Chapter 52 Colon and Rectum
No comprehensive discussion of colorectal anatomy is complete without a thorough understanding of the genesis of the gastrointestinal (GI) tract. Knowledge of the developmental anatomy of the foregut, midgut, and hindgut establishes a context in which to consider mature structural and functional anatomic relationships.
The endodermal roof of the yolk sac gives rise to the primitive gut tube. At the beginning of the third week of development, the gut tube is divided into three regions—the midgut, which opens ventrally, positioned between the foregut in the head fold and the hindgut in the tail fold. Development progresses through the stages of physiologic herniation, return to the abdomen, and fixation. The acquisition of length and formation of dedicated blood and lymphatic supplies takes place during this time (Fig. 52-1).
FIGURE 52-1 A, At the third week of development, the primitive tube can be divided into three regions—the foregut in the head fold, the hindgut with its ventral allantoic outgrowth in the smaller tail fold, and the midgut between these two portions. Stages of development of the midgut are physiologic herniation (B), return to the abdomen (C), and fixation (D). At the sixth week, the urogenital septum migrates caudally (E) and separates the intestinal and urogenital tracts (F, G).
(From Corman ML [ed]: Colon and rectal surgery, ed 4, Philadelphia,1998, Lippincott-Raven, p 2.)
Foregut-derived structures end at the second portion of the duodenum and rely on the celiac artery for blood supply. The midgut, extending from the duodenal ampulla to the distal transverse colon, is based on the superior mesenteric artery (SMA). The distal third of the transverse colon, descending colon, and rectum evolve from the hindgut fold and are supplied by the inferior mesenteric artery (IMA). Venous and lymphatic channels mirror their arterial counterparts and follow the same embryologic divisions. At the dentate line, endoderm-derived tissues fuse with the ectoderm-derived proctodeum, or ingrowth from the anal pit.
Distal rectal development is complex. The cloaca is a specialized area of the primitive distal rectum composed of endoderm- and ectoderm-derived tissues. This area is incorporated into the anal transition zone, which surrounds the dentate line in the adult. The cloaca exists in a continuum with the hindgut but, at approximately the sixth week, it begins to divide and differentiate into anterior urogenital and posterior anal and sphincter elements. Simultaneously, the urogenital and GI tracts are separated by caudal migration of the urogenital septum. During the 10th week of development, the external anal sphincter is formed from the posterior cloaca as the descent of the urogenital septum becomes complete. The internal anal sphincter is formed by the 12th week from enlarged circular muscle layers of the rectum.
The colon and rectum constitute a tube of variable diameter approximately 150 cm in length. The terminal ileum empties into the cecum through a thickened, nipple-shaped invagination, the ileocecal valve. The cecum is a capacious saclike segment of the proximal colon, with an average diameter of 7.5 cm and length of 10 cm. Although it is distensible, acute dilation of the cecum to a diameter more than 12 cm, which can be measured by a plain abdominal radiograph, can result in ischemic necrosis and perforation of the bowel wall. Surgical intervention may be required when this degree of cecal distention is caused by obstruction or pseudo-obstruction (Fig. 52-2).
FIGURE 52-2 Anatomy of the colon and rectum, coronal view. The diameter of the right colon is larger than the diameter of the left side. Note the higher location of the splenic flexure compared with the hepatic flexure and the extraperitoneal location of the rectum.
The appendix extends from the cecum approximately 3 cm below the ileocecal valve as a blind-ending elongated tube, 8 to 10 cm in length. The proximal appendix is fairly constant in location, whereas the end can be located in a wide variety of positions relative to the cecum and terminal ileum. Most commonly, it is retrocecal (65%), followed by pelvic (31%), subcecal (2.3%), preileal (1.0%), and retroileal (0.4%). Clinically, the appendix is found at the convergence of the taeniae coli. Another clinical aid useful for detecting the location of the appendix through a small abdominal incision is the identification of the fold of Treves, the only antimesenteric epiploic appendage normally found on the small intestine, marking the junction of the ileum and cecum.
The ascending colon, approximately 15 cm in length, runs upward toward the liver on the right side; like the descending colon, the posterior surface is fixed against the retroperitoneum, whereas the lateral and anterior surfaces are true intraperitoneal structures. The white line of Toldt represents the fusion of the mesentery with the posterior peritoneum. This subtle peritoneal landmark serves as a guide for the surgeon for mobilizing the colon and mesentery from the retroperitoneum.
The transverse colon is approximately 45 cm in length. Hanging between fixed positions at the hepatic and splenic flexures, it is completely invested in visceral peritoneum. The nephrocolic ligament secures the hepatic flexure and directly overlies the right kidney, duodenum, and porta hepatis. The phrenocolic ligament lies ventral to the spleen and fixes the splenic flexure in the left upper quadrant. The angle of the splenic flexure is higher, more acute, and more deeply situated than that of the hepatic flexure. The splenic flexure is typically approached by dissecting the descending colon along the line of Toldt from below and then entering the lesser sac by reflecting the omentum from the transverse colon. This maneuver allows mobilization of the flexure to be achieved, with minimal traction required for exposure. Attached to the superior aspect of the transverse colon is the greater omentum, a fused double layer of visceral and parietal peritoneum (four total layers) that contains variable amounts of stored fat. Clinically, it is useful in preventing adhesions between surgical abdominal wounds and underlying bowel and is often used to cover intraperitoneal contents as incisions are closed. The omentum can be mobilized and placed between the rectum and vagina after repair of a high rectovaginal fistula, or used to fill the pelvic and perineal space left after excision of the rectum. The living tissue of the greater omentum makes a good patch in difficult situations, such as treatment of a perforated duodenum, when closure of inflamed and friable tissues is impossible or ill-advised.
