Residents’ Section • Pat tern of the Month Chang et al. Gastrointestinal Tract Filling Defects in Pediatric Patients
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Residents’ Section Pattern of the Month
Residents
inRadiology Patricia T. Chang1 Edward Y. Lee1 Ricardo Restrepo 2 Ronald L. Eisenberg 3 Chang PT, Lee EY, Restrepo R, Eisenberg RL
Keywords: gastrointestinal filling defects, pediatric patients DOI:10.2214/AJR.13.12421 Received December 13, 2013; accepted without revision January 24, 2014. 1
Department of Radiology, Boston Children’s Hospital, Harvard Medical School, Boston, MA. 2
Department of Radiology, Miami Children’s Hospital, Miami, FL. 3
Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, 300 Brookline Ave, Boston, MA 02215. Address correspondence to R. L. Eisenberg ([email protected]). WEB This is a web exclusive article. AJR 2014; 203:W3–W13 0361–803X/14/2031–W3 © American Roentgen Ray Society
Gastrointestinal Tract Filling Defects in Pediatric Patients
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iscrete gastrointestinal filling defects can result from developmental obstructive lesions of the small intestine, neoplastic causes, infectious causes, or foreign body ingestion (Table 1). Many pediatric patients with gastrointestinal filling defects present with symptoms of bowel obstruction, including abdominal pain and distention, vomiting, and obstipation. Radiography is often the initial imaging study, sometimes followed by fluoroscopy, CT, or MRI. The combination of imaging, age of the patient, clinical history, and laboratory data can usually permit substantial narrowing of the differential diagnosis and optimization of patient management. Congenital Causes Duodenal Web Duodenal web is a rare developmental anomaly caused by failure of the primitive foregut to recanalize between the ninth and 11th weeks of gestation. Associated anomalies include annular pancreas, midgut malrotation, imperforate anus, and Down syndrome. Among the different types of duodenal webs are complete duodenal atresia (imperforate web), imperforate intraluminal duodenal diverticulum (windsock web), and perforated duodenal web (intraluminal duodenal diverticulum with either a central or eccentric opening). Affected patients typically present early with feeding intolerance and bilious or nonbilious vomiting. Later symptoms include nausea, abdominal pain, progressive vomiting, and even acute pancreatitis. On abdominal radiographs, severe obstruction can lead to dilatation of the stomach and proximal duodenum, producing the classic double-bubble sign. On fluoroscopy, a windsock deformity obstructing the duodenum beyond the origin of the web can produce gradual ballooning of the duodenal diaphragm (Fig. 1). Another fluoroscopic sign is
a “duodenal dimple,” which can occur when the tip of a nasogastric tube presses on the contrast-filled web distally causing dimpling of the duodenal wall contour at the web attachment sites. Treatment options include surgical or endoscopic resection of the web or duodenoduodenostomy if there is a complete obstruction. The prognosis is usually excellent with treatment. Meckel Diverticulum Meckel diverticulum is the most common congenital abnormality of the gastrointestinal tract, occurring in approximately 2% of the population. Resulting from incomplete resorption of the omphalomesenteric (vitelline) duct, the embryonic communication between the yolk sac and the developing midgut, TABLE 1: Filling Defects in the Bowel in Children Type Congenital Duodenal web Meckel diverticulum Meconium ileus Choledochocele Neoplastic Polyps Juvenile polyposis Gardner syndrome Bannayan-Riley-Ruvalcaba syndrome Lymphoma Infectious Parasitic infection Foreign Bodies Radiopaque foreign bodies Radiolucent foreign bodies Bezoars
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Chang et al. Meckel diverticulum typically arises within 2 feet (61 cm) of the ileocecal valve on the antimesenteric border of the ileum. Most affected patients develop clinical symptoms before age 2 years. Common complications include bleeding (when the diverticulum contains ectopic gastric mucosa), bowel obstruction, inflammation, and perforation. Abdominal radiographs may be nonspecific or rarely show a right lower quadrant mass, displacement of bowel loops, and obstruction. Ultrasound may show a thickwalled, mixed echogenicity tubular structure in the right lower quadrant. An inflamed Meckel diverticulum can also present as a cyst on ultrasound, but the mucosal layers are more irregular than those typically found in an intestinal duplication. On CT, a Meckel diverticulum can be found incidentally originating from the ileum as a blind-ending structure that may show contrast opacification. The findings of an inflamed Meckel diverticulum can be similar to appendicitis, with a thick-walled blind-ending structure near the cecum associated with surrounding inflammatory changes. Therefore, it is important to differentiate these entities by documenting the presence of the normal appendix. Symptomatic Meckel diverticulum commonly manifests as a small-bowel obstruction due to volvulus and internal hernia around a mesodiverticular band, intussusception, or incarceration of the diverticulum in an umbilical or inguinal hernia. The CT findings of a small-bowel obstruction caused by Meckel diverticulum are nonspecific and similar to those resulting from other entities causing obstruction. If an intussusception cannot be reduced, a small-bowel obstruction related to a Meckel diverticulum should be considered (Fig. 2). The most specific test for Meckel diverticulum is a 99mTc pertechnetate scan, with accuracy of approximately 90%, in which the radionuclide accumulates in the mucin-secreting cells of the ectopic gastric mucosa in the diverticulum. Treatment involves surgical resection with primary closure of the small intestine. An appendectomy is also typically performed. Meconium Ileus Meconium ileus is a manifestation of intestinal and pancreatic dysfunction leading to neonatal obstruction of the distal ileum due to abnormally thick tenacious inspissated intraluminal meconium. It is the earliest presenting illness in 10–20% of patients with cystic fibrosis, which occurs in about
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90% of patients with meconium ileus. Microcolon results from distal bowel obstruction and failure of meconium to pass into the colon. Complications of meconium ileus include segmental volvulus, atresia, necrosis, and perforation with meconium peritonitis. On abdominal radiographs, there is usually a nonspecific pattern of distal small-bowel obstruction with a bubbly appearance of intestinal contents in the right lower quadrant (Fig. 3A). Intramural calcifications can also be seen as well as peritoneal calcification if there is in utero perforation. A contrast enema shows a microcolon and multiple filling defects in the distal ileum from meconium plugs (Fig. 3B). On ultrasound, there are dilated thick-walled loops of small bowel containing heterogeneous meconium. Peritoneal calcifications, echogenic ascites, and sometimes pseudocyst formation with in utero perforation can also be identified. On fetal MRI, high T1 signal intensity meconium can be identified in the microcolon or obstructed small-bowel loops. Any patient presenting with meconium ileus should be tested for cystic fibrosis. Uncomplicated meconium ileus is treated with serial hyperosmotic water-soluble enemas. Surgery is typically reserved for patients with decompensation, failed enemas, or perforation. In complicated meconium ileus, surgery is the treatment of choice, which involves resection of abnormal bowel, removal of the meconium, and primary anastomosis or temporary enterostomy. Choledochocele According to the Todani classification system, a choledochocele is a type III choledochal cyst that presents as dilatation of the intraduodenal segment of the common bile duct. Rare congenital malformations of the intrahepatic biliary tree, choledochal cysts primarily affect girls, are particularly prevalent in Japanese patients, and are thought to be risk factors for the development of cholangiocarcinoma. The classic clinical symptoms in pediatric patients are a triad of abdominal pain, palpable right upper quadrant mass, and jaundice. Patients with choledochal cysts also often present with recurrent cholangitis. Ultrasound and MRCP are currently the imaging modalities of choice for evaluating choledochal cysts in pediatric patients. Choledochoceles typically occur within the duodenal wall and protrude as a mass into the duodenal lumen. Representing 4% of choledochal cysts, they may be lined with duo-
