Chapter 2: Under Colon
JJ
Skip to Main content

Colon
Related terms:
Bowel Obstruction
Neoplasm
Serositis
Lesion
Diarrhea
Small Intestine
Rectum
View all Topics
Development, Structure, and Function of the Tubal Gut
F.T. Bosman, P. Yan, in Pathobiology of Human Disease, 2014
Large Intestine
The basic structure of the large intestine is rather similar to that of the small intestine but there are characteristic differences. In addition to the usual two muscular layers, three longitudinal ribbons of smooth muscle compose the taeniae coli, which when contracted are responsible for the typical bulges in the colon, known as haustra. Even though the proximal colon is derived from the midgut whereas the distal part is derived from the hindgut, there are no striking morphological differences between these compartments. The mucosa is not arranged in regular folds and its surface is flat, without villi. The mucosal epithelium is organized in regular crypts, similar to those in the small intestine but somewhat deeper. The crypts are compartmentalized, as in the small intestine, with stem cells in the crypt basis along with enteroendocrine cells. Each crypt is a monoclonal structure: derived from a single stem cell. Usually Paneth cells are absent. Enterocytes are less abundant than in the small intestine and not as well equipped for absorption: they are somewhat shorter and have fewer and irregular microvilli. Their absorptive function is largely the uptake of water. Smooth passage of the solidifying fecal mass is assured by mucus (largely composed of MUC2) produced by the more abundant goblet cells. Lymphoid follicles in the mucosa and submucosa are abundant. This might reflect a state of symbiosis between the large intestinal flora and the bowel wall, a subject of increasing interest.
Implications for pathology
Large bowel infections are quite common. The peculiar luminal microenvironment and the mucosa-associated lymphoid system might well be important players in what is generically called inflammatory bowel disease (notably ulcerative colitis and Crohn's disease).
Of particular importance is adenocarcinoma of the large bowel. Even though the small bowel is a much bigger organ with a relative proliferative activity equal to that in the colon, adenocarcinomas are rare in the small but frequent in the large bowel. This may be related to the function of the large bowel: concentration of the fecal mass along with slower passage might increase the exposure of the mucosa to harmful xenobiotics. Recently, the notion that the large bowel microbiota might play a role has emerged.
View chapterPurchase book
Imaging of Nontraumatic Abdominal Conditions
Joshua Broder MD, FACEP, in Diagnostic Imaging for the Emergency Physician, 2011
X-ray in Large-Bowel Obstruction
The large bowel is located on the periphery of the abdomen and can usually be differentiated from the small bowel, which is normally located centrally within the abdomen.111 The normal appearance of the large bowel on x-ray includes scattered irregular areas of gas, caused by the production of gas by anaerobic organisms in stool. Air–fluid levels are sometimes normally seen within the large bowel. Markings of haustra are sometimes seen; these soft-tissue ridges incompletely cross the diameter of the large bowel, in contrast to plicae circularis, which fully cross the diameter of the small bowel. The normal diameter of the large bowel on x-ray is less than 5 cm,112 although dilatation beyond this degree can occur with ileus. A large bowel greater than 8 cm in diameter suggests mechanical obstruction, although diameters as great as 10 cm have been observed in ileus (see Figure 9-32).111 If the ileocecal valve is not competent, large-bowel obstruction may lead to small-bowel dilatation, because large-bowel contents reflux through the ileocecal valve. When the ileocecal valve is competent, it can result in massive dilatation of the large bowel, because retrograde reflux of large-bowel contents is prevented. In this circumstance, the cecum may exceed 9 to 13 cm, with risk for perforation. Pseudoobstruction caused by fecal impaction can also occur and has a similar x-ray appearance with dilated large bowel (see Figure 9-50). Prone and lateral decubitus x-rays are sometimes used to distinguish ileus from mechanical large-bowel obstruction. In ileus, air can fill the rectum with repositioning of the patient; in mechanical obstruction, air cannot pass the point of obstruction to reach the rectum. In most cases today, these additional x-ray maneuvers should be forgone in favor of CT, which provides more information about the nature and location of the obstruction, as well as complications such as perforation.
X-ray has a reported sensitivity of 84% and specificity of 72% for large-bowel obstruction, when clinical history is provided to the radiologist.113 However, large studies with appropriate blinding have not been performed.
View chapterPurchase book
Intestinal Obstruction
Thorsten Braun, Wolfgang Henrich, in Obstetric Imaging: Fetal Diagnosis and Care (Second Edition), 2018
Imperforate Anus
Definition
Large bowel anomalies are rare and less frequent than small bowel anomalies. Large bowel anomalies include anorectal atresia, persistent common cloaca as a complicated form of anorectal atresia, and Hirschsprung disease. Synonyms for anorectal atresia are anal atresia and imperforate anus. In its simplest form, imperforate anus results from a failure of the anal canal to perforate during bowel development.
