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AT THE FOCAL POINT| VOLUME 92, ISSUE 5, P1133-1135, NOVEMBER 01, 2020
Sigmoid colon tumor with G-nas mutation presenting unique morphology
Gota Sudo, MD
Hironori Aoki, MD, PhD
Yuko Omori, MD, PhD
Hiromu Suzuki, MD, PhD
Hiroshi Nakase, MD, PhD
Published:June 09, 2020DOI:https://doi.org/10.1016/j.gie.2020.06.002
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A 64-year-old man presented to our center for follow-up colonoscopy. The colonoscopy revealed a 20-mm laterally spreading tumor in the sigmoid colon, which had elevated portions and a slightly depressed portion ( A). The magnifying endoscopic findings showed that the oral-side elevated portion had type II-like and type IV-like pit patterns, and the anal-side elevated portion had type II- and type V-like pit patterns. However, we could not assess the slightly depressed portion according to Kudo's pit pattern classification because both chromoendoscopy with indigo carmine and magnifying endoscopy with crystal violet showed microvillous structures ( B, C). On the basis of the endoscopic findings, we diagnosed this tumor as early colonic cancer and performed endoscopic submucosal dissection for removal of the tumor. Histopathologic analysis showed a low to focally high-grade adenomatous lesion with dilated cystic glands including mucin inside; stained with hematoxylin and eosin ( D). The elevated portions consisted of dilatated glands resulting from mucin production, and the surface glands were serrated. The slightly depressed portion had a thin, spirelike villous pattern, which mimicked an intestinal-type intraductal papillary mucinous neoplasm (IPMN) of the pancreas ( E). Of note, molecular biologic analysis revealed activating G-nas and K-ras mutations, whereas BRAF mutation, CpG island methylator phenotype, MLH1 methylation were not detected.
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Published online: June 09, 2020
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DOI: https://doi.org/10.1016/j.gie.2020.06.002
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© 2020 by the American Society for Gastrointestinal Endoscopy
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Colon
Large bowel containing meconium is typically T1 hyperintense and T2 hypointense, with buildup of meconium after 20 weeks facilitating identification of the rectum.
From: Clinics in Perinatology, 2009
Related terms:
Bowel Obstruction
Neoplasm
Serositis
Lesion
Diarrhea
Small Intestine
Rectum
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Development, Structure, and Function of the Tubal Gut
F.T. Bosman, P. Yan, in Pathobiology of Human Disease, 2014
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.
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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.
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Miscellaneous Abnormalities of the Colon
Richard M. Gore MD, ... Stephen E. Rubesin MD, in Textbook of Gastrointestinal Radiology (Third Edition), 2008
Diverticulitis
Large bowel obstruction is the result of diverticular disease in about 12% of cases. Diverticulitis can cause both small and large bowel obstruction. Partial colonic obstruction can complicate acute diverticulitis as a consequence of edema and pericolic inflammation or abscess formation. High-grade obstruction is uncommon; it is far more frequently caused by carcinoma of the colon. More commonly, obstruction follows recurrent attacks of diverticulitis with marked fibrosis of the colon wall leading to narrowing and eventually stricture formation. The site of obstruction is usually in the sigmoid colon, near the site of inflammation. Obstruction of the transverse or right colon attributable to diverticulitis is rare.49,50
Clinically, patients with sigmoid diverticulitis complain of left lower quadrant pain, fever, and abnormal bowel habits. It is important for these symptoms to be differentiated from those of carcinoma of the colon, an often difficult task both clinically and radiologically (Fig. 66-3 and Table 66-3). Symptoms of sigmoid colon cancer are usually more insidious, with rectal bleeding, constipation, and weight loss.51–53
Patients with suspected nonobstructing diverticulitis may benefit from CT examination as the initial study. In the acutely obstructed patient, a water-soluble contrast enema should be performed to locate the site and cause of obstruction.54–56 A more complete discussion of diverticular disease can be found in Chapter 59.