The descending colon lies ventral to the left kidney and extends downward from the splenic flexure for approximately 25 cm. It is smaller in diameter than the ascending colon. At the level of the pelvic brim, there is a transition between the relatively thin-walled, fixed, descending colon and the thicker, mobile sigmoid colon. The sigmoid colon varies in length from 15 to 50 cm (average, 38 cm) and is very mobile. It is a small-diameter, muscular tube on a long floppy mesentery that often forms an omega loop in the pelvis. The mesosigmoid is frequently attached to the left pelvic sidewall, producing a small recess in the mesentery known as the intersigmoid fossa. This mesenteric fold is a surgical landmark for the underlying left ureter.
The rectum, along with the sigmoid colon, serves as a fecal reservoir. There is some controversy regarding the definition of the proximal and distal extent of the rectum. Some consider the rectosigmoid junction to be at the level of the sacral promontory; others consider it to be point at which the taeniae converge. Anatomists consider the dentate line the distal extent of the rectum, whereas surgeons typically view this union of columnar and squamous epithelium as existing within the anal canal and consider the end of the rectum to be the proximal border of the anal sphincter complex. The rectum is 12 to 15 cm in length and lacks taeniae coli or epiploic appendices. It occupies the curve of the sacrum in the true pelvis and the posterior surface is almost completely extraperitoneal, in that it is adherent to presacral soft tissues and thus is outside the peritoneal cavity. The anterior surface of the proximal third of the rectum is covered by visceral peritoneum. The peritoneal reflection is 7 to 9 cm from the anal verge in men and 5 to 7.5 cm in women. This anterior peritonealized space is called the pouch of Douglas, pelvic cul-de-sac, or rectouterine pouch and may serve as the site of so-called drop metastases from visceral tumors. These peritoneal metastases can form a mass in the cul-de-sac (called Bloomer’s shelf) that can be detected by a digital rectal examination.
The rectum possesses three involutions or curves, known as the valves of Houston. The middle valve folds to the left and the proximal and distal valves fold to the right. These valves are more properly called folds because they have no specific function as impediments to flow. They are lost after full surgical mobilization of the rectum, a maneuver that may provide approximately 5 cm of additional length to the rectum, greatly facilitating the surgeon’s ability to fashion an anastomosis deep in the pelvis.
The posterior aspect of the rectum is invested with a thick, closely applied mesorectum. A thin layer of investing fascia (fascia propria) coats the mesorectum and represents a distinct layer from the presacral fascia against which it lies. During proctectomy for rectal cancer, mobilization and dissection of the rectum proceed between the presacral fascia and fascia propria. Total mesorectal excision is a well-described oncologic maneuver that makes good use of the tissue planes investing the rectum to achieve a relatively bloodless rectal and mesorectal dissection. The lymphatics are contained within the mesorectum, and total mesorectal excision adheres to the basic surgical oncologic principle of removal of the cancer in continuity with its blood and lymphatic supplies. Resection of the rectum using this technique, and based on a thorough understanding of anatomy, has been shown to reduce markedly the incidence of subsequent local recurrence of rectal cancer.
The endopelvic fascia is a thick layer of parietal peritoneum that lines the walls and floor of the pelvis. The portion that is closely applied to the periosteum of the anterior sacrum is the presacral fascia. The fascia propria of the rectum is a thin condensation of the endopelvic fascia that forms an envelope around the mesorectum and continues distally to help form the lateral rectal stalks. The lateral rectal stalks or ligaments are actually anterolateral structures containing the middle rectal artery. The stalks reside in close proximity to the mixed autonomic nerves, containing sympathic and parasympathetic nerves, and division of these structures close to the pelvic sidewall may result in injury to these nerves, resulting in impotence and bladder dysfunction (Fig. 52-3).
FIGURE 52-3 Endopelvic fascia.
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 10.)
The rectosacral fascia, or Waldeyer’s fascia, is a thick condensation of endopelvic fascia connecting the presacral fascia to the fascia propria at the level of S4 that extends to the anorectal ring. Waldeyer’s fascia is an important surgical landmark, and its division during dissection from an abdominal approach provides entry to the deep retrorectal pelvis. Dissection between the fascia propria and presacral fascia follows the principles of surgical oncology and minimizes the risk for vascular or neural injuries. Disruption of the presacral fascia may lead to injury of the basivertebral venous plexus, resulting in massive hemorrhage. Disrupting the fascia propria during an operation for rectal cancer may significantly increase the incidence of subsequent recurrence of cancer in the pelvis if mesorectum is then left behind.
The muscles of the pelvic floor, like those of the anal sphincter mechanism, arise from the primitive cloaca. The pelvic floor, or diaphragm, consists of the pubococcygeus, iliococcygeus, and puborectalis, a group of muscles that together form the levator ani. The pelvic diaphragm resides between the sacrum, obturator fascia, ischial spines, and pubis. It forms a strong floor that supports the pelvic organs and, with the external anal sphincter, regulates defecation. The levator hiatus is an opening between the decussating fibers of the pubococcygeus that allows egress of the anal canal, urethra, and dorsal vein in men and the anal canal, urethra, and vagina in women. The puborectalis is a strong, U-shaped sling of striated muscle coursing around the rectum just above the level of the anal sphincters. Relaxation of the puborectalis straightens the anorectal angle and permits descent of feces; contraction produces the opposite effect. The puborectalis is in a state of continual contraction, a factor vital to the maintenance of continence. Puborectalis dysfunction is an important cause of defecation disorders. The pubococcygeus and iliococcygeus most likely participate in continence by applying lateral pressure to narrow the levator hiatus (Figs. 52-4 and 52-5).
FIGURE 52-4 Levator muscles.
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 18.)
