Published on 10/05/2015 by admin

Filed under Gastroenterology and Hepatology

Last modified 10/05/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 1.2 (31 votes)

This article have been viewed 9124 times


Figure 3-1 Normal ampulla of Vater (arrow).

Imaging Evaluation of the Duodenum

Historically visualization of the duodenum involved UGI contrast studies, but this has now been largely replaced by esophagogastroduodenoscopy (EGD). UGI contrast studies are now usually reserved to evaluate postoperative situations rather than disease de novo. The CT evaluation of the duodenum, though, has become more important. At fluoroscopy and UGI, the duodenal bulb had typically been the area of greatest interest, mainly because of the propensity of duodenal ulcers in the past. These ulcers are now far less common because of effective medications targeting gastric acid production and antibiotic treatment for Helicobacter pylori bacteria (see later in chapter). Good single-contrast or double-contrast technique is required to fully evaluate the duodenal bulb. The double-contrast technique, like optimized evaluation of the stomach, is somewhat of an art, and considerable expertise is required to assess patients with the variable anatomy, disease, or both.
The duodenal bulb is typically situated in a posterolateral axis (this can readily be appreciated through observation of its position at axial computed tomography [CT]), knowledge of which is required to fully evaluate bulb disease. The bulb will likely fill adequately with contrast once the patient is positioned in the right side down partial decubitus position. Once filled with barium, the bulb should be brought en face (perpendicular) to the x-ray beam, which usually requires positioning the patient right side up (right anterior oblique). At this point, the bulb should be adequately coated and distended with gas as a double-contrast view. Sometimes the bulb projects directly posteriorly and can be hard to view en face, but rotation of the patient into various positions (e.g., lateral) should bring the bulb en face, sometimes with the patient in a semiprone rather than semisupine position. Other times, the bulb can only be best viewed with the patient standing, which permits the weight of the gastric antrum to “fall away,” exposing the relatively fixed duodenal bulb.
Duodenal folds are usually best evaluated in the semisupine (right side up) position, and compression paddles may be required to move the gastric antrum away. In this semisupine position, ulcers may be seen as the pooling of barium on the posterior wall or radiolucent areas on the anterior wall (because the denser barium is now dependent on the posterior wall). Conversely, with the patient in a semiprone position (left side up or left anterior oblique), the barium will pool into ulcers on the anterior wall and not the posterior wall. As with any contrast fluoroscopic technique, any identified disease must be viewed tangentially, and multiple spot views must be taken. Ulcers may not be seen within duodenal folds, unless they are seen tangentially as they protrude outside the duodenal mucosa.
Hypertonic duodenography is a valuable tool for the evaluation of duodenal disease, including the bulb, but is now rarely performed. Hypertonic duodenography is achieved through temporary duodenal spasm after the administration of antispasmodics (glucagon or anticholinergics). Glucagon is relatively contraindicated in diabetics, and patients who are receiving anticholinergic agents should not drive vehicles for up to 4 hours because of the loss of visual accommodation. With appropriate bulb positioning, distortions in the duodenal wall, usually from ulcer disease, should be readily appreciated. If an abnormality is identified, views in multiple planes must be obtained to extract the most diagnostic information from the imaging examination. The second, third, and fourth parts of the duodenum are usually evaluated with single-contrast studies, although hypertonic duodenography should also temporarily distend at least the second part of the duodenum.
CT is not the primary modality for investigating the duodenum but can provide an excellent visualization of gross duodenal disease, including some congenital anomalies, duodenitis, and mural neoplastic lesions, particularly malignant masses. Positron emission tomography/computed tomography (PET/CT) is rarely used unless metastatic spread of duodenal malignancies is being evaluated, in which case it can identify small metastatic nodes that might otherwise be considered indeterminate by CT.

