The abdominal mesenteries are important peritoneal structures that give rise to a wide spectrum of abnormalities, including solid mesenteric masses. Despite similarities in appearance, solid masses in the mesentery may have diverse etiologies, ranging from benign to highly malignant. While metastases are the most common cause of solid masses in the mesentery, other less common conditions are also important diagnostic considerations. This article reviews four pathologic entities (sclerosing mesenteritis, carcinoid tumors, desmoids tumors, and gastrointestinal stromal tumors) that may be manifested on abdominal imaging examinations by one or more mesenteric masses. These four pathologic entities are used to present a systematic approach to the radiographic characterization of solid mesenteric masses based on the morphology of the lesions, locoregional effects, and distant findings on various abdominal imaging examinations.
Background Thromboembolism from nonstenosing carotid plaques may be an underrecognized cause of embolic strokes of undetermined source ( ESUS ). We evaluated the association between features of nonstenosing atherosclerotic plaque on computed tomographic angiography and ESUS . Methods and Results We identified consecutive acute ischemic stroke patients from 2011 to 2015 who had unilateral anterior territory infarction on brain magnetic resonance imaging and a neck computed tomographic angiography. We included ESUS cases and as controls, cardioembolic strokes. Patients with ≥50% internal carotid artery atherosclerotic stenosis ipsilateral to the stroke were excluded from this analysis. Reviewers blinded to infarct location and stroke cause retrospectively evaluated computed tomographic angiography studies for specific plaque features including thickness of the total, soft, and calcified plaque; presence of ulceration; and perivascular fat attenuation. Paired t tests and McNemar's test for paired data were used to compare plaque features ipsilateral versus contralateral to the side of infarction. Ninety‐one patients with ESUS or cardioembolic stroke were included in this study. Total plaque thickness was greater on the infarcted side (2.1±2.0 mm) than the contralateral side (1.2±1.5 mm) ( P =0.006) among ESUS cases, but not among cardioembolic cases (1.9±1.6 mm versus 1.8±1.6 mm) ( P =0.32). Conclusions Among ESUS cases, total plaque thickness was greater ipsilateral to the side of infarction than on the contralateral, stroke‐free side. No such side‐to‐side differences were apparent in cardioembolic strokes. Our findings suggest that nonstenosing large‐artery atherosclerotic plaques represent one underlying mechanism of ESUS .
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