Knowledge of the embryologic development of the intestinal tract provides an excellent foundation for understanding the anatomic blood supply. The foregut is supplied by the celiac artery, the midgut by the SMA, and the hindgut by the IMA (Figs. 52-6 and 52-7). Anatomic redundancy confers survival advantages and, in the intestinal tract, this feature is provided by extensive communication between the major arteries and collateral blood supply (Fig. 52-8). The territory of the SMA ends at the distal portion of the transverse colon and that of the IMA begins in the region of the splenic flexure. A large collateral vessel, the marginal artery, connects these two circulations and forms a continuous arcade along the mesenteric border of the colon. Vasa recta from this artery branch off at short intervals and supply the bowel wall directly (Fig. 52-9). The SMA supplies the entire small bowel, giving off 12 to 20 jejunal and ileal branches to the left and up to three main colonic branches to the right. The ileocolic artery is the most constant of these branches; it supplies the terminal ileum, cecum, and appendix. The right colic artery is absent in 2% to 18% of specimens; when present, it may arise directly from the SMA or as a branch of the ileocolic or middle colic artery. It supplies the ascending colon and hepatic flexure and communicates with the middle colic artery through collateral marginal artery arcades. The middle colic artery is a proximal branch of the SMA. It generally divides into right and left branches, which supply the proximal and distal transverse colon, respectively. Anatomic variations of the middle colic artery include complete absence in 4% to 20% and the presence of an accessory middle colic artery in 10% of specimens. The left branch of the middle colic artery may supply territory also supplied by the left colic artery through the collateral channel of the marginal artery. This collateral circulation in the area of the splenic flexure is the most inconsistent of the entire colon and has been referred to as a watershed area, vulnerable to ischemia in the presence of hypotension. In some studies, up to 50% of specimens were found to lack clearly identified arteries in a small segment of colon at the confluence of the blood supplies of the midgut and hindgut. These individuals rely on adjacent vasa recta in this area for arterial supply to the bowel wall. In practice, surgeons avoid making anastomoses in the region of the splenic flexure, fearing that the blood supply will not be sufficient to permit healing of the anastomosis, a situation that could lead to anastomotic leak and sepsis.
FIGURE 52-6 Arterial supply of the colon.
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 23.)
FIGURE 52-7 Arterial supply of the rectum.
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 24.)
FIGURE 52-8 Pathologic anatomy and occlusion of the SMA and IMA. A, Occlusion of SMA. B, Occlusion of the IMA. C, Ligating the IMA. 1, Correct location of ligation (see inset); 2, Incorrect location of ligation.
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 28.)
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 26.)
The IMA originates from the aorta at the level of L2 to L3, approximately 3 cm above the aortic bifurcation. The left colic artery is the most proximal branch, supplying the distal transverse colon, splenic flexure, and descending colon. Two to six sigmoid branches collateralize with the left colic artery and form arcades that supply the sigmoid colon and contribute to the marginal artery.
The arc of Riolan is a collateral artery, first described by Jean Riolan (1580-1657), that directly connects the proximal SMA with the proximal IMA and may serve as a vital conduit when one or the other of these arteries is occluded. It is also known as the meandering mesenteric artery and is highly variable in size. Flow can be forward (IMA stenosis) or retrograde (SMA stenosis), depending on the site of obstruction. Such obstruction results in increased size and tortuosity of this meandering artery, which may be detected by arteriography; the presence of a large arc of Riolan thus suggests occlusion of one of the major mesenteric arteries (Fig. 52-10).
FIGURE 52-10 Arc of Riolan.
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 27.)
The IMA terminates in the superior rectal (superior hemorrhoidal) artery, which courses behind the rectum in the mesorectum, branching and then entering the rectal submucosa. Here, the capillaries form a submucosal plexus in the distal rectum at the level of the anal columns. The anal canal also receives arterial blood from the middle rectal (hemorrhoidal) and inferior rectal (hemorrhoidal) arteries. The middle rectal artery is a branch of the internal iliac artery. It is variable in size and enters the rectum anterolaterally, passing alongside and slightly anterior to the lateral rectal stalks. It has been reported to be absent in 40% to 80% of specimens studied. The inferior rectal artery is a branch of the pudendal artery, which itself is a more distal branch of the internal iliac. From the obturator canal, it traverses the obturator fascia, ischiorectal fossa, and external anal sphincter to reach the anal canal. This vessel is encountered during the perineal dissection of an abdominoperineal resection.
The venous drainage of the colon and rectum mirrors the arterial blood supply. Venous drainage from the right and proximal transverse colon empties into the superior mesenteric vein, which coalesces with the splenic vein to become the portal vein. The distal transverse colon, descending colon, sigmoid, and most of the rectum drain into the inferior mesenteric vein, which empties into the splenic vein to the left of the aorta. The anal canal is drained by the middle and inferior rectal veins into the internal iliac vein and subsequently the inferior vena cava. The bidirectional venous drainage of the anal canal accounts for differences in patterns of metastasis from tumors arising in this region (Fig. 52-11).
FIGURE 52-11 Venous drainage of the colon and rectum.
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 30.)
Lymphatic drainage also follows the arterial anatomy. The wall of the large bowel is supplied with a rich network of lymphatic capillaries that drain to extramural channels paralleling the arterial supply. Lymphatics from the colon and proximal two thirds of the rectum ultimately drain into the para-aortic nodal chain, which empties into the cisterna chyli. Lymphatics draining the distal rectum and anal canal may drain to the para-aortic nodes or laterally, through the internal iliac system, to the superficial inguinal nodal basin. Although the dentate line roughly marks the level where lymphatic drainage diverges, classic studies by Block and Enquist using dye injection demonstrated that spread through lymphatic channels occurs to adjacent pelvic organs, such as the vagina and broad ligament, when injections are administered as high as 10 cm proximal to the dentate line (Figs. 52-12 and 52-13).
FIGURE 52-12 Lymphatic drainage of the colon.
(From Corman ML [ed]: Colon and rectal surgery, ed 4, Philadelphia,1998, Lippincott-Raven, p 21.)
(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 32.)