TABLE 2: Classification of Intestinal Polyposis Syndromes Classification Hereditary Familial multiple polyposis Gardner syndrome Peutz-Jeghers syndrome Turcot syndrome Nonhereditary Cronkhite-Canada syndrome Juvenile polyposis (occasionally hereditary)
denal mucosa, biliary mucosa, or both. On MRCP, a choledochocele may appear as an intramural filling defect exerting mass effect on the duodenum (Fig. 4). Surgical resection is the current management of choice in pediatric choledochoceles, especially those causing symptoms. Choledochoceles less than 3 cm in diameter can be excised endoscopically with sphincterotomy, whereas larger lesions are resected via a transduodenal approach. Neoplastic Causes Polyps Intestinal polyposis syndromes are rare entities that can be classified as hereditary or nonhereditary (Table 2). In the pediatric age group, juvenile polyps are the most common polypoid lesions in the colon. Findings suggesting an intestinal polyposis syndrome include an alimentary tract polyp found in any young patient, two or more polyps identified in any patient, development of colon cancer in a patient under 40 years old, and presence of characteristic cutaneous manifestations associated with some of these syndromes. In familial juvenile polyposis syndrome, hamartomatous polyps can affect the entire gastrointestinal tract. This condition usually presents in childhood, unlike the adult onset of syndromes with adenomatous polyps. Patients with familial juvenile polyposis syndrome have an increased risk of developing adenocarcinoma in the stomach as well as colorectal cancer. In about 20% of patients, germline mutations involved in transforming growth factor β signaling have been identified. Barium enema or MRI can show multiple pedunculated filling defects (Fig. 5). Gardner syndrome is an autosomal dominant subtype of familial adenomatous polyposis. Caused by a mutation in the adenomatous polyposis coli gene on chromosome 5q21, it is
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Gastrointestinal Tract Filling Defects in Pediatric Patients characterized by adenomatous intestinal polyps; multiple osteomas in the skull, maxillae, and mandible; and multiple epidermoids and desmoids. Nearly all adenomatous polyps undergo malignant transformation if not treated. Patients with Gardner syndrome also have a four times increased risk of developing pancreatic adenocarcinoma and a risk of hepatoblastoma that is more than 800 times that of the general population. On barium enema or CT, Gardner syndrome appears as multiple tiny polypoid filling defects that may be associated with soft-tissue desmoids (Fig. 6). Bannayan-Riley-Ruvalcaba syndrome is a rare autosomal-dominant hamartomatous disorder linked to mutations of the PTEN gene. It is characterized by macrocephaly, hamartomatous intestinal polyps, subcutaneous and visceral lipomas, and pigmented macules involving the genitalia. BannayanRiley-Ruvalcaba syndrome typically arises in childhood, with delayed motor and intellectual development. Mural polyps can be seen on barium enema or CT (Fig. 7), although no instance of colorectal or smallbowel cancer has been reported. Most patients with polyps detected by barium enema should undergo colonoscopy to excise the polyp and search for additional neoplasms. Repeat colonoscopy should be performed in 3 years for patients at high risk for developing metachronous advanced adenomas. Colonoscopic surveillance should be considered for first-degree relatives of patients with adenomatous polyps. Lymphoma Lymphomas of the gastrointestinal tract are the most common type of primary extranodal lymphomas, representing 5–10% of all non-Hodgkin lymphomas. Primary gastrointestinal lymphomas account for 1–4% of all gastrointestinal tumors and represent about 15–20% of gastrointestinal lymphomas. Most gastrointestinal lymphomas are located in the stomach, with much fewer appearing in the small bowel, colon, and rectum. The most common signs and symptoms of lymphoma involving the gastrointestinal tract in pediatric patients include pain, weight loss, palpable mass, malabsorption, and diarrhea. Some affected pediatric patients are asymptomatic, whereas others may present with an acute abdomen due to obstruction or perforation. The most common appearance of pediatric gastrointestinal lymphoma on CT is an infiltrating form, which produces a circumferential sausage-shaped mass or aneurys-
mal dilatation on the antimesenteric border. Other intestinal manifestations of childhood lymphoma include a polypoid form producing a “target” lesion and a mesenteric form that appears as multiple round masses encasing mesenteric vessels, a larger lobulated heterogeneous mass with areas of necrosis displacing small-bowel loops, or ill-defined mesenteric fat infiltration. Intestinal lymphoma can also lead to intussusception due to abnormal bowel motility, particularly in the pediatric population (Fig. 8). Burkitt lymphoma is a highly aggressive form of non-Hodgkin lymphoma that, in the pediatric population, may present as an abdominal mass with gastrointestinal hemorrhage, abdominal pain, nausea, and intestinal obstruction caused by direct compression or intraluminal involvement. Up to 20% of patients with primary abdominal Burkitt lymphoma present with intussusception (Fig. 9). Treatment of intestinal lymphoma involves chemotherapy. Surgical resection is reserved for patients with lesions complicated by bleeding or perforation. Infectious Causes The gastrointestinal tract is the primary site of involvement by parasites during their life cycle. Although mostly endemic in underdeveloped or developing countries in which sanitation is poor, parasitic infections are now more commonly encountered in developed countries because of increased immigration and travel. Common intestinal parasitic infections include amebiasis, ascariasis, anisakiasis, strongyloidiasis, ancyclostomiasis, trichuriasis, and tapeworm disease. Ascaris lumbricoides is one of the most common parasitic infestations of the gastrointestinal tract worldwide, giardiasis is the most common protozoal disease in the United States, and amebiasis infests 10% of the world population. Common signs and symptoms of a parasitic infection include abdominal pain, diarrhea, nausea, vomiting, weight loss, malabsorption, fever, and gastrointestinal bleeding. Various parasitic infections have predilections for different locations in the body: ascariasis is typically found in the small bowel, colon, common bile duct, or pancreatic duct; giardiasis in the duodenum and jejunum; and amebiasis in the colon and liver. Ascariasis produces linear filling defects on sonographic and fluoroscopic imaging (Fig. 10). Giardiasis appears as thickened duodenal or jejunal folds on fluoroscop-
