The Gastrointestinal Tract: Colon
Endoscopy with biopsy and/or microbiological investigation is a definitive tool for the diagnosis of colonic diseases, whether inflammatory or tumoral. However, imaging techniques remain essential in the evaluation of some entities like:
Anorectal anomalies: atresia with or without fistulas (contrast examinations, US, and MR to determine its level and the presence of fistulas). Radiograph neither useful nor diagnostic.
Hirschsprung disease: a well-done low-pressure enema may detect the transition zone between the distal aganglionic segment and the proximal dilated colon, otherwise it is diff cult to assess even with biopsy
Appendicitis: US has high accuracy without radiation risks.
Diagnosis | Findings | Comments |
Neonates and Infants | ||
Congenital megacolon (aganglionic megacolon, Hirschsprung disease) Fig. 2.107a, b, p. 212 | Plain X-ray: similar to other forms of low SBO. Barium enema (lateral view): transition zone between the normal or relatively narrow aganglionic segment and the dilated bowel proximal to it. | Low intestinal obstruction caused by the absence of normal myenteric ganglion cells in a segment of the colon. Abdominal distention, failure to pass meconium in the first 24 h of life, constipation, and bilious vomiting are the predominant symptoms. |
Neonatal small left colon syndrome | (see Table 2.69 ) | |
Colonic atresia Fig. 2.108, p. 212 | Proximal dilatation with obstruction to the flow of contrast in contrast enema at the site of the atresia; distal microcolon (DD with ileal atresia). | Less common than ileal atresia. |
Post-neonatal period, infants, toddlers, and older children | ||
Organic or neurogenic megacolon | Marked air-filled colon with stools. | Organic: congenital stenosis, fibrotic strictures, post-NEC, etc. Neurogenic causes: spinal cord infarcts, cord transection, and cerebral palsy. DD: Hirschsprung disease by clinical findings and (rarely) radiographic examination. Suction biopsy. |
Chronic constipation Fig. 2.109, p. 212 Fig. 2.110, p. 213 | Large amounts of air mixed with stools throughout the entire large bowel. Acquired fecal retention, especially in the sigmoid colon and rectum. | Most common cause of colonic dilatation in infancy and school-age children. Causes: diff cult toilet training, neuropsychogenetic abnormalities, hypothyroidism, malnutrition, etc. |
Toxic megacolon | Marked dilatation of the transverse colon in particular. Nodular thickening and rigidity of the colonic wall. Increased perforation risk: air-fluid levels and ascites. | Infrequent complication of ulcerative colitis and other colitis. Enema is contraindicated. |
IT (see Table 2.68) | Predominant small bowel dilatation. A normal X-ray does not exclude intussesception (s). US is diagnostic. | Less than 5% of intussesception (s) are colocolic. |
Chilaiditi syndrome | Distended colon interposed between the liver and the anterior abdominal wall. | Common in neurologically impaired children. Abdominal wall muscle weakness promotes intestinal content accumulation. DD: subphrenic abscess. |
Sigmoid volvulus | “Coffee-bean” sign. Low obstruction | Unusual but possible. |
Neuronal degeneration | Radiographically resembles Hirschsprung disease. | |
Anal rhabdomyosarcoma | Circumferential narrowing without mucosal destruction. | Constipation. Palpable tumor. |
Other distal colonic obstructions | Huge distended bladder, hematoma, pelvic masses (abscess, tumors), hernia (diaphragmatic: transverse, inguinal: sigma). |
Diagnosis | Findings | Comments |
NEC Fig. 2.116a, b, p. 216 | Abdominal X-ray: linear or cystic pneumatosis intestinalis (submucosal or subserosal air). Portal vein gas: finely branching radiolucencies extending from the porta hepatis to the periphery of the liver. US: bright, shifting echogenic foci within the portal vein. | In premature infants weighing < 1500 g. Factors: ischemia, decreased mucus production, diminished immune response of the premature infants, Hirschsprung. Complications: perforation, strictures. |
Infectious colitis Fig. 2.117, p. 216 | Nonspecific moderate continuous and mostly generalized thickening of the colon wall. | Often due to Salmonella infection. Not a primary radiographic diagnosis. |
Chronic nonspecific enteritis: Crohn disease, ulcerative colitis (rare) Fig. 2.118, p. 216 | Crohn: Asymmetric changes in the wall. Skip lesions and fistulas. | Crohn: more frequent in the ileocecal region. DD: TB and amebic dysentery. Ulcerative colitis begins in the rectum and ascends. Fistulas are very rare. |
Pseudomembranous enterocolitis | Marked thickening of the colon wall. Mucosal irregularity and ulcerations. Pseudomembranes on contrast studies. | Complication of oral antibiotic therapy. Caused by Clostridium diff cile. |