Lymph nodes are commonly grouped into levels depending on their location. Epicolic nodes are located along the bowel wall and in the epiploic appendices. Nodes adjacent to the marginal artery are paracolic. Intermediate nodes are located along the main branches of the large blood vessels; primary nodes are located on the SMA or IMA. Lymph node invasion by metastatic cancer is an important prognostic factor for patients with colorectal cancer. Accurate pathologic assessment of lymph nodes is essential for accurate staging, which serves as a determinant for treatment of patients with colorectal cancer.
Preganglionic sympathetic nerves from T6 to T12 synapse in preaortic ganglia. Postsympathetic fibers then course along blood vessels to reach the right and transverse colons. The right and transverse colon parasympathetic supply comes from the right vagus nerve. Parasympathetic fibers follow branches of the SMA to synapse in the wall of the bowel. The left colon and rectum receive sympathetic supply from the preganglionic lumbar splanchnics of L1 to L3. These synapse in the preaortic plexus located above the aortic bifurcation and the postganglionic elements follow the branches of the IMA and superior rectal artery to the left colon, sigmoid, and rectum. The lower rectum, pelvic floor, and anal canal receive postganglionic sympathetics from the pelvic plexus. The pelvic plexus is adherent to the pelvic sidewalls and is adjacent to the lateral stalks. It receives sympathetic branches from the presacral plexus, which condense at the sacral promontory into the left and right hypogastric nerves. These sympathetic nerves, which descend into the pelvis dorsal to the superior rectal artery, are responsible for delivery of semen to the posterior prostatic urethra. Failure to preserve at least one of the hypogastric nerves during rectal dissection results in ejaculatory dysfunction in males.
The pelvic parasympathetic nerves, or nervi erigentes, arise from S2 to S4. Preganglionic parasympathetic nerves merge with postganglionic sympathetics after the latter emerge from the sacral foramina. These nerve fibers, through the pelvic plexus, surround and innervate the prostate, urethra, seminal vesicles, urinary bladder, and muscles of the pelvic floor. Rectal dissection may disrupt the pelvic plexus and its subdivisions, resulting in neurogenic bladder and sexual dysfunction. Rates of bladder and erectile dysfunction after rectal surgery are as high as 45%. The degree and type of dysfunction are affected by the level of the neurologic injury. A high IMA ligation severing the hypogastric nerves near the sacral promontory results in sympathetic dysfunction characterized by retrograde ejaculation and bladder dysfunction. Injury to the mixed parasympathetic and sympathetic periprostatic plexus results in impotence and an atonic bladder.
Generally speaking, the function of the colon is the recycling of nutrients, whereas the function of the rectum is the elimination of stool. The recycling of nutrients depends on the metabolic activity of the colonic flora, colonic motility, and mucosal absorption and secretion. Stool elimination involves dehydration of colonic contents and defecation.
During the digestive process, ingested nutrients are diluted within the intestinal lumen by biliopancreatic and GI secretions. The small intestine absorbs most ingested nutrients and some of the fluid and bile salts secreted into the lumen. However, the ileal effluent is still rich in water, electrolytes, and nutrients that resist digestion. The colon has the functional ability to recover these substances and avoid unnecessary losses of fluids, electrolytes, nitrogen, and energy. To accomplish this, the colon depends highly on its bacterial flora.
Nutrients are digested within the intestinal lumen with the aid of biliopancreatic and GI secretions. By the time the chyme reaches the terminal ileum, most of the nutrients have been absorbed, leaving a succus entericus composed of electrolyte-rich fluid, bile salts, and some proteins and starches that have resisted digestion. An enormous quantity of autochthonous flora, consisting of more than 400 bacterial species, resides in the large intestine. Large bowel contents may contain as many as 1011 to 1012 bacterial cells/g, contributing approximately 50% of fecal mass.1 Most these colonic species are anaerobes. These bacteria feed on proteins sloughed from the bowel wall and undigested complex carbohydrates.
Colonic microflora provide several important functions to the host, including barrier functions that help maintain epithelial integrity, nutritive functions that utilize plant polysaccharides, and developmental functions that stimulate epithelial cell differentiation and angiogenesis and, finally, immune functions via the gut. Gut associated lymphoid tissue contributes to both innate and adaptive immunity.1 Short-chain fatty acids (SCFAs) are produced by microbial breakdown and fermentation of dietary starches. These fatty acids are the principal source of nutrition for the colonocyte. Bacteroides species predominate throughout the colon, comprising two thirds of the total counts of the proximal colon and almost 70% of the bacteria in the rectum. Escherichia, Klebsiella, Proteus, Lactobacillus, and enterococci are the predominant species of facultative anaerobes.
Probiotics can be defined as dietary supplements that contain live cultures of bacteria and yeast that are beneficial to colonic and host function. The two most widely used agents are Lactobacillus and Bifidobacterium. Recent studies have indicated that probiotics may have widespread health benefits, including stimulation of immune function, anti-inflammatory effects, and suppression of enteropathogenic colonization.2 In addition, they may increase the digestibility of dietary proteins, enhance absorption of amino acids, and play a protective or therapeutic role against Clostridium difficile–associated diarrhea.3 The ultimate role of probiotics has not yet been determined. There is conflicting data in regard to whether they work more effectively as primary therapy or as prophylaxis against recurrent C. difficile–associated diarrhea. Indications for their use are evolving, but may include necrotizing enterocolitis in neonates, patients with HIV-AIDS, and neutropenic patients undergoing chemotherapy. Further research is needed, but the evidence for probiotic usage in various settings is encouraging.
Prebiotics are nondigestible oligosaccharides (e.g., inulin) that help the host by stimulating the growth of certain species of beneficial intestinal bacteria. There is a growing body of data suggesting health benefits; however, there is currently little evidence to guide recommendations for their use.
Unlike most of the mucosal lining of the proximal GI tract, colonic mucosa does not receive its primary nutrition from the bloodstream. Instead, nutrient requirements are fulfilled from the colonic luminal contents. The primary energy source for the colonocyte is the SCFA butyrate. The manner in which this interaction occurs illustrates the essential symbiotic interaction between the colon and its resident bacterial flora.