ic imaging, whereas amebiasis can present as diffuse ulcerating colitis or as a liver abscess on CT. Treatment regimens depend on the type of parasitic infection. Ascariasis is treated with antihelminthic chemotherapy with mebendazole, albendazole, or pyrantel pamoate. Giardiasis is treated with nitazoxanide or metronidazole, and amebiasis is treated with metronidazole. Foreign Bodies Foreign body ingestion is common in children, particularly those between 6 months and 3 years old. If occurring in a child younger than 6 months, foreign body ingestion should raise the suspicion of child neglect. Most swallowed objects pass through the gastrointestinal tract without difficulty. A foreign body that has progressed beyond the stomach rarely lodges in the rest of the alimentary tract. However, foreign bodies larger than 5 cm generally do not pass through the pylorus. If one foreign body is identified, the entire gastrointestinal tract from the nasopharynx to the anus should be examined to search for additional foreign bodies (Fig. 11). Complications of foreign body ingestion include perforation, obstruction, fistula or abscess formation, mediastinitis, peritonitis, and intussusception. Expulsion of an ingested foreign body should be documented either by checking the patient’s stool or with follow-up radiography. Unless there is spontaneous expulsion, all ingested radiopaque foreign bodies should be removed either endoscopically or by surgery. Radiopaque Foreign Bodies Radiopaque foreign bodies include most metallic objects (except aluminum), lead, mineral fragments (Fig. 12), and some medical pills. Coin ingestion is common in children (Fig. 13), although most cause no harm and pass through the gastrointestinal tract in a few days. However, if the coin enters the airway or becomes impacted at the thoracic inlet or the gastroesophageal junction, interventional therapy is warranted. Because of their small size and resemblance to a dime, disk (button) batteries are also commonly ingested by children. These batteries contain a variety of caustic and corrosive agents that can lead to perforation and systemic toxicity from heavy metal poisoning if the containers break. Batteries in the esophagus are especially dangerous and should be removed immediately (Fig. 14). Another dangerous scenario is the ingestion of multiple mag-
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Chang et al. netic objects, which can attract each other across the bowel walls and cause pressure necrosis of the bowel wall and subsequent perforation (Fig. 15). Children can also ingest marbles, which are not as dense as coins or magnets (Fig. 16). Sharp metallic objects are likely to penetrate the bowel or esophageal mucosal lining and cause significant injury to the bowel wall or frank perforation, which may not occur acutely or cause acute symptoms (Fig. 17). Radiolucent Foreign Bodies Radiolucent foreign bodies include most fish bones, wood, thorns, and plastics. The diagnosis of foreign body ingestion can be missed, especially if there is inadequate history or the swallowed object is not radiopaque. In selected cases, contrast-enhanced studies with barium impregnated cotton balls may help in the diagnosis of foreign body ingestion such as fish or chicken bones (Fig. 18). If there is an unusual opacity or lucency seen on radiography, CT may also be of value for further characterization and confirmation before either endoscopic or surgical removal. Bezoars Bezoars are aggregates of inedible or undigested material, which are found most commonly in the stomach. They have also been described in the esophagus and small and large intestines, although colonic bezoars are rare. Affected pediatric patients usually present with abdominal pain, nausea and vomiting, and early satiety. Complications of bezoars include obstruction, perforation, intussusception, pancreatitis, and appendicitis. Bezoars can be categorized into five major subgroups according to the type of substance: Trichobezoars and phytobezoars are the most common. Trichobezoars, which are more common in adolescent girls and patients with mental illness, can be composed of hair fibers, carpet, or string. They usually are at least partially contained within the stomach, although they can extend throughout the entire small bowel and cause
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obstruction (Rapunzel syndrome) (Fig. 19). Phytobezoars, which are composed of poorly digested fruit or vegetable material (persimmon, coconut fibers, celery, and banana seeds), are more common after gastric surgery. Lactobezoars are composed of undigested milk precipitates and typically occur in preterm infants fed with highly concentrated formula within the first few weeks of life (Fig. 20). Risk factors include poor gastric motility and dehydration. Pharmacobezoar is a complication of undissolved medication pills (Fig. 21), most frequently cholestyramine, sucralfate, enteric coated aspirin, aluminum hydroxide antacids, and such extended-release pills as nifedipine or verapamil. Lithobezoar is the name given to the ingestion of multiple foreign bodies as well as to ingestion of such miscellaneous substances as shellac, tar, dirt, and sand. The imaging appearance of a bezoar depends primarily on the types of ingested materials, which can be radiolucent or radiopaque. In general, radiographs often show increased opacities within the lumen, sometimes associated with dilated bowel loops suggesting secondary bowel obstruction. On ultrasound, they can be visualized as a hyperechoic intraluminal mass with marked acoustic shadowing. On CT or fluoroscopic imaging, the intraluminal mass can have a mottled appearance and contain contrast material or air bubbles. Treatment of bezoars depends on the underlying ingested materials but typically involves chemical dissolution or endoscopic or surgical removal. Conclusion Gastrointestinal filling defects can be caused by numerous entities, from congenital lesions to foreign body ingestions. Knowledge of the spectrum of causes is essential for timely and appropriate management of pediatric patients, particularly those presenting with bowel obstruction. Recognition of characteristic imaging features is important because it can guide treatment and may eliminate unnecessary invasive procedures such as biopsy or surgery.
Suggested Reading 1. Adeyiga AO, Lee EY, Eisenberg RL. Focal hepatic masses in pediatric patients. AJR 2012; 199:[web]W422–W440 2. Bhargava R, Au Yong KJ, Leonard N. BannayanRiley-Ruvalcaba syndrome: MRI neuroimaging features in a series of 7 patients. AJNR 2014; 35:402–406 3. Bhavsar AS, Verma S, Laba R, Lall CG, Koenigsknecht V, Rajesh A. Abdominal manifestations of neurologic disorders. RadioGraphics 2013; 33:135–153 4. Chaudry G, Navarro OM, Levine DS, Oudjhane K. Abdominal manifestations of cystic fibrosis in children. Pediatr Radiol 2006; 36:233–240 5. Crespo SM, Ramanathan RC, Kuan SF, Schoen RE. Gastric polyposis in familial juvenile polyposis. Gastrointest Endosc 2007; 66:821–822; discussion, 822 6. Elsayes KM, Menias CO, Harvin HJ, Francis IR. Imaging manifestations of Meckel’s diverticulum. AJR 2007; 189:81–88 7. Grajo JR, Kayton ML, Steffenson TS, Dragicevic N, Guidi CB. Presentation of ileal Burkitt lymphoma in children. J Radiol Case Rep 2012; 6:27–38 8. Hall JD, Shami VM. Rapunzel’s syndrome: gastric bezoars and endoscopic management. Gastrointest Endosc Clin N Am 2006; 16:111–119 9. Hunter TB, Taljanovic MS. Foreign bodies. RadioGraphics 2003; 23:731–757 10. Kotecha M, Bellah R, Pena AH, Jaimes C, Mattei P. Multimodality imaging manifestations of the Meckel diverticulum in children. Pediatr Radiol 2012; 42:95–103 11. Lee NK, Kim S, Jeon TY, et al. Complications of congenital and developmental abnormalities of the gastrointestinal tract in adolescents and adults: evaluation with multimodality imaging. RadioGraphics 2010; 30:1489–1507 12. Panjwani S, Bagewadi A, Keluskar V, Arora S. Gardner’s syndrome. J Clin Imaging Sci 2011; 1:65 13. Park MS, Kim KW, Ha HK, Lee DH. Intestinal parasitic infection. Abdom Imaging 2008; 33:166–171 14. Tam B, Salamon A, Bajtai A, et al. The real face of juvenile polyposis syndrome. J Gastrointest Oncol 2012; 3:362–368 15. Uyemura MC. Foreign body ingestion in children. Am Fam Physician 2005; 72:287–291
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Gastrointestinal Tract Filling Defects in Pediatric Patients Fig. 1—Duodenal web in 20-day-old infant with new vomiting. A, Upper gastrointestinal series image shows pooling of oral contrast material in dilated proximal duodenum (PD), with web causing abrupt obstruction. B, Delayed image shows eventual passage of contrast material through elongated stenotic segment (windsock diverticulum) (arrow).