Prevalence and Epidemiology
The reported incidence of anorectal malformations ranges from 1 : 1500 to 1 : 5000 newborns.74–76
Etiology and Pathophysiology
During the ninth week of gestation, the downward-growing urogenital septum separates the cloaca into the ventral urogenital sinus (which develops into the urinary bladder and urethra) and the dorsal rectum. Anorectal malformations occur by the 10th week from an abnormal partitioning of the cloaca by the urogenital septum. Imperforate anus appears if the membrane of the anal pouch does not perforate.
Anorectal malformations are classified by their termination in relation to the levator sling into high (supralevator) and low (infralevator) lesions. High lesions have a higher incidence of associated fistulas and genitourinary malformations and are more frequent.
Manifestations of Disease
Clinical Presentation
Passage of the first stool does not occur within 24 to 48 hours after birth.
Imaging Technique and Findings
Ultrasound.
The prenatal diagnosis of an imperforate anus is difficult and is seldom been made by prenatal US.77 Reports of prenatal diagnosis are from the third trimester; possible signs are dilated colon in the lower abdomen78–80 or intraluminal meconium calcifications proximal or distal to the site of obstruction (Fig. 26.8).81–83 These calcifications differ from linear calcifications seen in meconium peritonitis, which can occur in the upper abdominal cavity, often adjacent to the liver, and sometimes are seen in the scrotum.84 However, more recent reports show that US findings can be observed at 12 weeks' gestation.85–87 In the presence of associated urogenital malformations with bilateral renal obstruction, amniotic fluid can be decreased. Fetuses with imperforate anus tend to be small for gestational age.88 In maternal plasma, decreased alpha-fetoprotein levels have been observed in cases of imperforate anus.89
Magnetic Resonance Imaging.
MRI findings include pathologic dilatation of the distal colon and rectum.90
View chapterPurchase book
Large Intestine (Colon)
ROBERT E. PETRAS, WENDY L. FRANKEL, in Modern Surgical Pathology (Second Edition), 2009
Developmental Abnormalities
Agenesis, Atresia, and Stenosis
Large bowel agenesis and atresia are extremely rare.746,747 Congenital atresia and stenosis are associated with failure to pass meconium, abdominal distention, and vomiting. These conditions are often seen on a background of other congenital anomalies. Pathologically, one can see an imperforate septum, a portion of the colon replaced by fibrous cord, or the absence of a segment of colon and associated mesentery.
Malrotation
Colonic malrotation occurs with malrotation of the small bowel and is associated with abnormal anatomic relationships and fibrous bands; it may predispose patients to volvulus.747,748 Mispositioning of the cecum and appendix may lead to delayed diagnosis of acute appendicitis.
Congenital Duplications, Diverticula, and Developmental Cysts
Congenital duplications and diverticula are located within the mesentery and often occur in combination with other congenital malformations.749,750 Sometimes, the duplications are tubular, represent doubling of the bowel, and run parallel to the colon and rectum. Other duplications can become cystic and are often referred to as enterogenous cysts. Patients may have associated spine abnormalities. We classify tubular duplications that communicate with the lumen at one end as congenital diverticula. Small duplications and diverticula are usually asymptomatic. Larger ones may cause mass lesions, abdominal pain, constipation, or bleeding. Hindgut duplications may be associated with complex genital and urinary tract abnormalities.
Duplications and congenital diverticula usually have organized layers of smooth muscle sometimes with a nerve plexus within their walls. Mucosal linings if present resemble colon, respiratory epithelium, or gastric mucosa. As lesions enlarge to become cystic, the lining and the wall can become atrophic.751
The retrorectal space is a relatively common location for developmental cysts that can become symptomatic in adults.752-754 Epidermoid or dermoid cysts are unilocular, are lined by squamous epithelium, and may contain adnexal structures (dermoid cyst) and lack smooth muscle in the wall. Rectal duplications can become cystic. Rectal duplications are also unilocular, are lined by colonic, gastric, or respiratory epithelium, and have an organized muscular wall that recapitulates the muscularis externa. The retrorectal cystic hamartoma is often referred to as a tailgut cyst. This lesion manifests as a multilocular cystic and solid tumor (Fig. 23-106). The variably sized cysts can be lined by squamous, transitional, or glandular epithelium. Disorganized bundles of smooth muscle are found within the wall. Inflammatory changes such as a foreign body giant cell reaction are quite common. Developmental cysts in the retrorectal space are susceptible to infection and fistula, and associated malignancy has been reported.754 Therefore, total excision is recommended.
