosis. The superior hemorrhoidal (rectal) veins drain blood from the rectum and upper part of the anal canal, where the internal hemorrhoidal plexus is situated, into the portal system via the inferior mesenteric vein. The middle hemorrhoidal (rectal) veins drain the lower part of the rectum and upper part of the anal canal into the systemic circulation via the internal iliac veins. The inferior hemorrhoidal (rectal) veins drain blood from the lower rectum and anal canal, where the external hemorrhoidal plexus is located, via the internal pudendal veins into the systemic venous circulation via the internal iliac veins. In the setting of portal hypertension, the superior, middle, and inferior hemorrhoidal veins interact to shunt venous blood from the portal system into the systemic circulation.
Lymphatic drainage generally follows the arterial blood supply of the colon and rectum. In the anal canal, lesions above the dentate line drain into the inferior mesenteric lymph nodes. Lesions below the dentate line drain into the internal iliac lymph nodes but can also drain into the inferior mesenteric lymph nodes.
The colon possesses extrinsic and intrinsic (enteric) neuronal systems. The extrinsic system consists of sympathetic and parasympathetic nerves that inhibit or stimulate colonic peristalsis, respectively. The sympathetic innervation to the right colon originates from the lower thoracic segments of the spinal cord and travels in the thoracic splanchnic nerves to the celiac and superior mesenteric plexuses. Postganglionic fibers emerge from here and course along the superior mesenteric artery and its branches to the right side of the colon. The parasympathetic nerves originate from the right vagus nerve and travel along with the sympathetic nerves to the right side of the colon. The left side of the colon and the rectum receive sympathetic fibers that arise from L1 through L3 segments of the spinal cord. This passes through the ganglionated sympathetic chains and leaves as a lumbar sympathetic nerve to join the preaortic plexus. It extends along the inferior mesenteric artery as the mesenteric plexus and then becomes the presacral nerve or superior hypogastric plexus. These hypogastric nerves are identified at the sacral promontory 1 cm lateral to the midline. The key zones of sympathetic nerve damage are during ligation of the inferior mesenteric artery and during initial posterior rectal mobilization adjacent to the hypogastric nerves. The parasympathetic supply to the left side of the colon and the rectum comes from S2 through S4 spinal cord segments. The sacral nerve fibers become the nervi erigentes, which join the pelvic plexus at the pelvic side walls. To prevent injury during full mobilization of the rectum, the lateral ligament should be cut close to the rectal side wall. Both the sympathetic and parasympathetic nervous systems play a role in erection, in that damage to the parasympathetics can lead to erectile dysfunction, while retrograde ejaculation can occur with damage to sympathetic nerve injury.
The intrinsic, or enteric, nervous system consists of two groups of plexuses that are identified by their location within the colon wall. This system can function independently of the central nervous system and controls motility and exocrine and endocrine functions of the gut, and is involved in intestinal immune regulation and inflammatory responses. The Meissner plexus is located in the submucosa between the muscularis mucosae and the circular muscle of the muscularis propria and is important in secretory control. The myenteric plexus, also known as the Auerbach plexus, is located between the inner circular muscle and outer longitudinal muscle layers of the colon and primarily controls intestinal motility.4
The internal anal sphincter is supplied by the sympathetic and parasympathetic nerves that supply the lower rectum. The parasympathetic nerves are inhibitory. The external sphincter is supplied by the inferior rectal branch of the internal pudendal nerve and the perineal branch of S4. Sensation of the anal canal is from the inferior rectal nerve, a branch of the pudendal nerve.
The colon’s function is to absorb, store, digest carbohydrate and protein residues, and secrete mucus.
The colon absorbs water, sodium, and chloride and secretes potassium and bicarbonate. The physiologic control of colonic water and electrolyte transport requires careful integration of neural, endocrine, and paracrine components. Although colonic epithelium does not actively absorb glucose or amino acids as the small-intestinal epithelium does, the colon does absorb short-chain fatty acids and vitamins that are produced by bacterial breakdown of nonabsorbed carbohydrates and amino acids. These short-chain fatty acids, which include acetate, butyrate, and propionate, are absorbed in a concentration-dependent fashion. They are a major (70% of colonic mucosal energy) energy substrate for colonic epithelial cells and represent the major fecal anions.6
Approximately 1,500 mL of ileal effluent reaches the cecum in a 24-hour period, 90% of which is reabsorbed in the colon; 100 to 150 mL of water remains in stool. The colon has a tremendous capacity that allows it to absorb as much as 5 to 6 L of water within a 24-hour period. When colonic capacity is exceeded, diarrhea results.7 Normally formed feces consist of 70% water and 30% solid material. Almost half of the solid material is made up of bacteria and the other half is composed of undigested food material and desquamated epithelium. Water absorption in the colon is a passive process that depends primarily on the osmotic gradient established by the active transport of sodium across the colonic epithelium. The composition of ileal effluent and luminal flow rates also play an important role in water absorption. Upsetting the balance of these three factors results in diarrhea. The absorptive capacity is not the same throughout each segment of the colon. Salt and water absorption is greatest in the right colon. Patients undergoing a right hemicolectomy should therefore be counseled preoperatively that they may experience loose bowel movements in the early postoperative period. Patients should also be reassured that this will resolve with time as the remaining colon adapts.