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B Fig. 2—Meckel diverticulum in 5-year-old boy with abdominal pain. A, Ultrasound image shows layers of alternating echogenicity, consistent with intussusception (arrow). Meckel diverticulum serves as lead point and there is surrounding free fluid (F). B, Contrast-enhanced axial CT image shows Meckel diverticulum (arrow) as intussusceptum containing fat.
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Fig. 3—Meconium ileus in newborn infant with failure to pass meconium. A, Frontal abdominal radiograph shows numerous dilated bowel loops, consistent with distal obstruction. B, Contrast enema image shows microcolon, with distal ileal filling defects (arrows) representing meconium pellets.
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Fig. 4—Choledochocele in 12-year-old girl with intermittent episodes of upper abdominal pain. Coronal thin-slab MRCP image shows cystic dilatation of distal common bile duct and intramural mass (arrow), which causes mass effect on duodenum. GB = gall bladder.
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Fig. 5—Juvenile polyposis in 10-year-old boy with rectal bleeding. A, Air-contrast barium enema image shows multiple pedunculated colonic filling defects (arrows). B, Axial T2-weighted MR image of abdomen shows pedunculated polyp (arrow) in rectum.
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Gastrointestinal Tract Filling Defects in Pediatric Patients
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Fig. 6—Gardner syndrome in 21-year-old man with upper gastrointestinal bleeding, anorexia, and weight loss. A, Contrast-enhanced axial CT image shows multiple tiny polyps (arrows) projecting from gastric wall. B, Coned image shows soft-tissue desmoid (arrow), additional manifestation of Gardner syndrome.
Fig. 7—Bannayan-Riley-Ruvalcaba syndrome in 7-year-old boy with macrocephaly, dolichocephaly, cutis marmorata, and penile lentigines. Virtual colonoscopy CT image shows several mural polyps (asterisks).
Fig. 8—Intestinal lymphoma in 8-year-old boy who presented with signs of bowel obstruction. Contrastenhanced coronal CT image shows concentric layers of hyper- and hypodense tissue representing intussusception (arrow) caused by a leading point related to neoplastic process.
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Chang et al.
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Fig. 9—Gastric Burkitt lymphoma in 4-year-old boy with intermittent abdominal pain, anorexia, weight loss, constipation, and irritability. A, Contrast-enhanced axial CT image shows eccentric thickening (asterisks) of gastric wall. B, Contrast-enhanced axial CT image shows small-bowel intussusception (asterisks) due to lead point from lymphoma.
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Fig. 10—Ascariasis in 7-year-old boy from Turkey with abdominal pain and vomiting for 3 days. A, Ultrasound image shows cylindric structures (arrows) in small-bowel lumen. B, Small bowel follow-through image shows serpiginous filling defect (arrow) within small bowel, compatible with ascaris infestation.
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Gastrointestinal Tract Filling Defects in Pediatric Patients Fig. 11—Foreign body ingestion in 15-month-old girl with neck swelling and fever. A, Frontal chest radiograph reveals subtle incompletely imaged foreign body (arrow). B, Lateral radiograph of neck clearly shows foreign body (arrow) within cervical esophagus. This illustrates importance of obtaining radiographic series “from mouth to anus” in cases of suspected ingested foreign bodies.
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Fig. 13—Coin ingestion in 20-month-old girl with history of gagging. A, Frontal chest radiograph reveals coin (arrow) lodged in upper esophagus with characteristic en face appearance. B, Lateral chest radiograph confirms anatomic location of coin (arrow) within esophagus just behind trachea.
Fig. 12—Rock ingestion in 2-year-old boy. Frontal chest radiograph shows multiple irregular radiopaque foreign bodies (arrow) in esophagus.
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Fig. 14—Battery ingestion in 7-year-old girl with developmental delay who swallowed battery (unwitnessed). A, Frontal chest radiograph shows radiopaque battery (arrow), which was initially thought to represent overlying object outside of patient. Note secondary right pleural effusion. B, Image from repeat study obtained because of patient’s worsening symptoms shows interval insertion of right chest tube due to development of hydropneumothorax caused by esophageal and pleural erosion related to corrosive effects of ingested battery (arrow).
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Chang et al.
Fig. 15—Magnet ingestion in 9-year-old girl with abdominal pain. Frontal abdominal radiograph shows multiple radiopaque foreign bodies (arrow) clustered together and dilated loops of proximal small bowel (asterisks).
Fig. 16—Marble ingestion in 5-year-old boy. Frontal abdominal radiograph shows round radiopaque foreign body (arrow) overlying stomach. Note that marble is not as dense as coin or magnet.
Fig. 17—Safety pin ingestion in 6-month-old boy. Coned image from frontal radiograph of neck shows open safety pin in esophageal lumen.
Fig. 18—Chicken bone ingestion in 13-year-old boy with foreign body sensation in his throat after eating. A, Frontal radiograph of neck shows no definite radiopaque foreign body. B, Lateral radiograph from barium swallow reveals chicken bone (arrow) within esophagus, which was not seen on frontal view.
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Gastrointestinal Tract Filling Defects in Pediatric Patients
Fig. 19—Trichobezoar in 18-year-old woman who has anorexia nervosa. Contrast-enhanced axial CT image of abdomen shows filling defect (asterisk) in stomach.
Fig. 20—Lactobezoar in 35-week-old infant girl with history of continuous feedings with maltodextrinenriched infant formula who presented with food intolerance. Image from upper gastrointestinal series shows large filling defect (asterisk) in gastric lumen.
Fig. 21—Pharmacobezoar in 18-year-old woman with history of ingestion of multiple iron pills. Axial CT image shows massively dilated stomach filled with numerous undissolved pills.
