PMC6191602_01
Axial and coronary views of the dissecting superior mesenteric artery on enhanced computed tomography. Dissecting superior mesenteric artery (SMA) was clearly observed, and the false lumen was enhanced at the proximal SMA (A, large arrow). The SMA was dissected spirally and was occluded at the middle portion due to thrombus formation (B, large arrow). Intestinal edema and emphysema (B, small arrow) were observed, suggesting intestinal necrosis.
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Enhanced CT revealed SMA dissection (Fig. 1A, large arrow), with the SMA dissected spirally with thrombus formation in the false lumen (Fig. 1B, large arrow). Notably, the true lumen was compressed by a false lumen at the proximal portion of the SMA, and complete obstruction was detected at the middle part of the SMA, complicated with intestinal edema and emphysema (Fig. 1B, small arrow).
Intraoperative findings of the small intestine complicated with necrosis. An intraoperative observation revealed extensive necrosis of the small intestine and the ascending colon.
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Treitz as well as the ascending colon (Fig. 2).
Histopathological findings of the small intestine. Hematoxylin and Eosin staining were performed. The structure of the intestinal villi (A, large arrow) had been destroyed by edema, vessel dilatation (A, small arrow), and lymphocyte infiltration. These findings were compatible with congestion, increased permeability of the vessels, edema, and inflammation, suggesting acute malperfusion of the small intestine. Thickening of the intima and fat deposition were observed within the small vessels of the small intestinal tissue (B and C, small arrow). Foam cells were not observed in the present specimen.
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Therefore, the surgeons decided to perform extensive small intestinal resection and ascending colon resection, despite the risk that short-bowel syndrome may sometimes occur after such an operation. The histopathological findings of the intestine demonstrated that the structure of intestinal villi (Fig. 3A, large arrow) had been destroyed by severe edema, vessel dilatation (Fig. 3A, small arrow), and lymphocyte infiltration, all of which were compatible with acute malperfusion of the small intestine. Notably, atherosclerotic changes, such as thickening of the intima and fat deposition, were also observed within the small vessels of the intestinal tissue (Fig. 3B and C, small arrow).