View chapterPurchase book
Gastrointestinal, Hepatic, and Pancreatic Disorders in Systemic Lupus Erythematosus
Chi Chiu Mok, in Systemic Lupus Erythematosus, 2016
Lupus Colitis and Inflammatory Bowel Disease
The large bowel may occasionally be involved in lupus enteritis, leading to colitis and perforation.11 Active SLE in other organs is often present and the mortality is high.
Crohn's disease and ulcerative colitis (UC) are rarely reported in SLE patients. The prevalence of UC in SLE patients is around 0.4%.39 Clinically and pathologically, lupus colitis may be indistinguishable from UC. Symptoms include lower abdominal discomfort, per rectal bleeding, and persistent diarrhea that may be bloody. Cases of Crohn's disease presenting with persistent GI bleeding have been reported in patients with SLE.40
View chapterPurchase book
Small Bowel and Large Bowel Resection and Anastomosis
Oliver Zivanovic, Yukio Sonoda, in Principles of Gynecologic Oncology Surgery, 2018
Anatomy of the Large Intestine
The large intestine is approximately 1.5 m in length, beginning at the cecum and ending with the anus in the perineum.
The large bowel is characterized by full-thickness infoldings of the bowel wall, called haustra (Fig. 17.7). These infoldings correspond to transverse folds in the bowel lumen called plicae semilunares. The large bowel has three thickened bands of longitudinal muscle that run its length from the appendix to the rectum called taeniae coli (taenia omentalis, taenia libera, and taenia mesocolica). Contraction of the taeniae causes the haustra to become more prominent. The large bowel has small pouches of peritoneum filled with fat called appendices epiploicae that are most prominent on the descending and sigmoid colon.
The cecum is the most proximal portion of the large intestine (Fig. 17.8). It is a blind pouch that is 5 to 7 cm in length and projects caudal to the ileocecal junction in the right iliac fossa of the right lower quadrant. Usually, the cecum is entirely enveloped by peritoneum but does not have a mesentery. It is the widest part of the large intestine but also has the thinnest wall; thus, it is at highest risk for perforation in cases of large bowel obstruction. The appendix arises 2 to 3 cm inferior to the ileocecal junction. The appendix has its own short mesentery called the mesoappendix, which connects it to the inferior part of the mesentery of the ileum. The appendiceal artery is a branch off the ileocolic artery and runs in the mesoappendix. The ileum leads into the cecum and is separated by the ileocecal valve. Its function is to limit the reflux of colonic contents into the ileum. Approximately 2 L of fluid enters the colon daily through the ileocecal valve.
The ascending colon measures approximately 15 to 20 cm long and runs from the ileocecal valve to the hepatic flexure. It ascends as a retroperitoneal structure covered by peritoneum only on its anterior and lateral surfaces. It lies anterior to the quadratus lumborum, psoas, and transversus abdominis muscles; inferior pole of the right kidney; and descending portion of the duodenum. Lateral to the ascending colon is the white line of Toldt, which represents the fusion of the colonic mesentery with the parietal peritoneum. There may be congenital adhesions between the anterior aspect of the ascending colon and the right abdominal wall (Jackson membrane). The hepatic flexure may have several attachments to the liver and gallbladder. The ascending colon and hepatic flexure are supplied by the ileocolic and right colic arteries, and the venous drainage is through the ileocolic and right colic veins, which drain into the superior mesenteric vein. The lymphatic drainage of the ascending colon is via the paracolic and epicolic lymph nodes, which empty into the superior mesenteric lymph nodes.
The transverse colon is the portion of large bowel that lies between the hepatic and splenic flexures. It is the longest portion of the large bowel and usually measures 30 to 60 cm in length. Occasionally, a redundant transverse colon will reach into the pelvis. Unlike the ascending and descending colon, the transverse colon has its own mesentery, which is longest in the center, and is therefore considered an intraperitoneal structure. The root of the mesentery of the transverse colon covers the descending part of the duodenum, the pancreas, and a portion of the left kidney. At the hepatic and splenic flexures, the mesentery is very short and may place the transverse colon in contact with the duodenum and the head of the pancreas, which may be injured during mobilization of the hepatic flexure. The splenic flexure is connected to the diaphragm by the phrenocolic ligament and to the spleen by the lienocolic ligament. The transverse colon is attached to the greater curvature of the stomach by the cephalic portion of the greater omentum, which is also referred to as the gastrocolic ligament.