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Residents’ Section Pattern of the Month
Residents
inRadiology Patricia T. Chang1 Edward Y. Lee1 Ricardo Restrepo 2 Ronald L. Eisenberg 3 Chang PT, Lee EY, Restrepo R, Eisenberg RL
Keywords: gastrointestinal filling defects, pediatric patients DOI:10.2214/AJR.13.12421 Received December 13, 2013; accepted without revision January 24, 2014. 1
Department of Radiology, Boston Children’s Hospital, Harvard Medical School, Boston, MA. 2
Department of Radiology, Miami Children’s Hospital, Miami, FL. 3
Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, 300 Brookline Ave, Boston, MA 02215. Address correspondence to R. L. Eisenberg ([email protected]). WEB This is a web exclusive article. AJR 2014; 203:W3–W13 0361–803X/14/2031–W3 © American Roentgen Ray Society
Gastrointestinal Tract Filling Defects in Pediatric Patients
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iscrete gastrointestinal filling defects can result from developmental obstructive lesions of the small intestine, neoplastic causes, infectious causes, or foreign body ingestion (Table 1). Many pediatric patients with gastrointestinal filling defects present with symptoms of bowel obstruction, including abdominal pain and distention, vomiting, and obstipation. Radiography is often the initial imaging study, sometimes followed by fluoroscopy, CT, or MRI. The combination of imaging, age of the patient, clinical history, and laboratory data can usually permit substantial narrowing of the differential diagnosis and optimization of patient management. Congenital Causes Duodenal Web Duodenal web is a rare developmental anomaly caused by failure of the primitive foregut to recanalize between the ninth and 11th weeks of gestation. Associated anomalies include annular pancreas, midgut malrotation, imperforate anus, and Down syndrome. Among the different types of duodenal webs are complete duodenal atresia (imperforate web), imperforate intraluminal duodenal diverticulum (windsock web), and perforated duodenal web (intraluminal duodenal diverticulum with either a central or eccentric opening). Affected patients typically present early with feeding intolerance and bilious or nonbilious vomiting. Later symptoms include nausea, abdominal pain, progressive vomiting, and even acute pancreatitis. On abdominal radiographs, severe obstruction can lead to dilatation of the stomach and proximal duodenum, producing the classic double-bubble sign. On fluoroscopy, a windsock deformity obstructing the duodenum beyond the origin of the web can produce gradual ballooning of the duodenal diaphragm (Fig. 1). Another fluoroscopic sign is
a “duodenal dimple,” which can occur when the tip of a nasogastric tube presses on the contrast-filled web distally causing dimpling of the duodenal wall contour at the web attachment sites. Treatment options include surgical or endoscopic resection of the web or duodenoduodenostomy if there is a complete obstruction. The prognosis is usually excellent with treatment. Meckel Diverticulum Meckel diverticulum is the most common congenital abnormality of the gastrointestinal tract, occurring in approximately 2% of the population. Resulting from incomplete resorption of the omphalomesenteric (vitelline) duct, the embryonic communication between the yolk sac and the developing midgut, TABLE 1: Filling Defects in the Bowel in Children Type Congenital Duodenal web Meckel diverticulum Meconium ileus Choledochocele Neoplastic Polyps Juvenile polyposis Gardner syndrome Bannayan-Riley-Ruvalcaba syndrome Lymphoma Infectious Parasitic infection Foreign Bodies Radiopaque foreign bodies Radiolucent foreign bodies Bezoars
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Chang et al. Meckel diverticulum typically arises within 2 feet (61 cm) of the ileocecal valve on the antimesenteric border of the ileum. Most affected patients develop clinical symptoms before age 2 years. Common complications include bleeding (when the diverticulum contains ectopic gastric mucosa), bowel obstruction, inflammation, and perforation. Abdominal radiographs may be nonspecific or rarely show a right lower quadrant mass, displacement of bowel loops, and obstruction. Ultrasound may show a thickwalled, mixed echogenicity tubular structure in the right lower quadrant. An inflamed Meckel diverticulum can also present as a cyst on ultrasound, but the mucosal layers are more irregular than those typically found in an intestinal duplication. On CT, a Meckel diverticulum can be found incidentally originating from the ileum as a blind-ending structure that may show contrast opacification. The findings of an inflamed Meckel diverticulum can be similar to appendicitis, with a thick-walled blind-ending structure near the cecum associated with surrounding inflammatory changes. Therefore, it is important to differentiate these entities by documenting the presence of the normal appendix. Symptomatic Meckel diverticulum commonly manifests as a small-bowel obstruction due to volvulus and internal hernia around a mesodiverticular band, intussusception, or incarceration of the diverticulum in an umbilical or inguinal hernia. The CT findings of a small-bowel obstruction caused by Meckel diverticulum are nonspecific and similar to those resulting from other entities causing obstruction. If an intussusception cannot be reduced, a small-bowel obstruction related to a Meckel diverticulum should be considered (Fig. 2). The most specific test for Meckel diverticulum is a 99mTc pertechnetate scan, with accuracy of approximately 90%, in which the radionuclide accumulates in the mucin-secreting cells of the ectopic gastric mucosa in the diverticulum. Treatment involves surgical resection with primary closure of the small intestine. An appendectomy is also typically performed. Meconium Ileus Meconium ileus is a manifestation of intestinal and pancreatic dysfunction leading to neonatal obstruction of the distal ileum due to abnormally thick tenacious inspissated intraluminal meconium. It is the earliest presenting illness in 10–20% of patients with cystic fibrosis, which occurs in about
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90% of patients with meconium ileus. Microcolon results from distal bowel obstruction and failure of meconium to pass into the colon. Complications of meconium ileus include segmental volvulus, atresia, necrosis, and perforation with meconium peritonitis. On abdominal radiographs, there is usually a nonspecific pattern of distal small-bowel obstruction with a bubbly appearance of intestinal contents in the right lower quadrant (Fig. 3A). Intramural calcifications can also be seen as well as peritoneal calcification if there is in utero perforation. A contrast enema shows a microcolon and multiple filling defects in the distal ileum from meconium plugs (Fig. 3B). On ultrasound, there are dilated thick-walled loops of small bowel containing heterogeneous meconium. Peritoneal calcifications, echogenic ascites, and sometimes pseudocyst formation with in utero perforation can also be identified. On fetal MRI, high T1 signal intensity meconium can be identified in the microcolon or obstructed small-bowel loops. Any patient presenting with meconium ileus should be tested for cystic fibrosis. Uncomplicated meconium ileus is treated with serial hyperosmotic water-soluble enemas. Surgery is typically reserved for patients with decompensation, failed enemas, or perforation. In complicated meconium ileus, surgery is the treatment of choice, which involves resection of abnormal bowel, removal of the meconium, and primary anastomosis or temporary enterostomy. Choledochocele According to the Todani classification system, a choledochocele is a type III choledochal cyst that presents as dilatation of the intraduodenal segment of the common bile duct. Rare congenital malformations of the intrahepatic biliary tree, choledochal cysts primarily affect girls, are particularly prevalent in Japanese patients, and are thought to be risk factors for the development of cholangiocarcinoma. The classic clinical symptoms in pediatric patients are a triad of abdominal pain, palpable right upper quadrant mass, and jaundice. Patients with choledochal cysts also often present with recurrent cholangitis. Ultrasound and MRCP are currently the imaging modalities of choice for evaluating choledochal cysts in pediatric patients. Choledochoceles typically occur within the duodenal wall and protrude as a mass into the duodenal lumen. Representing 4% of choledochal cysts, they may be lined with duo-
