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Original Report |
1 Department of Radiology, Hospital of the University of Pennsylvania, 3400
Spruce St., Philadelphia, PA 19104.
2 Present address: Department of Radiology, Medical College of Virginia,
Richmond, VA 23298.
Received July 7, 2003;
accepted after revision October 21, 2003.
Address correspondence to M. S. Levine
(marc.levine{at}uphs.upenn.edu).
Abstract
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CONCLUSION. Our experience suggests that ulcers in the postbulbar duodenum are considerably larger than those in the duodenal bulb and that they constitute a greater percentage of all duodenal ulcers than has previously been recognized. It is important for radiologists to be familiar with the characteristic radiographic features of postbulbar ulcers because of the increased risk of serious upper gastrointestinal tract bleeding in patients with this condition.
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We recently encountered a number of postbulbar duodenal ulcers on upper gastrointestinal tract barium examinations. A review of the radiology literature revealed that earlier descriptions of these ulcers were based on the findings of single-contrast barium studies reported more than three decades ago [1, 2, 7]. Therefore, the purpose of our investigation was to review the findings in a series of patients with postbulbar duodenal ulcers on barium studies to better characterize the clinical and radiographic features of these ulcers.
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All eight patients underwent double-contrast upper gastrointestinal tract examinations performed as biphasic studies with double-contrast images of the duodenum using an effervescent agent (Baros [dimethicone], Lafayette Pharmaceuticals) and a high-density (250% weight/volume) barium suspension (E-Z-HD, E-Z-EM) and single-contrast images of the duodenum using a low-density (100% w/v) barium suspension (Entrobar, Lafayette Pharmaceuticals). Seven patients (88%) received our standard dose of 0.1 mg of IV glucagon, and one (13%) received 1.0 mg of IV glucagon to induce gastric and duodenal hypotonia. The studies were performed at our university hospital with digital fluoroscopic equipment (Diagnost 76 Plus, Philips) and at our Veterans Affairs medical center with conventional fluoroscopic equipment (400-speed RFXII, General Electric Medical Systems). All examinations were performed by residents, fellows, or attending physicians in gastrointestinal radiology, and all were originally interpreted by the attending gastrointestinal radiologists.
The radiographic images from these eight barium studies were reviewed retrospectively by two of the authors to determine the location and size of the postbulbar duodenal ulcers, the presence or absence of luminal narrowing or obstruction, and other associated radiographic findings. Medical records were also reviewed by one author to determine the clinical presentation and treatment.
Our institutional review board approved all aspects of this retrospective study and did not require informed consent from patients whose images or records were included in our study.
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The presumptive clinical diagnoses before the barium studies included nonulcer dyspepsia in four patients (50%), biliary disease in one (13%), irritable bowel disease in one (13%), and anxiety in two (25%). The patients previously had been treated with a variety of medications, including analgesic agents, anti-secretory agents (histamine receptor antagonists and proton pump inhibitors), stool softeners, and milk of magnesia.
One patient (13%) underwent upper endoscopy 1 month before the barium study, and no abnormalities were detected in the duodenum. However, none of the patients underwent endoscopy after the barium studies to confirm the presence of a postbulbar duodenal ulcer because these individuals were all treated on the basis of the radiographic findings. After the barium studies revealed postbulbar ulcers, three patients were found to have normal serum gastrin levels, excluding a diagnosis of Zollinger-Ellison syndrome. Serum gastrin levels were not determined for the remaining five patients.
Radiographic Findings
Barium studies of the upper gastrointestinal tract revealed solitary ulcers
in the proximal descending duodenum in all eight patients (Figs.
1A,
1B,
2,
3); three (38%) were located
just distal to the apex of the duodenal bulb and five (63%) were located more
inferiorly in the proximal descending duodenum above the papilla of Vater. In
all cases, the ulcers were located on the medial (i.e., inner) wall of the
postbulbar duodenum. All ulcers were 1 cm or larger in diameter (mean, 1.6 cm;
range, 1–2 cm), and they had a mean depth of 5 mm (range, 2–7 mm).