Congenital Duodenal Anomalies

Duodenal Atresia and Web

Duodenal atresia presents very early after birth because of the complete obstruction of the duodenum from the intrauterine failure of duodenal cannulation, which is often associated with Down syndrome. Patients vomit their feeding, and on plain image, a characteristic “double bubble” is identified representing a gas-filled duodenum proximal to the complete obstruction and an enlarged, gas-filled stomach (Fig. 3-2). Duodenal webs are a form of duodenal atresia, although the duodenal obstruction is not complete; rather there is a diaphragm or membrane or web that causes duodenal stenosis (Fig. 3-3). These may persist into adulthood and present with an intraluminal diverticulum. The thin membrane or web can become stretched and propelled toward the distal duodenal lumen by constant peristalsis, creating the so-called windsock deformity (Fig. 3-4).
Figure 3-2 Plain abdominal film in a neonate with dilatation of the stomach (large arrow) and duodenum (small arrow) creating the double bubble sign caused by duodenal atresia.
Figure 3-3 UGI swallow in a neonate demonstrating a duodenal obstruction (arrow) from a congenital duodenal web.
Figure 3-4 UGI series demonstrates a tubular filling defect (windsock) in the duodenum due to an intraluminal diverticulum (arrow).

Duodenal Duplication

Congenital duplication of the duodenum can be cystic or tubular and may or may not communicate with the lumen. Most are cystic and noncommunicating and located along the medial second part of the duodenum. Patients can have duodenal obstruction, and peptic ulceration or pancreatitis can also occur. At UGI series the affected duodenum is narrowed and displaced in the noncommunicating type, but contrast may fill the cyst when the duplication is communicating. The duplication may be more easily appreciated when it is extraluminal, often identified as a cystic structure medial to the duodenal C-sweep. CT or magnetic resonance imaging (MRI) will usually demonstrate the duplication better (Fig. 3-5). Other diagnoses, including choledochocele, pancreatic pseudocyst, and duodenal diverticulum, may have similar imaging appearances.
Figure 3-5 Coronal T2-weighted MRI in a 34-year-old woman with a hyperintense, smooth, rounded submucosal duodenal mass (arrow) due to duodenal duplication.

Midgut Malrotation

Midgut malrotation results from malrotation in utero as the duodenum rotates. It is the result of incomplete rotation that is recognized by the ligament of Treitz (represents the junction of the duodenum and jejunum) not migrating to its normal position to the left of the spine. Depending on the degree of malrotation, the ligament of Treitz will be located more inferiorly and to the right. In complete malrotation, it will be located to the right of the spine (Fig. 3-6). The cecal position will vary, usually in the left side of the abdomen with complete malrotation. The intestinal tract is susceptible to volvulus due to abnormal mesenteric anatomy (Fig. 3-7).
Figure 3-6 UGI series and follow-though demonstrating midgut malrotation. The duodenum fails to cross over the midline (arrow).
Figure 3-7 Coronal contrast-enhanced CT in a 33-year-old man demonstrating a left-sided liver (curved arrow) and right-sided bowel (arrow). The third and fourth parts of the duodenum do not cross the midline. Volvulus of the small bowel has also occurred, and there is small bowel obstruction.

Midgut Volvulus

Midgut volvulus is usually diagnosed in childhood and rarely in adulthood. It is an incomplete rotation of the midgut in utero that renders patients susceptible to a volvulus around a congenitally abnormal small bowel mesentery. At UGI series, there is an abrupt tapering of the third part of the duodenum, which is obstructed. Imaging is now usually performed with CT, which identifies a corkscrew or spiral appearance of the mesentery, with the duodenal-jejunal junction positioned inferiorly and to the right of its normal position at the ligament of Treitz (Fig. 3-8). The normal positioning of the superior mesenteric artery (SMA) and superior mesenteric vein (SMV) are frequently reversed (normally the SMA lies to the left of the SMV). UGI series can also demonstrate the corkscrew appearance (Fig. 3-8). An alternative cause of congenital volvulus is a Ladd band, which is an abnormal fibrous band of tissue at the root of the small bowel mesentery. This abnormality of the mesenteric root also predisposes the patient to malrotation.
Figure 3-8 UGI series (A) and axial contrast-enhanced CT (B) in a 54-year-old woman with a midgut volvulus (arrows) caused by Ladd bands.

