SAM most commonly affects the renal arteries, superior mesenteric artery, and celiac artery. Dissections and aneurysms are the most common imaging findings. Follow-up imaging studies show stability or regression in most patients.
Segmental arterial mediolysis (SAM) is an uncommon, non-atherosclerotic, non-inflammatory arteriopathy that tends to affect the medium-sized splanchnic branches of the aorta along with renal, carotid, cerebral, and coronary arteries. The clinical presentation ranges from asymptomatic to severe, life-threatening intra-abdominal hemorrhage and shock. SAM overlaps clinically and radiologically with other inflammatory vasculitides. This article describes the pathologic-radiologic correlation, imaging findings, and the management of the disease. Radiologists should be familiar with this disease entity as imaging plays a crucial role in the diagnosis.
Cardiopulmonary bypass (CPB) has been demonstrated to activate platelets, producing an increased number of circulating platelets that have undergone alpha-granule release and express granule membrane protein-140 (GMP-140) on their surface. In vitro, GMP-140 mediates activated platelet adhesion to neutrophils (PMN) and monocytes, causing the formation of leukocyte-platelet conjugates. Using a newly developed assay that measures the percentage of circulating leukocyte-platelet conjugates in whole blood, we studied 17 patients undergoing CPB and have determined that (1) monocyte-platelet conjugates increased significantly during CPB, from 18% +/- 1.5% to 44% +/- 4.5% (mean +/- SEM) by the end of CPB, while PMN-platelet conjugates increased only slightly and lymphocyte-platelet conjugates decreased; (2) the time course of the increase in monocyte- and PMN-platelet conjugates paralleled that of the increase in circulating activated platelets, as determined by the presence of surface GMP-140; and (3) monocyte activation, as assessed by increased surface expression of CD11b, showed a gradual increase similar to the increase in monocyte-platelet conjugates, while PMN surface CD11b peaked immediately after the start of CPB. We conclude that CPB, through increased platelet GMP-140 expression, causes formation of monocyte-platelet, and to a lesser extent, PMN-platelet conjugates. The activation of monocytes and PMN on CPB, as evidenced by CD11b expression, occurs with differing time courses.
Intervertebral disc degeneration of any etiology may be associated with the formation of spaces or clefts within the disc. Gas collects within these spaces and can be seen roentgenographically. A case is presented in which intradiscal gas herniated into a connective tissue capsule, displacing the left S-1 nerve root and producing symptoms and signs identical to those of a herniated nucleus pulposus. The pathophysiology of gas within a disc space and the possibility that it may herniate much like the nucleus pulposus is discussed.
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