The main source of energy for intestinal bacteria is dietary fiber, composed of complex carbohydrates (starches and nonstarch polysaccharides [NSPs]). This fiber is metabolized by the process of fermentation. Not all complex carbohydrates are fermented in the same manner, which underlies many of the dietary recommendations for bulking agents; lignin and psyllium are components of plants that are not fermented by human colonic flora. They are hydrophilic, thus leading to water resorption and stool bulking. Celluloses are partially fermented, whereas fruit pectins are completely metabolized by colonic bacteria. Diets high in nonfermentable NSPs contribute to stool bulk and increased transit time; highly fermentable NSPs provide minimal bulk, but enhanced colonocyte nutrition.
The end products of fermentation are SCFAs and gas—carbon dioxide, methane, and hydrogen. In addition to NSPs, colonic bacteria ferment poorly absorbed starches and proteins from the upper GI tract, known as resistant starches. Although highly variable from person to person, with daily variability dependent on diet, the gases produced by bacterial fermentation comprise approximately 50% to 75% of flatus, with the remainder consisting of swallowed air.
Protein fermentation, otherwise known as putrefaction, results in the formation of potentially toxic metabolites, including phenols, indoles, and amines. The production of these toxins is inhibited in many intestinal bacteria by the presence of alternate carbohydrate energy sources. This process becomes accentuated more distally in the colon as carbohydrate sources become scarcer. These deleterious end products of bacterial metabolism can lead to mucosal injury and reactive hyperproliferation, which have been hypothesized to promote carcinogenesis. Also, the presence of bulking agents decreases intracolonic pressures and may serve to prevent the formation of colonic diverticula. It can be seen, then, how providing adequate sources of various forms of dietary carbohydrates can serve positive roles in colonic health. These principles underlie the recommendations for dietary fiber, as do the evolving data on the helpful nature of probiotics and prebiotics.
The primary end products of bacterial fermentation are SCFAs. Absorption of SCFAs in the large intestine is efficient; only 5% to 10% are lost in the feces. The three primary fatty acids produced are acetate, propionate, and butyrate in a ratio of 3 : 1: 1. SCFAs have key roles in colonic and also overall human metabolism. They are metabolized in three main sites: (1) colonocytes use butyrate as their primary energy source; (2) hepatocytes metabolize all three SCFAs to various degrees for use in gluconeogenesis; and (3) muscle cells oxidize acetate to generate energy. Metabolism of the SCFAs can provide up to 70% of colonocyte energy needs, reduce glucose oxidation, and spare other essential amino acids for metabolism.4 SCFAs also influence GI motility via the ileocolonic brake mechanism, which is defined as the inhibition of gastric emptying and nutrients reaching the ileocolonic junction.
Acetate, the principal SCFA in the colon, is primarily absorbed and transported to the liver, where it is the primary substrate for cholesterol synthesis. Nonabsorbable, nonfermentable dietary fiber, such as psyllium, may decrease the production of acetate and may have a beneficial effect on cholesterol levels. Similarly, propionate, which has a glycolytic role in the liver, may also lower serum lipid levels by inhibiting cholesterol synthesis. Butyrate is the primary energy source for colonic epithelial cells and may also play an important role in maintaining cellular health by arresting the proliferation of neoplastic colonocytes, while paradoxically being trophic for normal colonocytes. In addition, butyrate serves to regulate and stabilize cell adhesion molecules.
It was long believed that urea is the end product of nitrogen metabolism in humans. This is true in the sense that humans, and mammals in general, do not produce urease. However, colonic bacteria are rich in urease. When urea is labeled with a tracer (e.g., radioisotope, heavy isotope) and injected IV, 10% of the urea nitrogen is not recovered in urine but is incorporated into body protein. Bacteria firmly adherent to the colonic epithelium mediate this process of urea recycling, which produces urease. A low-protein and high-fiber diet, such as that of the Papua New Guinea highlanders, further increases urea recycling. These individuals ingest only 10 mg of protein/kg/day and have normal health, with normal muscle mass and serum proteins. Adaptation to this low-protein diet has made the colon efficient in recycling nitrogen to the point that it may even absorb some essential amino acids (e.g., lysine). Urea recycling has been exploited as a therapy for renal failure by excluding nonessential amino acids from the diet to promote maximal urea recycling and diminish the need for dialysis.
However, one pathologic condition in which urea recycling is not beneficial is liver failure. When the liver cannot reuse the urea nitrogen absorbed by the colon, ammonia crosses the blood-brain barrier and produces false neurotransmitters, which result in hepatic coma.
The total absorptive area of the colon is estimated at approximately 900 cm2. Between 1000 and 1500 mL of fluid is poured into the cecum by the daily ileal effluent. The total volume of water in stool is only 100 to 150 mL/day. This 10-fold reduction in water across the colon represents the most efficient site of absorption in the GI tract per surface area. The net absorption of sodium is even higher. Although the ileal effluent contains 200 mEq/liter of sodium, stool contains only 25 to 50 mEq/liter. One major difference between sodium and water absorption in the colon is that although water is absorbed passively, sodium requires active transport. Sodium is transported against chemical and electrical gradients at the expense of energy consumption.
The colonic epithelium can use various fuels; however, n-butyrate is oxidized in preference to glutamine, glucose, or ketone bodies. Because mammalian cells do not produce n-butyrate, the colonic epithelium relies on luminal bacteria to produce it through the fermentation of dietary fiber. The lack of n-butyrate, such as that resulting from the inhibition of fermentation by broad-spectrum antibiotics, leads to less sodium and water absorption and thus diarrhea. Conversely, the perfusion of the colonic lumen with n-butyrate stimulates sodium and water absorption. n-Butyrate, acetate, and propionate are SCFAs produced through bacterial fermentation; these constitute the main anions in stool. Other physiologic effects of SCFAs on the colon include stimulation of blood flow, mucosal cell renewal, and regulation of intraluminal pH for homeostasis of the bacterial flora.