Paraduodenal Hernia

Paraduodenal hernias result from congenitally incomplete peritoneal fixation onto the posterior abdominal cavity, creating abnormal peritoneal spaces into which the duodenum and other small bowel can herniate. Therefore the small bowel can be seen in abnormal locations. If it is on the right, the second, third, and fourth parts of the duodenum can be displaced to the right. Left-sided paraduodenal hernias are more common, however, and can sequester large parts of the small bowel into the left upper quadrant, leaving only a small loop of bowel to connect to a normally positioned cecum.

Duodenal Diverticulum

Extraluminal diverticula are not true diverticula because they represent mucosal herniation through the muscular wall, but they are very common and are frequently identified incidentally at CT or UGI series, occurring mostly on the medial aspect of the second part of the duodenum at or just beyond the periampullary region (Figs. 3-9 and 3-10). Sometimes they can be very large (Fig. 3-11). Less commonly they are in the third and fourth parts of the duodenum (Fig. 3-12). They typically fill with fluid, gas, or both, and knowledge of their frequency, appearance, and location should avoid an erroneous diagnosis of a periduodenal mass or abscess. They are usually insignificant, but there is a risk of inadvertent perforation by endoscopy or feeding-tube placement. Diverticulitis can develop in large diverticula, resulting in fever and upper abdominal pain.
Figure 3-9 Axial contrast-enhanced CT in a 61-year-old man with a duodenal diverticulum (arrow) with an air/barium fluid level.
Figure 3-10 UGI series in a 38-year-old man with two medial duodenal diverticula (arrows).
Figure 3-11 UGI series in a 65-year-old man with a large medial duodenal diverticulum (arrow). Duodenal folds can be seen entering the diverticulum. There is an incidental inferior vena cava filter in situ.
Figure 3-12 UGI series in a 61-year-old woman with multiple duodenal diverticula (arrows).

Pancreatic Rests

Also known as ectopic pancreas, pancreatic rests are congenital remnants of pancreatic tissue that are most commonly found in the first and second part of the duodenum, although they have also been reported elsewhere in the small bowel and stomach. They are clinically insignificant and usually asymptomatic. They are identified at UGI series or EGD, where they appear as a smooth round or lobulated mucosal filling defect approximately 1 to 2 cm in diameter. A classic central dimple filled with barium, representing the pancreatic ductule remnant, may or may not be present, but it is diagnostic if it is present (Fig. 3-13).
Figure 3-13 UGI series demonstrating a small duodenal bulb mass with a central barium collection caused by a pancreatic rest (arrow).

Annular Pancreas

Annular pancreas is an embryological abnormality of pancreatic development that results in the narrowing of the second part of the duodenum because of circumferential constriction by the pancreas. Normal embryological pancreatic development involves a single dorsal and two ventral buds (which fuse early). With normal intestinal rotation at about 7 weeks of gestation, the fused ventral bud rotates behind the duodenum from right to left to fuse with the dorsal bud and forms part of the pancreatic head and the uncinate. Failure of the ventral bud to rotate normally leaves the duodenum encircled by pancreatic tissue. It may remain asymptomatic, particularly with incomplete forms, but complete forms, which may not become symptomatic until adulthood, may require a gastroenterostomy rather than the simple release of the pancreatic annular tissue. At UGI series there is a characteristic narrowed, band-like, and uniform circumferential stricture in the midportion of the second part of the duodenum (Fig. 3-14). CT readily identifies the circumferential pancreatic tissue (Fig. 3-15).
Figure 3-14 UGI series in a 45-year-old woman with a stricture of the second part of the duodenum (arrow) caused by an annular pancreas.
Figure 3-15 Axial (A) and coronal (B) contrast-enhanced CT in a 73-year-old woman with pancreatic annular pancreas (arrows) that almost completely occludes the duodenal lumen.