TABLE 2: Classification of Intestinal Polyposis Syndromes Classification Hereditary Familial multiple polyposis Gardner syndrome Peutz-Jeghers syndrome Turcot syndrome Nonhereditary Cronkhite-Canada syndrome Juvenile polyposis (occasionally hereditary)
denal mucosa, biliary mucosa, or both. On MRCP, a choledochocele may appear as an intramural filling defect exerting mass effect on the duodenum (Fig. 4). Surgical resection is the current management of choice in pediatric choledochoceles, especially those causing symptoms. Choledochoceles less than 3 cm in diameter can be excised endoscopically with sphincterotomy, whereas larger lesions are resected via a transduodenal approach. Neoplastic Causes Polyps Intestinal polyposis syndromes are rare entities that can be classified as hereditary or nonhereditary (Table 2). In the pediatric age group, juvenile polyps are the most common polypoid lesions in the colon. Findings suggesting an intestinal polyposis syndrome include an alimentary tract polyp found in any young patient, two or more polyps identified in any patient, development of colon cancer in a patient under 40 years old, and presence of characteristic cutaneous manifestations associated with some of these syndromes. In familial juvenile polyposis syndrome, hamartomatous polyps can affect the entire gastrointestinal tract. This condition usually presents in childhood, unlike the adult onset of syndromes with adenomatous polyps. Patients with familial juvenile polyposis syndrome have an increased risk of developing adenocarcinoma in the stomach as well as colorectal cancer. In about 20% of patients, germline mutations involved in transforming growth factor β signaling have been identified. Barium enema or MRI can show multiple pedunculated filling defects (Fig. 5). Gardner syndrome is an autosomal dominant subtype of familial adenomatous polyposis. Caused by a mutation in the adenomatous polyposis coli gene on chromosome 5q21, it is
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Gastrointestinal Tract Filling Defects in Pediatric Patients characterized by adenomatous intestinal polyps; multiple osteomas in the skull, maxillae, and mandible; and multiple epidermoids and desmoids. Nearly all adenomatous polyps undergo malignant transformation if not treated. Patients with Gardner syndrome also have a four times increased risk of developing pancreatic adenocarcinoma and a risk of hepatoblastoma that is more than 800 times that of the general population. On barium enema or CT, Gardner syndrome appears as multiple tiny polypoid filling defects that may be associated with soft-tissue desmoids (Fig. 6). Bannayan-Riley-Ruvalcaba syndrome is a rare autosomal-dominant hamartomatous disorder linked to mutations of the PTEN gene. It is characterized by macrocephaly, hamartomatous intestinal polyps, subcutaneous and visceral lipomas, and pigmented macules involving the genitalia. BannayanRiley-Ruvalcaba syndrome typically arises in childhood, with delayed motor and intellectual development. Mural polyps can be seen on barium enema or CT (Fig. 7), although no instance of colorectal or smallbowel cancer has been reported. Most patients with polyps detected by barium enema should undergo colonoscopy to excise the polyp and search for additional neoplasms. Repeat colonoscopy should be performed in 3 years for patients at high risk for developing metachronous advanced adenomas. Colonoscopic surveillance should be considered for first-degree relatives of patients with adenomatous polyps. Lymphoma Lymphomas of the gastrointestinal tract are the most common type of primary extranodal lymphomas, representing 5–10% of all non-Hodgkin lymphomas. Primary gastrointestinal lymphomas account for 1–4% of all gastrointestinal tumors and represent about 15–20% of gastrointestinal lymphomas. Most gastrointestinal lymphomas are located in the stomach, with much fewer appearing in the small bowel, colon, and rectum. The most common signs and symptoms of lymphoma involving the gastrointestinal tract in pediatric patients include pain, weight loss, palpable mass, malabsorption, and diarrhea. Some affected pediatric patients are asymptomatic, whereas others may present with an acute abdomen due to obstruction or perforation. The most common appearance of pediatric gastrointestinal lymphoma on CT is an infiltrating form, which produces a circumferential sausage-shaped mass or aneurys-
mal dilatation on the antimesenteric border. Other intestinal manifestations of childhood lymphoma include a polypoid form producing a “target” lesion and a mesenteric form that appears as multiple round masses encasing mesenteric vessels, a larger lobulated heterogeneous mass with areas of necrosis displacing small-bowel loops, or ill-defined mesenteric fat infiltration. Intestinal lymphoma can also lead to intussusception due to abnormal bowel motility, particularly in the pediatric population (Fig. 8). Burkitt lymphoma is a highly aggressive form of non-Hodgkin lymphoma that, in the pediatric population, may present as an abdominal mass with gastrointestinal hemorrhage, abdominal pain, nausea, and intestinal obstruction caused by direct compression or intraluminal involvement. Up to 20% of patients with primary abdominal Burkitt lymphoma present with intussusception (Fig. 9). Treatment of intestinal lymphoma involves chemotherapy. Surgical resection is reserved for patients with lesions complicated by bleeding or perforation. Infectious Causes The gastrointestinal tract is the primary site of involvement by parasites during their life cycle. Although mostly endemic in underdeveloped or developing countries in which sanitation is poor, parasitic infections are now more commonly encountered in developed countries because of increased immigration and travel. Common intestinal parasitic infections include amebiasis, ascariasis, anisakiasis, strongyloidiasis, ancyclostomiasis, trichuriasis, and tapeworm disease. Ascaris lumbricoides is one of the most common parasitic infestations of the gastrointestinal tract worldwide, giardiasis is the most common protozoal disease in the United States, and amebiasis infests 10% of the world population. Common signs and symptoms of a parasitic infection include abdominal pain, diarrhea, nausea, vomiting, weight loss, malabsorption, fever, and gastrointestinal bleeding. Various parasitic infections have predilections for different locations in the body: ascariasis is typically found in the small bowel, colon, common bile duct, or pancreatic duct; giardiasis in the duodenum and jejunum; and amebiasis in the colon and liver. Ascariasis produces linear filling defects on sonographic and fluoroscopic imaging (Fig. 10). Giardiasis appears as thickened duodenal or jejunal folds on fluoroscop-