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Abdominal and abdominal-wall abnormalities
David W. Pilling, in Textbook of Fetal Abnormalities (Second Edition), 2007
Large bowel pathology
The normal large bowel is not always clearly identified in the second trimester. In the third trimester, the appearances are very varied and frequently the meconium is of low echogenicity so that the colon stands out from the other abdominal contents and can be mistaken for dilated small bowel or ureters. The typical haustral pattern and peripheral position of the bowel in the abdomen almost always enables the normal large bowel to be differentiated from dilated small bowel. Dilatation of the large bowel has been described in imperforate anus,129–131 but this condition is more frequently diagnosed postnatally following a normal antenatal scan.
Intraluminal, large-bowel calcification has been described antenatally and postnatally in imperforate anus with communication between the large bowel and the urinary tract. The reaction between urine and meconium causes the calcification.132,133 Imperforate anus is often associated with the other anomalies of the VATER association (Table 11.2), the renal and sacral abnormalities being the most frequent.
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LARGE BOWEL OBSTRUCTION
In Surgery of the Anus, Rectum & Colon (Third Edition), 2008
DIVERTICULAR DISEASE
Acute large bowel obstruction due to diverticular disease is unusual. Thus between 1977 and 1983 Koruth et al (1985a) in Aberdeen saw 74 patients with large bowel obstruction; 55 had carcinoma but only 1 patient had a diverticular stricture. Similarly Nelson and Ellis (1984) between 1962 and 1983 treated 279 patients with large bowel obstruction at the Westminster Hospital in London: 84 patients (30%) had a carcinoma, whereas only 11 (3%) had diverticular disease. McConnell et al (2003) found that of 934 patients requiring surgical resection for diverticular disease, 61 (6.5%) presented with obstructive symptoms.
The management of large bowel obstruction caused by diverticular disease is not dissimilar to that outlined for malignant large bowel obstruction. However, the role of the self-expanding metal stent in obstruction due to diverticular disease is much less well defined (Tamim et al, 2000; Forshaw et al, 2005). The surgeon is often faced with a diagnostic dilemma if an inflammatory mass is found in the sigmoid colon which is the site of the obstruction. There may be diverticula present in the rest of the colon but this finding does not assist in differentiating between the two conditions. The best policy is to assume that the mass is a carcinoma and proceed accordingly. If resection is deemed to be the best therapy, this should be as radical as possible in order to encompass the spread of the 'tumour' and to ensure adequate removal of bowel containing diverticula. The relative merits of exteriorisation and primary anastomosis are discussed in the chapter on diverticular disease (see Chapter 33).
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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
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Vascular Imaging
In Primer of Diagnostic Imaging (Fifth Edition), 2011
Lower GI hemorrhage (Fig. 8-29)
Defined as bleeding distal to ligament of Treitz. 98% of hemorrhages are located in large bowel, and 2% are located in small bowel. Endoscopy is performed to exclude rectal bleeding. Unlike the outcome with UGI hemorrhage, endoscopy is often technically not successful because bleeding obscures visualization.
Causes
Large bowel, 98%
•
Diverticulosis (most common)
•
Angiodysplasia
•
Colon carcinoma
•
Polyps
•
Inflammatory bowel disease, other colitis
•
Rectal disease
Ulcer or tear
Hemorrhoids
Tumor
Small bowel, 2%
•
Leiomyoma
•
Arteriovenous malformation
•
Ulcer (steroid therapy or transplant patients)
•
Small bowel varices
•
Other
Inflammatory bowel disease (IBD)
Diverticulosis, Meckel's diverticulum
Small bowel tumors (e.g., metastases, Kaposi sarcoma)
Radiographic Features
Scintigraphic scans are sensitive and often helpful.
•
Threshold of detection is 0.1 mL/min.
•
If scintigraphy is negative, the angiographic likelihood of a positive study is very low.
•
Prolonged imaging can detect intermittent bleeding.
Selective SMA and IMA arteriograms
•
Multiple runs should be obtained to cover entire vascular bed (colonic flexures, rectum).
•
Anomalous arteries (e.g., middle colic) may require celiac arteriogram.
Angiographic Intervention (Fig. 8-30)
•
Intraarterial vasopressin is successful in 90%. Abdominal pain may indicate ischemia.
•
Rebleed rate, 30%
•
Compared with embolization of the upper GI tract, embolization of the lower GI tract has a higher rate of complications because of less collateralization. Bowel ischemia and/or infarction occurs in 25%.
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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.
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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
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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.