Sodium absorption by the colonic epithelium is an active cellular transport process similar to that seen in small-intestinal and renal epithelial cells.8 Initially, sodium absorption involves the passive movement of sodium across the apical membrane into the mucosal cell down an electrochemical gradient. To maintain an adequate electrochemical gradient, intracellular sodium is removed from the cell into the interstitial space in exchange for potassium at the basolateral membrane. This is an energy-dependent process that is controlled by Na+-K+-adenosine triphosphatase (ATPase). Mineralocorticoids (predominantly aldosterone) and glucocorticoids accelerate sodium absorption and potassium excretion in the colon by increasing Na+-K+-ATPase activity.9 Potassium movement into the colonic lumen is primarily a passive process that depends on the electrochemical gradient generated by the active transport of sodium across colonic epithelial cells. Chloride absorption in the colon is generally thought to be an energy-independent process that is associated with reciprocal exchange for bicarbonate at the luminal border of the mucosal cell.10 Patients with a ureterosigmoidoscopy may develop hyperchloremia and secrete excessive amounts of bicarbonate.
Twenty percent of urea synthesized by the liver is metabolized mainly in the colon. This is converted into 200 to 300 mL of ammonia each day, of which most is absorbed by passive coupled diffusion with bicarbonate and forms ammonia and carbon dioxide. Ammonia is also derived from dietary nitrogen, epithelial cells, and bacterial debris. Mucus is produced by goblet cells and secreted into the lumen via stimulation of the pelvic nerves.
13 commensal bacteria.10 The vast majority of the normal colonic flora consists of anaerobic bacteria, with Bacteroides species being most prevalent, particularly B. fragilis.11 Aerobic colonic bacteria are mainly coliforms and enterococci, with Escherichia coli being the most predominant coliform. The colonic flora is important for (a) digestion and absorption of complex macromolecules, (b) protecting the colon against invasion by noncommensal bacteria, and (c) development of mucosal immunity. Fermentation of carbohydrates generates short-chain fatty acids, including acetic acid, propionic acid, and butyrate, which is the primary nutrient for the colonic mucosa. Colonic bacteria also produce certain vitamins, such as vitamin K and B12, which are absorbed by the host. The enterohepatic circulation of bilirubin and bile acids depends on bacterial enzymes produced by fecal flora. The degradation of bile pigments by colonic bacteria gives stool its characteristic brown color. Colonic bacteria also play an important role in preventing infection by controlling the growth of potentially pathogenic bacteria such as Clostridium difficile.The bacterial flora of the colon is established soon after birth and depends in large part on dietary and environmental factors. The colon is populated by approximately 10
12 Changes in diet and use of antibiotics can dramatically alter the microbiome. Dysregulation of the flora has been implicated in the pathogenesis of inflammatory bowel disease, obesity and, to a lesser extent, colorectal cancer. Increasingly, dysregulation has also been linked to nongastrointestinal diseases including autism and other neurologic conditions. In animal studies, mice with certain immune deficiencies that make them prone to colitis fail to develop colitis when raised under germ-free conditions. Analysis of the microbiota of patients with inflammatory bowel disease revealed markedly different flora compositions in ulcerative colitis, Crohn disease, and healthy control patients. Similarly, certain genetically altered mice with a propensity to develop colorectal cancer fail to develop tumors in germ-free conditions. Although studies of human flora and colorectal cancer are limited, preliminary studies have raised interest in modulating the colonic flora as a way to treat and/or prevent colitis and other diseases of the colon.Host and colonic flora have a mutualistic relationship; however, disturbances of this coexistence can lead to human disease.