Superior Mesenteric Artery Syndrome

Although SMA syndrome is a congenital abnormality, it usually presents in adulthood, often after significant weight loss from severe acute illness. The theory is that as the retroperitoneal fat is metabolized, the angle between the proximal SMA and aorta becomes more acute, thereby compressing the duodenum that passes left to right immediately beneath this angle. Duodenal and gastric distention then occurs near the obstruction. The diagnosis is made in the correct clinical setting with contrast-enhanced CT demonstrating the features of a dilated duodenum, marked narrowing of the duodenum as it passes behind the SMA, and a relative paucity of retroperitoneal fat (Fig. 3-16). Duodenal narrowing at the level of the SMA, though, can also be a normal finding, and correlation with clinical symptoms is required.
Figure 3-16 UGI (A) and axial (B) contrast-enhanced CT in a 65-year-old woman demonstrating gastric and duodenum dilatation (arrow in A) and stricture formation (arrow in B) due to superior mesenteric artery syndrome.

Duodenal Bulb Disease

There are a finite number of duodenal bulb diseases, most of which are benign (Box 3-1). Malignant lesions are rare. Normal anatomical structures can impress upon the duodenum (colon and gallbladder), which creates a smooth effacement of the duodenal bulb (Fig. 3-17).
Box 3-1   Duodenal Bulb Abnormalities
Heterotopic gastric mucosa
Brunner gland hypertrophy and adenoma
Flexural pseudotumor
Peptic erosions and ulcer
Neoplastic (GIST, adenoma, carcinoma, lymphoma)

GIST, Gastrointestinal stromal tumor.

Figure 3-17 UGI series in a 39-year-old woman with smooth effacement of the duodenal bulb (arrow) caused by duodenal compression by the gallbladder.

Heterotopic Gastric Mucosa

Heterotopic gastric mucosa represents ectopic gastric mucosa most often situated in the duodenal bulb, although it can occur in the esophagus, jejunum, and even ileum. It can be recognized usually only at double-contrast UGI (or EGD) as small, plaque-like filling defects in a mosaic-like pattern (Fig. 3-18).
Figure 3-18 UGI in a 61-year-old woman with multiple small filling defects in the duodenal bulb (arrow) caused by ectopic gastric mucosa.

Brunner Gland Hyperplasia

Brunner glands secrete alkali, protecting the proximal small intestine from the hyperacidity produced by the gastric mucosa. The cause of their enlargement is uncertain, but multiple Brunner glands can be seen in the duodenal bulb, extending for a short distance into the second part of the duodenum. They are visualized on UGI series, particularly with double-contrast views, which demonstrate multiple small (<5 mm) nodular filling defects (strawberry-like) in the distended duodenal bulb (Fig. 3-19). When there is only one, it is known as Brunner gland adenoma or hamartoma. This can have an appearance similar to flexural pseudotumor if situated at the inferior margin between the duodenal bulb and second part of the duodenum.
Figure 3-19 UGI series in a 55-year-old man with multiple nodular filling defects in the duodenal bulb caused by Brunner gland hypertrophy (arrow).

Duodenal Flexural Pseudotumor or Pseudopolyp

Duodenal flexural pseudotumor or pseudopolyp is a normal variant in which the angle between the duodenal apex and the descending duodenum is particularly acute, and it is more common in thin, asthenic individuals. The duodenal mucosa on the inner (inferior) aspect of this abrupt angle is sometimes heaped up into the duodenal lumen, giving the spurious appearance of a mass (Fig. 3-20). Repositioning the patient on the fluoroscopy table, though, should diminish the abnormality or make it disappear altogether, which clarifies the diagnosis. At CT, it can appear as a definitive duodenal mass or polyp.
Figure 3-20 UGI series demonstrating a smooth duodenal polyp, identified as a duodenal flexural pseudopolyp (arrows).


Most causes of gastritis also cause duodenitis because of the duodenum’s proximity to the stomach (see Chapter 2). The imaging features also mimic features of gastritis, including fold thickening and erosions (Fig. 3-21). More severe ulceration can progress to a duodenal ulcer. At CT, there is duodenal wall thickening and thickened folds, but these findings are nonspecific (Fig. 3-22).
Figure 3-21 UGI in a 22-year-old woman with antral and duodenal mucosal thickening caused by gastritis (arrow) and secondary duodenitis.
Figure 3-22 Coronal (A) and axial (B) contrast-enhanced CT in a 49-year-old woman with duodenal wall thickening (arrows) caused by duodenitis.

