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Case Report |
1
Mallinckrodt Institute of Radiology, Washington University School of Medicine,
St. Louis, MO 63110.
2
Department of Radiology, F. Edward Hébert
School of Medicine, Uniformed Services University of the Health Sciences,
Bethesda, MD 20814.
3
Department of Radiology, National Naval Medical Center, 8901 Wisconsin Ave.,
Bethesda, MD 20889-5600.
Received March 19, 2001;
accepted after revision April 26, 2001.
The opinions and assertions contained herein are the private views of the
authors and are not to be construed as official or as reflecting the views of
the Department of the Navy or the Department of Defense.
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The patient was admitted to a hospital where he was given an oral corticosteroid; cyclophosphamide was withheld. Upon transfer to our center, he was placed on empiric antibiotic therapy (including clindamycin) for continued temperature spikes. Cylcophosphamide was started shortly thereafter, at which time he developed crampy abdominal pain and guaiac-positive diarrhea. CT of the abdomen was performed to evaluate for C. difficile colitis; findings showed no evidence of bowel wall thickening or pericolonic inflammation (Fig. 1A). Air-space consolidation was present at the lung bases (Fig. 1B). The patient was placed on IV metronidazole pending stool assay for C. difficile cytotoxin.
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Several days later, however, his abdominal symptoms greatly worsened. Repeated CT of the abdomen revealed marked interval change with diffuse wall thickening and mural striation of both small and large bowel with extensive surrounding inflammatory changes (Figs. 1C and 1D). Because the co-existence of small- bowel findings was more indicative of ischemia caused by vasculitis than of C. difficile colitis, high-dose pulsed steroid therapy was initiated.
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Unfortunately, the patient's condition deteriorated, and he was brought to the operating room for exploratory laparotomy. Partial jejunoileal resection and subtotal colectomy were performed because he had advanced ischemia with necrosis. Portions of the remaining small bowel showed scattered foci of purplish discoloration.
Pathologic examination of the resected bowel showed extensive inflammation, hemorrhage, and transmural necrosis (Fig. 1E). Vasculitis involving small-sized vessels was identified in sections of both the mesentery and the bowel wall with acute necrotizing inflammation, fibrin deposition, and thrombosis. No granulomas were identified.
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A stormy postoperative course ensued that included three additional laparotomies with further partial resections of the duodenum, ileum, and jejunum. Remarkably, after his 6-week hospitalization, the patient was discharged to home on cyclophosphamide and corticosteroids.
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The frequency of gastrointestinal involvement in Wegener's granulomatosis is uncertain, because the few well-documented cases describe only severe disease [4, 5]. Abdominal pain, diarrhea, and hematochezia are the most common symptoms. Most textbooks and review articles covering small-vessel vasculitis of the gastrointestinal tract understandably devote their attention to the more common causes, such as Henoch-Schönlein purpura, Behçet's disease, and systemic lupus erythematosus. This stance is supported by a study of 158 patients with Wegener's granulomatosis in which no intestinal manifestations were reported [6]. However, another study involving 45 patients found abdominal symptoms in four [4]. An autopsy study of 56 cases showed necrotizing intestinal arteriolitis in 24% [1].
Unlike in the respiratory tract, granulomas are rarely identified in the intestine at pathologic examination [5]. Severe gastrointestinal involvement manifested during the early stages of disease in all previously reported cases, as in our patient. However, our patient's case appears to represent the first report of severe gastrointestinal disease without concomitant renal disease [5].
The CT findings of Wegener's granulomatosis of the bowel are not well known but are likely nonspecific when compared with other small-vessel vasculitides. Such findings include multifocal or diffuse bowel wall thickening, abnormal bowel wall enhancement, mesenteric vascular engorgement, and ascites. Associated extraintestinal findings, such as the pulmonary parenchymal infiltrates seen in our patient, may suggest a multisystemic process. In a recent radiologic review of 81 cases of vasculitis involving the gastrointestinal tract, no cases of Wegener's granulomatosis were included [7]. We were able to find only a single case report that described the CT findings of colonic involvement by Wegener's granulomatosis [8].
To our knowledge, the CT appearance of small-bowel involvement has not been previously reported. Nonetheless, the small-bowel findings in our patient were important with regard to clinical treatment because they clearly favored the diagnosis of progressive vasculitis over the clinical diagnosis of C. difficile colitis. This case report also reveals the fulminant potential of Wegener's granulomatosis as shown by serial CT examinations. Overall, CT is a useful tool for difficult clinical scenarios such as this, and it often directs appropriate patient treatment.
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  F M Shaikh, C B Sabu, T H Peirce, and S A Naqvi Extensive intestinal ischaemic necrosis in Wegener's granulomatosis. Gut, September 1, 2006; 55(9): 1368 - 1369. [Full Text] [PDF]
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