Hemolytic uremic syndrome | Thickening of the colon with irregular narrowing of the lumen and “thumbprinting” pattern due to intramural hemorrhage. Lost of bowel wall layering. | Hemolytic anemia, renal failure, and thrombocytopenia. DD: Henoch-Schönlein purpura predominates in the small bowel and shows flow on Doppler US. US examination of the kidneys. |
Acute appendicitis | (see Table 2.68 ) | Nonfilling of the appendix occurs in 30% of normal contrast studies. |
Appendiceal abscess | Deformed cecum or rectum and adjacent bowel loops. | DD: gynecological pathology. |
Complications postappendectomy Fig. 2.120, p. 218 | Cecal filling defect due to an inflamed appendiceal stump. Cecal fistulas. | Particularly significant when they appear soon after surgery. |
Benign Tumors | ||
Lymphoid hyperplasia | Small (2–3 mm) mucosal follicles with central umbilication. | Considered normal variant. |
Juvenile polyp | Often pedunculated solitary filling defect. | Benign hyperplastic polyp; autoamputation is frequent. |
Juvenile colonic polyposis | Multiple round filling defects. | Malignant degeneration has not been described. |
Generalized juvenile gastrointestinal polyposis | Changes throughout the GI tract. | Histology. |
Hereditary adenomatous colonic polyposis | Multiple polyps of various sizes. | Premalignant; autosomal dominant (AD); histology. |
Adenomatous polyps of the colon (Gardner and Turcot syndromes) | Sessile or pedunculated. | Malignant degeneration is described. |
Cavernous hemangioma Fig. 2.121a, b, p. 218 | Nodular or polypoid wall thickening with flow detected on Doppler US; phleboliths. | Prone to hemorrhage; may involve any segment of GI tract. |
Malignant Tumors | ||
Non-Hodgkin lymphoma Fig. 2.122a, b, p. 218 | Several patterns; homogenously hypoechoic high vascularized lesions. | Predominate in the ileocecal region; intussesception. |
Carcinoma of the colon Fig. 2.123, p. 219 | Irregular polypoid filling defect, mural rigidity, erosions crater, stenosis. | Secondary to inflammatory intestinal disease, adenomatous polyposis, sporadic. |
Diagnosis | Findings | Comments |
High anomaly without fistula | Blind-ending pouch above the I-point (lowest point of the pubis or below the tip of the ischium). Voiding cystourethrogram (VCUG). | MRI may be of help. |
Intermediate anomaly without fistula Fig. 2.125, p. 220 | Blind-ending pouch at the level of the I-point. | MRI. |
Rectourethral fistula, rectovaginal/vestibular | Demonstration of fistula with VCUG in boys or contrast filling from the anus in girls. | May present with air in bladder or meconium in urine. |
Perineal and vulvar fistulas | Retrograde contrast evaluation. | Always low anomalies. |
Transscrotal fistulas | Retrograde contrast evaluation. | Intermediate anomaly. |
Diagnosis | Findings | Comments |
Diverticulum | Isolated colonic diverticulum. | Rare. |
Duplications | The cecum accounts for about 40% of cystic colonic duplications, and its imaging features are similar to those of small bowel duplications. US: a cystic image with echogenic inner rim and outer hypoechoic muscle layers (“double-halo” sign) is highly suggestive. | Colonic duplications can be cystic or tubular, the second being more frequent in the rectum. If the cyst contains ectopic gastric mucosa or pancreatic tissue and communicates with the rectum, rectal bleeding may occur. |
Diagnosis | Findings | Comments |
Pneumatosis intestinalis (small and large bowel; see Table 2.54) | Abdominal X-ray: linear or cystic (submucosal or subserosal) air in intestinal wall. | In NEC (perforation risk). May also occur in obstruction, Hirschsprung disease, cystic fibrosis, immunosuppression, etc. |
Gastric pneumatosis | Linear or cystic lucencies in the gastric wall. | Tube malposition, after endoscopy, volvulus, ulcer disease, and from chemical damage. |
Diagnosis | Findings | Comments |
Appendicolith and foreign body | Often single round or oval calcification in the RLQ. Specific finding (just seen in the 10% of appendicitis). | Delayed surgery is indicated even if asymptomatic due to the increased risk of perforated appendicitis. |
Foreign bodies | Abdominal radiograph. | Coins, stones, marbles, metallic toys, ingested soil (geophagia). |
Calcified meconium Fig. 2.116a, b, p. 216 | Small flecks of calcification in the lumen with meconium ileus and other congenital forms of obstruction. | Neonates. |
Enterolith | Due to chronic fecal retention with anorectal anomalies. Begins as a soft-tissue density and later increased in density due to peripheral apposition of calcium salts. | |
Enterolith in a Meckel diverticulum | Rare. |