In addition to recovering sodium and water, the colonic mucosa absorbs bile acids. The colon absorbs bile acids that escape absorption by the terminal ileum, thus making the colon part of the enterohepatic circulation. Bile acids are passively transported across the colonic epithelium by nonionic diffusion. When the colonic absorptive capacity is exceeded, colonic bacteria deconjugate bile acids. Deconjugated bile acids can then interfere with sodium and water absorption, leading to secretory, or choleretic, diarrhea. Choleretic diarrhea is seen early after right hemicolectomy as a transient phenomenon and more permanently after extensive ileal resection.
The physiologic role of colon secretion is demonstrated in patients with chronic renal failure. Uremic patients can remain normokalemic while ingesting a normal amount of potassium before requiring dialysis. This phenomenon is associated with a compensatory increase in colonic secretion and fecal excretion of potassium. This effect is blocked by spironolactone, which illustrates the effect of aldosterone on colonic potassium secretion. Potassium secretion requires both Na+,K+-ATPase and Na+-K+-2Cl− cotransport on the basolateral membrane and an apical potassium channel.
Many forms of colitis are associated with increased potassium secretion, such as inflammatory bowel disease (IBD), cholera, and shigellosis. In addition, some forms of colitis impair colonic absorption or produce secretion of chloride, such as collagenous and microscopic colitis and congenital chloridorrhea. Chloride is secreted by colonic epithelium at a basal rate, which is increased in pathologic conditions such as cystic fibrosis and secretory diarrhea. Secretion of chloride also requires the coupling of Na+,K+-ATPase and Na+-K+-2Cl− cotransport to exit passively through the apical membrane. Calcium and cyclic adenosine monophosphate both stimulate chloride secretion, whereas bicarbonate and SCFAs inhibit chloride secretion.
Colonic secretion of H+ and bicarbonate is coupled to the absorption of Na+ and Cl−, respectively. It is through these exchangers that the colon is linked to systemic acid-base metabolism. The supply of H+ and bicarbonate for these exchangers is maintained by the hydration of CO2, catalyzed by colonic carbonic anhydrase. Changes in systemic pH induce changes in the activity of carbonic anhydrase, eliciting elimination of H+ or bicarbonate as needed to bring the systemic pH back to normal.
Colonic motility is a highly complex process, made difficult to investigate by a lack of standardized terminology and measurements. Additionally, movement through the colon is relatively slow compared with the proximal GI tract, and studies require prolonged observation.
Colonic motility patterns may be more simply divided into two primary patterns, segmental activity and propagated activity. Segmental activity consists of single contractions or rhythmic bursts of contractions. The purpose of these segmental contractions is to propel fecal matter distally via a directed pressure gradient toward the rectum in discrete distances and allow for mixing, which promotes optimal absorption. The second pattern is propagated activity, commonly classified on the basis of amplitude as low-amplitude or high-amplitude propagated contractions.5 High-amplitude propagated contractions have been historically referred to as mass movements, or migrating motor complexes whose role is shifting large quantities of contents through the colon. These have an important role in defecation, with mass movements propelling larger volumes of fecal matter to the distal colon and emptying of the descending colon into the sigmoid colon and rectum. Little is known about low-amplitude propagated contractions, but they are associated with distention of the viscous and passage of flatus.
Not surprisingly, food ingestion results in an increase of overall colonic motility for approximately 2 hours. This reflex is stimulated not only by gastric distention but also by the central nervous system (CNS), initiated by visualization of food. Additionally, meal composition affects colonic responses. Increased activity in response to carbohydrate meals is fairly short-lived, whereas fatty meals elicit longer term responses.
Ultimately, transit in the colon is controlled by the autonomic nervous system. Parasympathetic innervation reaches the colon through the vagus and pelvic nerves. The enteric nervous system in the colon is arranged in several plexuses—subserosal, myenteric (Auerbach), submucosal (Meissner), and mucosal plexuses. Sympathetic innervation originates in the superior and inferior mesenteric ganglia and reaches the colon via perivascular plexuses.
The frequency of defecation is just as variable among individuals as is their perception of abnormal stool frequency. An individual who passes more than three loose stools daily is considered as having diarrhea, whereas fewer than three weekly stools is considered constipation. Any frequency within that range is considered normal, although many individuals will still seek medical attention for what they perceive as diarrhea or constipation. Many factors influence colonic transit rate. Colonic transit is longer in women than in men and longer in premenopausal than postmenopausal women. Conversely, colonic transit time is shortened in smokers. In normal subjects, supplementation with NSPs does not shorten colonic transit time, although it does increase fecal weight. In patients with idiopathic constipation, however, NSPs, in the form of psyllium seeds, shorten colonic transit time and increase stool weight.
Normal defecation requires adequate colonic transit time, stool consistency, and fecal continence. Fecal continence implies deferment of stool elimination, discrimination among gas, liquid, and solid stool, and selective elimination of gas without stool. There is some controversy regarding the actual role of the rectum under resting conditions. Some have proposed that the rectum is simply a conduit, which under resting conditions should be empty. If stool arrives at the rectum, the anorectal inhibitory reflex is triggered, forcing the subject to hold defecation by voluntary contraction of the external sphincter. However, any surgeon who performs routine rigid proctosigmoidoscopies in the office is well aware that a patient can have a rectum full of stool without any awareness. This leads to the opposing view, which regards the rectum as a reservoir. Just as stool triggers the anorectal inhibitory reflex, it also triggers a rectocolic reflex. This reflex allows continuous filling of the rectum with fecal material until the colon is emptied.