The descending colon is approximately 20 to 25 cm in length; it begins at the splenic flexure and ends at the pelvic brim with the start of the sigmoid colon, which is demarcated by its intraperitoneal mesentery. The proximal part of the descending colon is attached to the peritoneum overlying the left kidney by the phrenicocolic ligament. Similar to the ascending colon, the descending colon is a retroperitoneal structure that is covered by peritoneum only on its anterior and lateral surfaces. Lateral to the descending colon is the white line of Toldt, which demarcates the correct plane to enter the retroperitoneal space to mobilize the descending colon.
The sigmoid colon begins at the pelvic brim, curves inferiorly along the left pelvic side wall over the bifurcation of the left common iliac artery, and finally runs in the midline. It is usually 45 cm long, but variations in length are very common. The taenia coli are wider than in the rest of the colon. The sigmoid mesocolon begins at the pelvic brim and becomes longer to the midpoint of the sigmoid colon and then decreases in size as it travels inferiorly. Thus the sigmoid colon is significantly longer than its mesentery.
The sigmoid colon becomes the rectum in front of the sacrum at the level at which the sigmoid colon mesentery ends and the appendices epiploicae disappear. The taeniae coli become more diffuse around the rectum and form a complete outer layer of longitudinal muscle. The longitudinal muscles merge with the perineal body and with muscles of the external sphincter. The rectum is 15 to 18 cm in length. Proximally it is of similar diameter as the sigmoid colon, but more distally it widens to the infraperitoneal ampulla, which is capable of significant distention. The upper third of the rectum is covered by peritoneum anteriorly and laterally, the middle third is covered only anteriorly, and the lower third is without peritoneal covering. The peritoneum is tented forward to the upper vagina to form the rectouterine pouch of Douglas. The rectum passes inferiorly through a ligamentous gate formed by the left and right ligamentum sacrouterinum and travels posterior to the vagina. This surgical plane between the posterior vagina and the rectum is an important landmark during surgical procedures for gynecologic cancer because here the retroperitoneum can be entered below the peritoneal reflection and the perirectal fat and the anterior rectum can be developed in preparation for the resection.
View chapterPurchase book
PREBIOTICS
M.B. Roberfroid, in Encyclopedia of Food Sciences and Nutrition (Second Edition), 2003
Fermentation in the Large Bowel: the Prebiotic Effect
The large bowel is by far the most heavily colonized segment of the human gastrointestinal tract, with up to 1012 (mostly anaerobic) bacteria per gram of gut content. These bacteria belong to a wide variety of genera, species, and strains. Through the process of fermentation, these colonic bacteria produce a wide variety of metabolites, among which the short-chain fatty acids represent salvage of part of the energy of malabsorbed food components, especially malabsorbed carbohydrates, and they play important systemic physiological roles.
Evidence for the fermentation of inulin-type fructans by bacteria colonizing the large bowel has come from in vitro and in vivo studies. At nutritional doses (up to 20–40 g per day), these malabsorbed carbohydrates are fermented quantitatively and are not excreted in the feces; the products of fermentation are gases and short-chain fatty acids, mainly acetate, butyrate, and propionate. Compared with most other malabsorbed carbohydrates (e.g., resistant starch and dietary fiber), the colonic fermentation of inulin-type fructans is accompanied by a significant change in the composition of the colonic microbiota due to selective proliferation of bifidobacteria and a concomitant reduction in the number of other bacteria, like bacteroides, fusobacteria, and pathogenic clostridia. On the basis of the results of well-designed human studies that have shown significant changes in the composition of human fecal flora, it can be concluded that inulin-type fructans (5–15 g per day for a few weeks) are prebiotic. But even though some studies showed a significant reduction in the number of pathogenic clostridia, the health benefits (e.g., reducing the risk of intestinal infections) of such a change in the composition of the colonic microbiota have yet to be established. A recent report has shown that oligofructose (daily dose of 6 g (3 × 2 g)) had no therapeutic value in patients with irritable bowel syndrome. But in an experimental model of necrotizing enterocolitis in quails, data have been reported that support the hypothesis that oligofructose might prevent overgrowth of the bacteria known to play a role in this pathology in preterm neonates.