Duodenal Ulcer

Although it still an important disease, duodenal ulcer is far less common now that H. pylori is known as a causative agent and its treatment is well understood. Furthermore, most patients are now evaluated by EGD, so radiologists will now be unlikely to see many duodenal ulcers in the course of their clinical work.
Duodenal ulcers are two to three times more common than gastric ulcers, but unlike gastric ulcers, almost all duodenal ulcers are benign. Approximately 95% occur in the duodenal bulb, with 5% being postbulbar. Ulcers arise from gastric hyperacidity or other caustic agents such as alcohol or drugs, especially aspirin and nonsteroidal antiinflammatory agents. The disease is frequently associated with the features of peptic disease in the stomach (concomitant gastric fold thickening is common).

Their appearance is best evaluated with single-contrast and double-contrast UGI series, where a persistent pooling of contrast material within the ulcer crater can be observed, especially when the ulcer crater is in the dependent position. There are smooth folds that converge on the acute ulcer (Fig. 3-23). Some ulcers form beyond the bulb and are termed postbulbar ulcers (Fig. 3-24). Most ulcers cannot be seen with CT, but deep ones are occasionally identified (Fig. 3-25). Postbulbar ulcers are more common in patients with severe gastric hyperacidity such as Zollinger-Ellison syndrome (see Chapter 2). The hyperacidity can be so severe that duodenitis continues into the fourth part of the duodenum and even into the jejunum (Fig. 3-26).
Figure 3-23 UGI series in a 44-year-old man with thickened folds (vertical arrow) radiating toward an ulcer crater (horizontal arrow) from an acute duodenal ulcer.
Figure 3-24 UGI series in a 61-year-old woman with a postbulbar ulcer (large arrow) and radiating thickened duodenal folds (small arrows).
Figure 3-25 Axial contrast-enhanced CT in a 46-year-old woman with a perforated duodenal ulcer. There is wall thickening of the proximal duodenal wall, mild surrounding edema, and a sliver of extraluminal gas (arrow).
Figure 3-26 Axial contrast-enhanced CT in a 36-year-old man with a duodenal gastrinoma (large arrow) and Zollinger-Ellison syndrome with marked duodenal and jejunal mucosal thickening (small arrows).
The ulcer typically heals by fibrosis distorting the normal architecture of the duodenal bulb, although both acute ulcers and chronic findings can be seen at the same time (Fig. 3-27). Occasionally the ulcers can be very large, known as giant duodenal ulcers, and may mimic the configuration of the bulb itself, potentially leading the radiologist to think that the ulcer is a normal bulb. There should, however, be no duodenal folds within the ulcer itself, and there is persistent pooling of contrast rather than the contrast passing on down the duodenum from the normal peristaltic waves.
Figure 3-27 UGI series in a 66-year-old woman with proximal duodenal narrowing and distortion (large arrow) caused by healing from chronic duodenal ulcer disease. A tiny acute ulcer is also present (small arrow).
The most serious complication is perforation caused by transmural penetration of the ulcer, which mainly occurs into the peritoneum because most (95%) bulbar ulcers are on the anterior wall. Less commonly, retroperitoneal perforation occurs from the rarer posterior wall ulcers. Subtle perforation may require CT analysis with lung “window” contrast settings; otherwise, subtle extraluminal gas may be missed. Perforation can also cause severe hemorrhage with profuse hematemesis or melena. The ulcer itself is often not identified at CT, but the diagnosis is strongly suggested by duodenal mucosal thickening and periduodenal inflammation (stranding), fluid, and gas (Fig. 3-28). Sometimes there is profuse gas that can be both intraperitoneal and extraperitoneal (Fig. 3-29

Buy Membership for Gastroenterology and Hepatology Category to continue reading. Learn more here