The mechanisms involved in fecal continence are not fully understood. A certain reservoir capacity is needed to achieve fecal continence. A stiff nondistensible rectum, such as in radiation proctitis, may produce incontinence, even when the sphincter muscles are competent. Some of the internal and external sphincter muscle fibers are necessary for adequate continence, although many patients have part of the sphincter severed during a fistulotomy and are still continent. Probably, the only factor needed for fecal continence is innervation of the sphincter. The motor nerve fibers, which produce contraction of the sphincter fibers, and also all the sensory innervation are important to empty the rectum adequately.
Purging the feces and reducing the concentration of colonic intraluminal bacteria before operations on the colon have long been basic tenets of surgery. The normal, or autochthonous, microbial organisms in the colon comprise up to 90% of the dry weight of feces, reaching concentrations of up to 109 organism/mL of feces. The anaerobic Bacteroides is the most common colonic microbe, whereas Escherichia coli is the most common aerobe. Pseudomonas, Enterococcus, Proteus, Klebsiella, and Streptococcus spp. are also present in large numbers.
The process of preparing the colon for an elective operation has traditionally involved two factors, purging the fecal contents (mechanical preparation) and administration of antibiotics effective against colonic bacteria. Tradition has held that an unprepared colon (i.e., one that contains intraluminal feces) poses an unacceptably high rate of failure of the anastomosis to heal. However, experience with primary repair of colonic injuries by trauma surgeons, along with reports from European surgeons describing elective operations conducted safely without the use of preoperative purging, have led to reconsideration of the true value of purging the colon before colonic surgery. Because the colonocytes receive nutrition from intraluminal free fatty acids produced by fermentation from colonic bacteria, there are concerns that purging may actually be detrimental to the healing of a colonic anastomosis. However, in the United States at present, the colon is generally cleansed in preparation for colonic operations. Effective cleansing is mandatory for adequate colonoscopy or the administration of contrast enema.
Although the use of preoperative parenteral antibiotics is well accepted and validated, the related issue of preoperative oral antibiotic use is controversial. A multiplicity of bowel preparation regimens and antibiotic combinations are in current use. A clear superiority of one over another has not been found; however, for some patients, certain bowel preparations may have adverse physiologic consequences. Knowledge of the history of bowel preparation practices, current controversies, and data is useful.
Mechanical bowel cleansing methods are used for colonoscopy and elective surgery. Complete bowel obstruction and free perforation are absolute contraindications to bowel preparation. For colonoscopy, properties of various preparations are judged by safety, patient tolerance, and efficacy or preparation quality. In the past, 4 to 5 days of clear liquids, along with laxatives such as senna, castor oil, and bisacodyl, whole bowel nasogastric irrigation, mannitol irrigation, and repeated enemas were some of the regimens used. Patient tolerance of these methods is poor and is associated with dehydration, electrolyte abnormalities, and severe abdominal cramping, and are generally not well tolerated by older or infirm patients.
In the 1980s, polyethylene glycol (PEG) solution, a nonabsorbed, sodium sulfate–based liquid, was developed as an oral mechanical bowel preparation. Patients are required to drink at least 2 to 4 liters of the solution, along with additional fluids. Abdominal cramping, nausea, and vomiting are common side effects of the preparation, and prophylactic antiemetics are often administered routinely. Sodium phosphate solution (Fleet’s Phospho-soda) was developed in response to patient dissatisfaction with the large fluid volume required for PEG preparation and has been found in most trials to be a more tolerable preparation, with higher rates of patient satisfaction and compliance. The smaller volume (45 mL taken twice) seems to be the main benefit because the side effects are similar. Sodium phosphate pills (Visicol) were introduced as an alternative to liquids. The regimen consists of ingesting a total of 40 pills, with three pills taken every 15 minutes with 8 oz of fluid. Sodium phosphate, in liquid or pill form, has been linked more frequently than PEG to rare but serious electrolyte imbalances. In patients with impaired renal function, hyperphosphatemia, hypernatremia, hypokalemia, and hypocalcemia can occur. Thus, PEG is the recommended bowel preparation in patients with renal insufficiency, cirrhosis, ascites, or congestive heart failure. Investigation comparing the efficacy of mechanical bowel preparations has focused on comparisons between PEG and sodium phosphate solutions.
Cohen and colleagues have demonstrated a 90% excellent or good bowel preparation with sodium phosphate versus 70% with 4 liters of PEG. Frommer has found that sodium phosphate results in a cleaner bowel than PEG, with no difference in infectious complications. On the other hand, Poon and associates have found that there is no difference in bowel cleanliness when the volume of PEG is reduced to 2 liters and compared with 90 mL of sodium phosphate, and that the reduced volume enhances patient compliance. A Canadian study has found the use of sodium phosphate to be associated with increased patient compliance and an eightfold cost reduction when compared with PEG. Ultimately, patient comfort and economic factors may determine mechanical bowel preparation practices if the efficacy is similar.
For patients undergoing colonoscopy, the quality of the bowel preparation is essential for performing an accurate examination. For segmental resections, however, the necessity of mechanical bowel preparation has come under scrutiny. Zmora and coworkers, in a study comparing infectious complications in mechanically prepared bowel (PEG solution) versus unprepared bowel in patients undergoing segmental resection, found no differences in any type of infectious complication. Both groups received parenteral antibiotics. The study looked at left-sided anastomoses only and found that there was no significant difference between overall infection rates in unprepared (13.2%) versus prepared bowel (12.5%). Also, the wound infection rates in this study did not significantly differ, 6.6% in the prepared group and 10% in the unprepared group. Although studies of this type have been relatively small and significantly underpowered, they indicate the future possibility of avoiding the discomfort of bowel preparation and the small attendant risk for electrolyte irregularities and dehydration.