Circumferential narrowing was seen at the level of the ulcer in four patients
(Figs. 1A,
1B and
2) and eccentric narrowing in
the remaining four (predominantly lateral in three and medial in one)
(Fig. 3). Despite this
narrowing, no evidence was seen of proximal luminal dilatation or delayed
emptying of barium from the duodenum in any patient.
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The duodenal bulb appeared normal in seven patients and was mildly deformed in one, presumably as a result of scarring from previous peptic ulcer disease. Other radiographic findings included gastroesophageal reflux in six patients, hiatal hernias in four, reflux esophagitis in two, and gastritis in four.
One patient underwent a repeated double-contrast study 4 weeks after the original study because of increasing abdominal pain. The follow-up study revealed a continued postbulbar ulcer with circumferential narrowing of the proximal descending duodenum, proximal dilatation, and delayed emptying of barium from the duodenum. Another patient underwent a repeated double-contrast study 4 months after the original study that showed complete healing of the ulcer crater.
Treatment
Three (38%) of the eight patients with postbulbar duodenal ulcers underwent
urea breath tests for Helicobacter pylori infection; one test was
positive and the other two were negative for this infection. The one patient
with proven H. pylori infection and two others with presumed H.
pylori infection (who were not tested for H. pylori) underwent
combination therapy with antibiotics and proton pump inhibitors. The two
patients without H. pylori infection and two others who were not
tested for H. pylori underwent treatment only with proton pump
inhibitors. Finally, the one patient who had duodenal obstruction on a
follow-up barium study underwent open laparotomy with a diverting
gastrojejunostomy. Unfortunately, we did not have adequate clinical follow-up
to assess patient response to surgery.
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Several aspects of their clinical presentation differentiate postbulbar duodenal ulcers from more typical ulcers in the duodenal bulb. Although bulbar ulcers are more common in men than in women, postbulbar ulcers have a striking male predominance; more than 90% having been reported in men [2, 5, 8, 9]. Similarly, in our study, all eight patients (100%) with postbulbar duodenal ulcers were men, although this finding could be related to selection bias because one of the two hospitals used for our study was a Veterans Affairs medical center in which the patient population is predominantly male. Postbulbar ulcers have also been diagnosed in patients who are, on average, 10 years older than those with bulbar ulcers [2, 5, 9, 10]. In our study, the mean age of patients with postbulbar duodenal ulcers was 63 years. Thus, postbulbar ulcers are more likely than ulcers in the duodenal bulb to be encountered in older men.
The most common presenting symptom in patients with postbulbar duodenal ulcers is chronic abdominal pain [2, 5, 7]. As in our study, however, the pain is often nonspecific and can radiate to multiple locations, including the right upper quadrant, flanks, and back, so the clinical findings may erroneously be attributed to biliary or pancreatic disease, abdominal aortic aneurysms, or even psychogenic disorders [4, 5].
The prevalence of upper gastrointestinal tract bleeding (including hematemesis, melena, and hematochezia) ranges from 35% to 87% in patients with postbulbar duodenal ulcers versus 19–44% in those with bulbar ulcers [2, 4–6, 8, 10]. Patients with postbulbar duodenal ulcers therefore appear to have a higher risk of bleeding than those with bulbar ulcers. Also, when bleeding develops in patients with postbulbar ulcers, it has been described as massive in 70–86% of patients [4, 8]. In our study, upper gastrointestinal tract bleeding occurred in six (75%) of eight patients with postbulbar duodenal ulcers, and two of these patients had massive bleeding. Therefore, patients with postbulbar ulcers are more likely to require intensive medical treatment or surgery for severe gastrointestinal bleeding than those with ulcers in the duodenal bulb.
Despite the importance of prompt diagnosis of postbulbar duodenal ulcers, these ulcers can be difficult to detect at endoscopy because of technical problems in visualizing the postbulbar duodenum with forward-viewing endoscopes [11]. In our series, a postbulbar ulcer was missed at endoscopy in the one patient who underwent this procedure. The diagnosis can even be missed at surgery because the duodenum may have a normal external appearance [7, 10]. The limitations of endoscopy and surgery in detecting postbulbar ulcers underscore the importance of accurate radiographic diagnosis of these lesions.
