Peptic duodenal stricture causing gastric outlet obstruction: CT diagnosis with endoscopic correlation

Clinical History

A 68-year-old woman with unremarkable past medical history complained of recurrent, worsening upper abdominal pain, with associated nausea and pyrosis, unrelieved by self-prescribed antacid medications. Further questioning revealed a 10-kg weight loss during the past year.
Abnormal laboratory tests included leukocytosis, 11 mg/L C-reactive protein, 1.6 mg/dl serum creatinine, altered electrolytes.

Imaging Findings

Plain abdominal radiographs (Fig.1) showed gastric overdistension by intraluminal stagnant fluid despite recent fasting. Further investigation with contrast-enhanced multidetector CT (Fig. 2) confirmed overdistended stomach with normal mural thickness. On multiplanar image review, the contracted pylorus and proximal duodenum showed moderate, circumferential hypoenhancing mural thickening with a focal, depressed thinning of the enhancing mucosal contour. No other abnormal findings were noted, particularly concerning liver, peritoneum and lymph nodes.
After relieving gastric distension by nasogastric tube, endoscopy showed a post-pyloric ulcer with fibrinous base, oedematous hyperaemic periphery, slightly irregular mucosal surface (Fig. 3a) associated with moderately irregular stricture of the proximal duodenum (Fig. 3b). Biopsies excluded presence of neoplasia.
After intravenous hydration, proton-pump inhibitor and anti-Helicobacter pylori therapy, repeated endoscopy confirmed persistence of an impassable stricture, which ultimately required surgical treatment with duodenotomy, partial resection and Roux-en-Y gastro-enteroanastomosis. Surgical and pathologic findings confirmed peptic stricture with chronic inflammation and fibrosis. The patient did well postoperatively.

Discussion

The incidence of peptic ulcer disease (PUD) decreased worldwide since the availability of Helicobacter pylori (HP) eradication therapy and the declining prevalence of HP infection. However, despite effective medications such as H2-receptor antagonists and proton pump inhibitors, symptomatic PUD still pose a significant health concern. Partly related to use of nonsteroidal anti-inflammatory drugs including low-dose aspirin, PUD is nowadays predominantly encountered in advanced age with a 1.5:1 male predominance. Complications of PUD include endoluminal bleeding, perforation, gastric outlet obstruction (GOU) and fistulization in descending order of frequency [1-3].
GOU accounts for a minority (below 2%) of all digestive tract obstructions, and refers to blocked passage of gastric contents into the duodenum from partial or complete obstacle located at the distal stomach, pylorus, or proximal duodenum. GOU is a rare (2-3%) complication of PUD, and generally (almost 80% of cases) secondary to untreated or long-standing duodenal bulb ulcer with severe mural inflammation and/or fibrosis [1-4].
Radiographically, GOU is heralded by stomach overdistension with scarce or no air distally. Similar appearances may also result from neurogenic or medication-induced delayed gastric emptying. Before performing endoscopy to visualize the obstruction and take biopsies, further investigation with contrast-enhanced multidetector CT allows confirming mechanical obstruction and assessing its level (transition point) and probable cause. The stagnant gastric content provides luminal distension without administering oral contrast, which is poorly tolerated due to nausea and vomiting, and may potentially cause inhalation. Multiplanar CT interpretation at the workstation is recommended to elucidate the regional anatomy. PUD causing GOU is suggested by more or less symmetric, hypoattenuating pyloric-duodenal mural thickening corresponding to submucosal oedema, with interrupted mucosal enhancement or a frank ulcer outpouching through the wall, without solid tissue adjacent to the ulcer, with associated inflammatory stranding of the surrounding fat [4-6].
Compared to PUD, other causes of GOU are much more prevalent: malignancies of the pancreatic head, distal stomach and duodenum should be strongly suspected in individuals over 50 years of age. Alternatively, GOU may occur in the setting of severe acute pancreatitis, which commonly affects the medial duodenal wall and includes periduodenal fat inflammation and sometimes compression by collections. More rarely, duodenal narrowing may complicate chronic pancreatitis as consequence of fibrotic changes occurring within the duodenal wall and paraduodenal tissues, or secondary to external mechanical compression from pseudocysts [4, 7-9].

Differential Diagnosis List

Final Diagnosis

Surgically treated peptic ulcer and stricture of the duodenal bulb.

URL:	https://www.eurorad.org/case/13857
DOI:	10.1594/EURORAD/CASE.13857
ISSN:	1563-4086