Antibiotic use in colorectal surgery is a well-established practice that reduces infectious complications. Elective colorectal cases are classified as clean-contaminated and, as such, benefit from routine single-dose administration of parenteral antibiotics 30 minutes before an incision. It has been shown that when operative times are prolonged, additional doses at 4-hour intervals reduce wound infection. When the operation is completed, postoperative administration of antibiotics for a clean-contaminated case, such as a routine segmental resection, does not reduce infectious complications further and may promote C. difficile colitis, Candida infection, and the emergence of bacterial antibiotic resistance. Polk and Lopez-Mayer showed a reduction in postoperative infection rates from 30% to 8% with the routine use of preoperative parenteral antibiotics; Gomez-Alonzo and colleagues repeated these results, showing a decrease from 39% to 9%. Antibiotics active against both aerobes and anaerobes are ideal; second- or third-generation cephalosporins alone, or a combination of a fluoroquinolone plus metronidazole or clindamycin, is typical. The use of additional oral antibiotics, theoretically to reduce the bacterial load further, is widely accepted, but not as well validated. In a survey of colon and rectal surgeons, 87% indicated that both oral and parenteral antibiotic usage is part of their routine preparation for elective colon operations. A typical preparation consists of erythromycin base (1 g) and neomycin (1 g) given in three preoperative doses the day before surgery. However, this regimen is associated with a high incidence of nausea and abdominal cramps, and some surgeons prefer to prescribe oral ciprofloxacin or metronidazole.
In studies comparing oral and parenteral antibiotics, a decrease in wound infection rate from 36% to 6.5% was seen with IV administration, whereas others comparing a combination of oral plus parenteral antibiotics, versus oral alone, found that the addition of IV antibiotics reduced infectious complications by half (22% to 11%). It is notable that there have been no prospective randomized trials examining this issue and that most retrospective reviews are poorly powered. Although it is clear that preoperative parenteral antibiotics reduce wound infection rates, oral antibiotics do not clearly benefit the patient by reducing wound infection or decreasing intra-abdominal abscess or leaks. The rate of intra-abdominal abscess is more dependent on technical factors affecting anastomotic integrity than on antibiotic prophylaxis.
A diverticulum is an abnormal sac or pouch protruding from the wall of a hollow organ, which is, for the purposes of this discussion, the colon. A true diverticulum is composed of all layers of the intestinal wall, whereas a false diverticulum, or pseudodiverticulum, lacks a portion of the normal bowel wall. The diverticula that commonly occur in the human colon are protrusions of mucosa through the muscular layers of the intestine. Because these mucosal herniations are devoid of the normal muscular layers, they are pseudodiverticula (Fig. 52-14).
Diverticulosis and diverticular disease are terms used to indicate the presence of colonic diverticula. Diverticulosis is a common condition of Western society and seems to be an unfortunate product of the Industrial Revolution. It is interesting that there seem to be no specimens of colonic diverticulosis in anatomic or medical museums in Europe that were archived before the Industrial Revolution. The process of roller-milling wheat flour was introduced in Europe approximately a quarter of a century earlier than the appearance of diverticulosis, which was initially observed in the first decade of the 20th century. It has been postulated that the decreased consumption of unprocessed cereals and increased consumption of sugar and meat by the general population are factors largely responsible for the appearance of diverticulosis. During the past 80 years or so, the amount of fiber consumed by individuals in North America and Western Europe has decreased, whereas the prevalence of diverticulosis has increased significantly. The formation of diverticula is also related to aging. Diverticula are rare in individuals younger than 30 years, but at least two thirds of Americans will have developed colonic diverticula by the age of 80 years.
Further evidence that a diet low in fiber and high in carbohydrates and meat contributes to the incidence of diverticulosis is the observation that diverticulosis is rare in sub-Saharan African blacks who consume a high-fiber diet; however, blacks in Johannesburg who consume a low-fiber diet have the same incidence of diverticulosis as South African whites.
Diverticula are actually herniations of mucosa through the colon at sites of penetration of the muscular wall by arterioles. These sites are on the mesenteric side of the antimesenteric taeniae. In some cases, the arteriole penetrating the wall can be displaced over the dome of the diverticulum. This close relationship between the artery and diverticulum is responsible for the massive hemorrhage that can occasionally complicate diverticulosis (Fig. 52-15).
FIGURE 52-15 Pathogenesis of diverticular disease. Diverticula are herniations of the mucosa through the points of entry of blood vessels across the muscular wall. Because the diverticula are formed only by the mucosa rather than by the entire wall of the intestine, they are called false diverticula. Note that the diverticula form only between the mesenteric taenia and each of the two lateral taeniae. Because there are no perforating vessels, diverticula do not form on the antimesenteric side of the colon.
There is often a striking hypertrophy of the muscular layers of the colonic wall associated with diverticulosis. This thickening of the colonic wall, usually affecting the sigmoid colon, may precede the appearance of diverticula. Diverticula most commonly affect the sigmoid colon and are confined to the sigmoid in approximately 50% of patients with diverticulosis. The next most common area involved is the descending colon (≈40% of affected individuals), and the entire colon has diverticula in 5% to 10% of patients with diverticulosis. Even in patients with diverticula involving the entire colon, the muscular thickening characteristic of the disease is usually confined to the sigmoid (Fig. 52-16).
The sigmoid colon, the most common site of diverticula formation, is also the segment of colon with the smallest luminal diameter. If the colonic lumen contains a large volume of fiber, the contractile pressure required to propel the feces forward is low. In such circumstances, the colonic pressure in the sigmoid is only slightly higher than atmospheric pressure. However, with the decreased amount of fiber provided by today’s typical dietary regimens, there is decreased colonic luminal content, requiring the generation of increased colonic pressures to propel the feces forward. Colonic pressures as high as 90 mm Hg can be generated by contraction of the narrow sigmoid colon. These high intraluminal pressures are thought to be responsible for the herniations of mucosa through the anatomically weak points in the colonic wall.
It has long been conjectured that factors contributing to diverticular disease, or at least diverticulitis, is the consumption of nuts, popcorn, and small seeds, such as are found in tomatoes, and patients with diverticular disease are often counseled to avoid these foods. However, a large prospective study of men without known diverticular disease has failed to detect an increase in the risk of diverticulosis or diverticular complications.11