Postbulbar duodenal ulcers are classically manifested on single-contrast barium studies by discrete ulcer craters on the medial wall of the proximal duodenum with marked narrowing of the adjacent lumen (proximal to the papilla of Vater) because of edema and spasm or actual fibrosis and stricture formation [1, 2, 7, 8]. Similarly, all eight of our patients with postbulbar duodenal ulcers who underwent barium studies had discrete ulcer craters on the medial wall of the postbulbar duodenum above the papilla of Vater, with circumferential or eccentric narrowing of the adjacent duodenum, presumably because of some combination of edema, spasm, and scarring (Figs. 1A, 1B, 2, 3). In one patient with less severe spasm, it was possible to obtain double-contrast images of the duodenum that showed a discrete area of mass effect from edema surrounding the ulcer (Fig. 3). In most patients, however, it was difficult to obtain double-contrast images of the duodenum in the region of the ulcers because of the degree of edema and spasm (Figs. 1A, 1B and 2). This problem may be related to the fact that seven (88%) of our eight patients received a standard dose of 0.1 mg of IV glucagon rather than a larger dose (1.0 mg) to overcome such spasm. Whatever the explanation, our experience suggests that postbulbar duodenal ulcers have a similar appearance on double-contrast and single-contrast barium studies. In earlier reports, the edema and spasm accompanying postbulbar ulcers could be so severe that they prevented visualization of the ulcers on single-contrast barium studies [2, 7]. Although we are not aware of any proven postbulbar ulcers that were undetected on barium studies in our patients, we have no way of determining how often postbulbar ulcers were missed in these individuals.
All of our patients with postbulbar duodenal ulcers had sizable ulcer craters that were 1 cm or larger in diameter. In contrast, most ulcers in the duodenal bulb are less than 1 cm in diameter [12]. The larger size of ulcers in the postbulbar duodenum could indicate that they have a poorer response to medical therapy than those in the duodenal bulb. Whatever the explanation, the greater size of postbulbar ulcers presumably is responsible for the increased risk of serious upper gastrointestinal tract bleeding in these individuals.
In various studies, the prevalence of H. pylori infection has been found to range from 95% to 100% in patients with ulcers in the duodenal bulb [12]. However, to our knowledge, few data are available about the prevalence of H. pylori infection in patients with ulcers in the postbulbar duodenum. In our study, H. pylori infection was documented in only one (33%) of three patients who underwent testing for this organism. These numbers are too small to draw any firm conclusions. However, if a substantial percentage of patients with postbulbar duodenal ulcers are found not to have H. pylori infection, the larger size and increasing frequency of these ulcers compared with ulcers in the duodenal bulb could indicate that H. pylori–negative ulcers in the postbulbar duodenum are more refractory to combination therapy with antibiotics and antisecretory agents than are H. pylori–positive ulcers in the duodenal bulb. Because of the implications for patient treatment, further investigation is needed to determine whether the development of postbulbar duodenal ulcers is related to different etiologic factors from ulcers in the duodenal bulb.
Our study has a number of limitations. Because of its retrospective nature, selection bias was unavoidable. We may also have overstated the mean size of postbulbar duodenal ulcers by failing to detect small ulcers in this portion of the duodenum. Finally, only one (13%) of the eight patients in our series underwent endoscopy and only three (38%) underwent testing for H. pylori infection, so correlation of the radiographic findings with the endoscopic findings or H. pylori status of the patients was not possible in most cases.
In conclusion, our experience suggests that ulcers in the postbulbar duodenum are considerably larger than those in the duodenal bulb and that they constitute a greater percentage of all duodenal ulcers than has previously been recognized. In all cases, the ulcers appeared on barium studies as discrete niches on the medial wall of the proximal descending duodenum with circumferential or eccentric luminal narrowing but no evidence of obstruction. It is important for radiologists to be familiar with the characteristic radiographic features of postbulbar duodenal ulcers because of the increased risk of serious upper gastrointestinal tract bleeding in patients with this condition.
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