ic imaging, whereas amebiasis can present as diffuse ulcerating colitis or as a liver abscess on CT. Treatment regimens depend on the type of parasitic infection. Ascariasis is treated with antihelminthic chemotherapy with mebendazole, albendazole, or pyrantel pamoate. Giardiasis is treated with nitazoxanide or metronidazole, and amebiasis is treated with metronidazole. Foreign Bodies Foreign body ingestion is common in children, particularly those between 6 months and 3 years old. If occurring in a child younger than 6 months, foreign body ingestion should raise the suspicion of child neglect. Most swallowed objects pass through the gastrointestinal tract without difficulty. A foreign body that has progressed beyond the stomach rarely lodges in the rest of the alimentary tract. However, foreign bodies larger than 5 cm generally do not pass through the pylorus. If one foreign body is identified, the entire gastrointestinal tract from the nasopharynx to the anus should be examined to search for additional foreign bodies (Fig. 11). Complications of foreign body ingestion include perforation, obstruction, fistula or abscess formation, mediastinitis, peritonitis, and intussusception. Expulsion of an ingested foreign body should be documented either by checking the patient’s stool or with follow-up radiography. Unless there is spontaneous expulsion, all ingested radiopaque foreign bodies should be removed either endoscopically or by surgery. Radiopaque Foreign Bodies Radiopaque foreign bodies include most metallic objects (except aluminum), lead, mineral fragments (Fig. 12), and some medical pills. Coin ingestion is common in children (Fig. 13), although most cause no harm and pass through the gastrointestinal tract in a few days. However, if the coin enters the airway or becomes impacted at the thoracic inlet or the gastroesophageal junction, interventional therapy is warranted. Because of their small size and resemblance to a dime, disk (button) batteries are also commonly ingested by children. These batteries contain a variety of caustic and corrosive agents that can lead to perforation and systemic toxicity from heavy metal poisoning if the containers break. Batteries in the esophagus are especially dangerous and should be removed immediately (Fig. 14). Another dangerous scenario is the ingestion of multiple mag-
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Chang et al. netic objects, which can attract each other across the bowel walls and cause pressure necrosis of the bowel wall and subsequent perforation (Fig. 15). Children can also ingest marbles, which are not as dense as coins or magnets (Fig. 16). Sharp metallic objects are likely to penetrate the bowel or esophageal mucosal lining and cause significant injury to the bowel wall or frank perforation, which may not occur acutely or cause acute symptoms (Fig. 17). Radiolucent Foreign Bodies Radiolucent foreign bodies include most fish bones, wood, thorns, and plastics. The diagnosis of foreign body ingestion can be missed, especially if there is inadequate history or the swallowed object is not radiopaque. In selected cases, contrast-enhanced studies with barium impregnated cotton balls may help in the diagnosis of foreign body ingestion such as fish or chicken bones (Fig. 18). If there is an unusual opacity or lucency seen on radiography, CT may also be of value for further characterization and confirmation before either endoscopic or surgical removal. Bezoars Bezoars are aggregates of inedible or undigested material, which are found most commonly in the stomach. They have also been described in the esophagus and small and large intestines, although colonic bezoars are rare. Affected pediatric patients usually present with abdominal pain, nausea and vomiting, and early satiety. Complications of bezoars include obstruction, perforation, intussusception, pancreatitis, and appendicitis. Bezoars can be categorized into five major subgroups according to the type of substance: Trichobezoars and phytobezoars are the most common. Trichobezoars, which are more common in adolescent girls and patients with mental illness, can be composed of hair fibers, carpet, or string. They usually are at least partially contained within the stomach, although they can extend throughout the entire small bowel and cause
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obstruction (Rapunzel syndrome) (Fig. 19). Phytobezoars, which are composed of poorly digested fruit or vegetable material (persimmon, coconut fibers, celery, and banana seeds), are more common after gastric surgery. Lactobezoars are composed of undigested milk precipitates and typically occur in preterm infants fed with highly concentrated formula within the first few weeks of life (Fig. 20). Risk factors include poor gastric motility and dehydration. Pharmacobezoar is a complication of undissolved medication pills (Fig. 21), most frequently cholestyramine, sucralfate, enteric coated aspirin, aluminum hydroxide antacids, and such extended-release pills as nifedipine or verapamil. Lithobezoar is the name given to the ingestion of multiple foreign bodies as well as to ingestion of such miscellaneous substances as shellac, tar, dirt, and sand. The imaging appearance of a bezoar depends primarily on the types of ingested materials, which can be radiolucent or radiopaque. In general, radiographs often show increased opacities within the lumen, sometimes associated with dilated bowel loops suggesting secondary bowel obstruction. On ultrasound, they can be visualized as a hyperechoic intraluminal mass with marked acoustic shadowing. On CT or fluoroscopic imaging, the intraluminal mass can have a mottled appearance and contain contrast material or air bubbles. Treatment of bezoars depends on the underlying ingested materials but typically involves chemical dissolution or endoscopic or surgical removal. Conclusion Gastrointestinal filling defects can be caused by numerous entities, from congenital lesions to foreign body ingestions. Knowledge of the spectrum of causes is essential for timely and appropriate management of pediatric patients, particularly those presenting with bowel obstruction. Recognition of characteristic imaging features is important because it can guide treatment and may eliminate unnecessary invasive procedures such as biopsy or surgery.
Suggested Reading 1. Adeyiga AO, Lee EY, Eisenberg RL. Focal hepatic masses in pediatric patients. AJR 2012; 199:[web]W422–W440 2. Bhargava R, Au Yong KJ, Leonard N. BannayanRiley-Ruvalcaba syndrome: MRI neuroimaging features in a series of 7 patients. AJNR 2014; 35:402–406 3. Bhavsar AS, Verma S, Laba R, Lall CG, Koenigsknecht V, Rajesh A. Abdominal manifestations of neurologic disorders. RadioGraphics 2013; 33:135–153 4. Chaudry G, Navarro OM, Levine DS, Oudjhane K. Abdominal manifestations of cystic fibrosis in children. Pediatr Radiol 2006; 36:233–240 5. Crespo SM, Ramanathan RC, Kuan SF, Schoen RE. Gastric polyposis in familial juvenile polyposis. Gastrointest Endosc 2007; 66:821–822; discussion, 822 6. Elsayes KM, Menias CO, Harvin HJ, Francis IR. Imaging manifestations of Meckel’s diverticulum. AJR 2007; 189:81–88 7. Grajo JR, Kayton ML, Steffenson TS, Dragicevic N, Guidi CB. Presentation of ileal Burkitt lymphoma in children. J Radiol Case Rep 2012; 6:27–38 8. Hall JD, Shami VM. Rapunzel’s syndrome: gastric bezoars and endoscopic management. Gastrointest Endosc Clin N Am 2006; 16:111–119 9. Hunter TB, Taljanovic MS. Foreign bodies. RadioGraphics 2003; 23:731–757 10. Kotecha M, Bellah R, Pena AH, Jaimes C, Mattei P. Multimodality imaging manifestations of the Meckel diverticulum in children. Pediatr Radiol 2012; 42:95–103 11. Lee NK, Kim S, Jeon TY, et al. Complications of congenital and developmental abnormalities of the gastrointestinal tract in adolescents and adults: evaluation with multimodality imaging. RadioGraphics 2010; 30:1489–1507 12. Panjwani S, Bagewadi A, Keluskar V, Arora S. Gardner’s syndrome. J Clin Imaging Sci 2011; 1:65 13. Park MS, Kim KW, Ha HK, Lee DH. Intestinal parasitic infection. Abdom Imaging 2008; 33:166–171 14. Tam B, Salamon A, Bajtai A, et al. The real face of juvenile polyposis syndrome. J Gastrointest Oncol 2012; 3:362–368 15. Uyemura MC. Foreign body ingestion in children. Am Fam Physician 2005; 72:287–291
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Gastrointestinal Tract Filling Defects in Pediatric Patients Fig. 1—Duodenal web in 20-day-old infant with new vomiting. A, Upper gastrointestinal series image shows pooling of oral contrast material in dilated proximal duodenum (PD), with web causing abrupt obstruction. B, Delayed image shows eventual passage of contrast material through elongated stenotic segment (windsock diverticulum) (arrow).