For the other NDOs, studies in vivo have been performed with doses ranging from 3 to 15 g per day, given for periods of 1, 2, or 3 weeks. For soybean oligosaccharides, a dose of 10 g given twice daily for 3 weeks significantly increased the number of bifidobacteria, whilst slightly decreasing clostridia counts. A dose of 3 g per day increased bifidobacteria, bacteroides, and eubacteria. For the galactooligosaccharides, an increase in bifidobacteria and lactobacilli in response to doses ranging from 3 to 10 g per day has been reported. Similarly, a daily dose (5 or 10 g) of galactosylsucrose stimulated the growth of bifidobacteria after 1 and 2 weeks of ingestion. A dose of isomaltooligosaccharide of 13.5 g per day for 2 weeks significantly increased the number of bifidobacteria in adult and elderly volunteers. Early results suggest that platinose condensate may stimulate the growth of bifidobacteria. For all these NDOs, except the galactooligosaccharides, only a single human intervention study has been performed, and this will need to be repeated before any prebiotic effect can be substantiated. Moreover, as discussed above, great care should be taken to quantify the component species of the fecal microflora and to identify changes in its composition.
View chapterPurchase book
Cancer of the Colon
Bruce D. Minsky MD, ... Alan P. Venook MD, in Leibel and Phillips Textbook of Radiation Oncology (Third Edition), 2010
Anatomy
The large bowel is divided into the colon and rectum.13,14 The cecum, transverse colon, and sigmoid loop are mobile structures that lie free in the peritoneal cavity and are completely covered with serosa (visceral peritoneum). The dorsal or posterior aspect of the ascending and descending colon, and both flexures are frequently without serosa. Tumor spread from these segments may involve the retroperitoneal soft tissues, kidney, ureter, and pancreas. Although the rectum is frequently considered to be extraperitoneal, the anterior surface of the proximal third of the rectum is covered with serosa and is therefore intraperitoneal. Anatomically, the transition from sigmoid colon to rectum is marked by the fusion of the tenia of the sigmoid colon to the circumferential longitudinal muscle of the rectum at the level of the sacral promontory. This occurs approximately 12 to 15 cm from the dentate line. Patterns of recurrence of proximal rectal cancer may depend upon whether the location of the tumor is anterior or posterior.
The overall rationale of the use of adjuvant radiation therapy in colon cancer is based on the patterns of failure following potentially curative surgery. The primary determinant of failure patterns in colorectal cancer is the location of the tumor in reference to the posterior peritoneal reflection. In contrast to tumors located at or below the posterior peritoneal reflection (rectosigmoid and rectum), most tumors located above the peritoneal reflection (cecum-sigmoid), have a higher incidence of failure within the abdominal cavity.15-18 This is because colon tumors have easier access to a free peritoneal surface.
Representative series examining the patterns of failure after potentially curative surgery are seen in Table 40-2. There is much variation as to what defines failure, the method by which failure is determined, the staging system used, and whether patients with metastatic disease are excluded from analysis. Failure patterns will be lowest in series which use clinical and/or radiographic evidence of first failure,15 whereas they will be highest in series which use reoperation and/or autopsy evidence of cumulative failure.18
Treatment recommendations are based on stage and the location of tumor in reference to the posterior peritoneal reflection. If the tumor is completely above the posterior reflection it is treated as a colon cancer. If any portion is at or below the reflection, it is treated as a rectal cancer. However, if a sigmoid or cecal cancer is adherent to a pelvic structure (cT4), the local recurrence rate is similar to a rectal cancer, and it is treated as such with preoperative combined chemotherapy and radiation.
View chapterPurchase book
Gastrointestinal Diseases
Ashwin N. Ananthakrishnan, Ramnik J. Xavier, in Hunter's Tropical Medicine and Emerging Infectious Diseases (Tenth Edition), 2020
Megacolon
Patients with large bowel dilatation may be ill appearing with abdominal pain, distension, and tenderness. Toxic megacolon can complicate any of the infectious colitides. It is also seen in fulminant colitis from the inflammatory bowel diseases and is rarely due to drug-induced intestinal hypomotility. Abdominal examination is remarkable for a distended abdomen with absence of bowel sounds. Plain film of the abdomen shows a markedly distended colon. Stool should be sent for bacterial culture, C. difficile toxin, and examination for ova and parasites. However, regardless of the etiology, in the setting of toxicity the treatment is colectomy, as the risk of bowel perforation and peritonitis is high without such treatment. In contrast, some patients may have chronic large bowel dilatation without systemic toxicity. This results in constipation due to chronic intestinal pseudo-obstruction. It may be due to acquired absence of the ganglions in the enteric nervous plexus, as in Chagas disease. Treatment of such cases is often supportive with a bowel regimen and avoiding agents with antimotility properties.
View chapterPurchase book

About ScienceDirect
Remote access
Shopping cart
Advertise
Contact and support
Terms and conditions
Privacy policy
Weekly Power Status
-- Power
Ranking 
-- Power
stone