Motor activity varies greatly throughout the colon. There are two patterns of colonic motility: segmental contractions, which are single or clustered contractions, and propagated activity, which is either high-amplitude (>100 mm Hg) propagated contractions (HAPCs) or low-amplitude (<60 mm Hg) propagated contractions (LAPCs). Segmental contractions are intermittent contractions of the longitudinal and circular muscles that result in the segmented appearance of the colon.13 These contractions propel luminal contents in a back-and-forth pattern over short distances, slowing aboral transit and allowing for water reabsorption.14 Propagated activity consists of strong, propulsive contractions of the smooth muscle that involve a long segment of colon.15 The LAPCs move luminal contents forward at a rate of 0.5 to 1.0 cm/s and typically last for 20 to 30 seconds.13 HAPCs occur three to four times per day, primarily after awakening, exercise, and after meals.
The orderly progression of colonic luminal contents from cecum to anus requires the coordination of smooth muscle contractions. Calcium-dependent cyclic depolarization and repolarization of the colonic smooth muscle cell membrane generates a basic electrical pattern of slow-wave activity. This activity allows each smooth muscle cell to control its own contraction and to couple with adjacent smooth muscle cells.16 The extrinsic (autonomic) and intrinsic (enteric) neuronal systems also interact to influence colonic motility.
As the fecal mass enters the rectum, the internal anal sphincter relaxes, while the external anal sphincter contracts to maintain continence. Distention of the rectum in this setting is the primary stimulus for defecation to begin. At this point, the urge to defecate may be suppressed by conscious contraction of the external anal sphincter. Receptive relaxation of the rectal ampulla accommodates the fecal mass and the urge to defecate passes unless the volume of feces is extremely large or the sphincter mechanism is impaired. If the subject voluntarily accedes to the urge to defecate, a Valsalva maneuver occurs, which increases the intra-abdominal pressure to overcome the resistance of the external anal sphincter. Relaxation of the pelvic muscles causes the pelvic floor to descend and the anorectal angle to straighten. Conscious inhibition of the external anal sphincter then allows passage of the feces. On completion, the pelvic floor returns to its resting position and the anal sphincter muscles return to their resting activity, closing the anal canal. Under normal circumstances, this process occurs once every 24 hours; however, the interval between bowel movements may vary between 8 and 12 hours and 2 to 3 days in normal subjects.
The frequency of defecation is influenced by multiple environmental and dietary factors. The gastrorectal reflex occurs as postprandial defecation. An increase in rectal tone results in increased pressure from the fecal mass on the rectal wall, providing heightened sensation.
There are varying degrees of anal continence, with a spectrum from complete control to complete lack of control. Maintaining continence is complex, as both voluntary and involuntary mechanisms play a role in anal continence. The most important mechanisms involve the internal anal sphincter, which contributes 52% to 85% of the pressure generated to maintain continence.17,18 The rest of the contribution to the anal basal pressure includes the following: 30% from the external anal sphincter and 15% from the hemorrhoidal cushions. The internal sphincter is supplied by dual extrinsic innervation: sympathetic outflow (S5) via the hypogastric nerve provides motor supply and inhibition by parasympathetic outflow (S1–S3). The external sphincter nerve supply is dependent on the pudendal nerve (S2–S4) and maintains tonic activity at rest. When stool enters the rectum, the contents of the rectum are sampled by sensors in the anal canal to determine whether the contents are solid, liquid, or gas. By discriminating between the consistency of the stool, the pelvic floor and sphincter muscles are able to coordinate a complex mechanism through angulation of the pelvic floor and contraction of the anal sphincter muscles. Other mechanisms contributing to continence include stool consistency and volume. Modification of the stool consistency to more solid and less voluminous stool may allow a patient to recapture fecal control. Reservoir function of the rectum consists of lateral angulations of the sigmoid colon and the valves of Houston as a mechanical barrier to slow the progression of stool.
DISORDERS OF COLONIC MOTILITY AND ANAL CONTINENCE
19 Colorectal surgeons, gastroenterologists, gynecologists, and family medicine physicians are frequently called upon to treat constipation.20 To evaluate constipation, the clinician must ask focused questions about bowel function. Constipation can mean infrequent bowel movements, straining, or hard stools. The Rome criteria were developed to help standardize the diagnosis (Table 64-1). Constipation can be caused by lifestyle choices, side effects of medications taken for other reasons, medical conditions (such as hypothyroidism), structural abnormalities of the colon, pelvic floor dysfunction, and colonic inertia (Table 64-2). Evaluation of the constipated patients includes a thorough history, a physical examination including a rectal examination, and evaluation for sources of pelvic floor dysfunction such as rectocele. Colonoscopy may be necessary to eliminate a structural bowel obstruction as the cause of constipation.Constipation is common and may affect up to 15% of people, but only a portion of affected individuals seek medical help.
Table 64-1 Rome III Criteria for the Diagnosis of Constipation