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B Fig. 2—Meckel diverticulum in 5-year-old boy with abdominal pain. A, Ultrasound image shows layers of alternating echogenicity, consistent with intussusception (arrow). Meckel diverticulum serves as lead point and there is surrounding free fluid (F). B, Contrast-enhanced axial CT image shows Meckel diverticulum (arrow) as intussusceptum containing fat.
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Fig. 3—Meconium ileus in newborn infant with failure to pass meconium. A, Frontal abdominal radiograph shows numerous dilated bowel loops, consistent with distal obstruction. B, Contrast enema image shows microcolon, with distal ileal filling defects (arrows) representing meconium pellets.
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Fig. 4—Choledochocele in 12-year-old girl with intermittent episodes of upper abdominal pain. Coronal thin-slab MRCP image shows cystic dilatation of distal common bile duct and intramural mass (arrow), which causes mass effect on duodenum. GB = gall bladder.
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Fig. 5—Juvenile polyposis in 10-year-old boy with rectal bleeding. A, Air-contrast barium enema image shows multiple pedunculated colonic filling defects (arrows). B, Axial T2-weighted MR image of abdomen shows pedunculated polyp (arrow) in rectum.
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Gastrointestinal Tract Filling Defects in Pediatric Patients
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Fig. 6—Gardner syndrome in 21-year-old man with upper gastrointestinal bleeding, anorexia, and weight loss. A, Contrast-enhanced axial CT image shows multiple tiny polyps (arrows) projecting from gastric wall. B, Coned image shows soft-tissue desmoid (arrow), additional manifestation of Gardner syndrome.
Fig. 7—Bannayan-Riley-Ruvalcaba syndrome in 7-year-old boy with macrocephaly, dolichocephaly, cutis marmorata, and penile lentigines. Virtual colonoscopy CT image shows several mural polyps (asterisks).
Fig. 8—Intestinal lymphoma in 8-year-old boy who presented with signs of bowel obstruction. Contrastenhanced coronal CT image shows concentric layers of hyper- and hypodense tissue representing intussusception (arrow) caused by a leading point related to neoplastic process.
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Fig. 9—Gastric Burkitt lymphoma in 4-year-old boy with intermittent abdominal pain, anorexia, weight loss, constipation, and irritability. A, Contrast-enhanced axial CT image shows eccentric thickening (asterisks) of gastric wall. B, Contrast-enhanced axial CT image shows small-bowel intussusception (asterisks) due to lead point from lymphoma.
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Fig. 10—Ascariasis in 7-year-old boy from Turkey with abdominal pain and vomiting for 3 days. A, Ultrasound image shows cylindric structures (arrows) in small-bowel lumen. B, Small bowel follow-through image shows serpiginous filling defect (arrow) within small bowel, compatible with ascaris infestation.
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Gastrointestinal Tract Filling Defects in Pediatric Patients Fig. 11—Foreign body ingestion in 15-month-old girl with neck swelling and fever. A, Frontal chest radiograph reveals subtle incompletely imaged foreign body (arrow). B, Lateral radiograph of neck clearly shows foreign body (arrow) within cervical esophagus. This illustrates importance of obtaining radiographic series “from mouth to anus” in cases of suspected ingested foreign bodies.
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Fig. 13—Coin ingestion in 20-month-old girl with history of gagging. A, Frontal chest radiograph reveals coin (arrow) lodged in upper esophagus with characteristic en face appearance. B, Lateral chest radiograph confirms anatomic location of coin (arrow) within esophagus just behind trachea.
Fig. 12—Rock ingestion in 2-year-old boy. Frontal chest radiograph shows multiple irregular radiopaque foreign bodies (arrow) in esophagus.
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Fig. 14—Battery ingestion in 7-year-old girl with developmental delay who swallowed battery (unwitnessed). A, Frontal chest radiograph shows radiopaque battery (arrow), which was initially thought to represent overlying object outside of patient. Note secondary right pleural effusion. B, Image from repeat study obtained because of patient’s worsening symptoms shows interval insertion of right chest tube due to development of hydropneumothorax caused by esophageal and pleural erosion related to corrosive effects of ingested battery (arrow).
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Fig. 15—Magnet ingestion in 9-year-old girl with abdominal pain. Frontal abdominal radiograph shows multiple radiopaque foreign bodies (arrow) clustered together and dilated loops of proximal small bowel (asterisks).
Fig. 16—Marble ingestion in 5-year-old boy. Frontal abdominal radiograph shows round radiopaque foreign body (arrow) overlying stomach. Note that marble is not as dense as coin or magnet.
Fig. 17—Safety pin ingestion in 6-month-old boy. Coned image from frontal radiograph of neck shows open safety pin in esophageal lumen.
Fig. 18—Chicken bone ingestion in 13-year-old boy with foreign body sensation in his throat after eating. A, Frontal radiograph of neck shows no definite radiopaque foreign body. B, Lateral radiograph from barium swallow reveals chicken bone (arrow) within esophagus, which was not seen on frontal view.
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Gastrointestinal Tract Filling Defects in Pediatric Patients
Fig. 19—Trichobezoar in 18-year-old woman who has anorexia nervosa. Contrast-enhanced axial CT image of abdomen shows filling defect (asterisk) in stomach.
Fig. 20—Lactobezoar in 35-week-old infant girl with history of continuous feedings with maltodextrinenriched infant formula who presented with food intolerance. Image from upper gastrointestinal series shows large filling defect (asterisk) in gastric lumen.
Fig. 21—Pharmacobezoar in 18-year-old woman with history of ingestion of multiple iron pills. Axial CT image shows massively dilated stomach filled with numerous undissolved pills.
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