With extensive vascular injuries in which a vascular conduit is required, there is controversy as to whether an autogenous or prosthetic graft is preferable. The authors reviewed their experience with 91 extremity arterial injuries in which autogenous tissue was used to repair vascular injuries of the extremities. Twenty-two patients also had concomitant repair of associated venous injuries with autogenous vein grafts. Ten patients required amputations, despite patent grafts in five patients, because of severe muscle necrosis. Two patients had thrombosis of their vein grafts develop in the early postoperative period but did not require amputation. The authors identified only one late vein graft failure in a patient in whom an infected pseudoaneurysm developed. Three patients with extensive soft tissue injuries had infection develop in vein grafts, with subsequent massive bleeding that ultimately required arterial ligation. Among the 22 patients with repair of their venous injuries, occlusion of popliteal vein repairs was documented in two patients and suspected in three others. The remainder of patients had satisfactory results. The excellent results obtained in the vast majority of the authors' patients with extremity vascular injuries reinforces their preference for using autogenous tissue whenever a vascular conduit is required. Exceptions include patients with extensive soft tissue loss precluding adequate graft coverage, the repair of large vessels, and life-threatening emergencies when there is insufficient time to harvest and prepare a vein.
By using a videomicroscopy system, images of toe nail fold capillaries from 33 male smokers with atherosclerosis, 19 healthy male smoker controls, and 19 healthy male nonsmoker controls were recorded on video tape. Control subjects did not have clinical evidence of atherosclerosis. Capillary diameters were measured from the video tape with an image shearing device. The mean diameters ( t SD) for the atherosclerotic patients, nonsmoker controls, and smoker controls were 13.7 p m (k4.7 pm), 11.1 pm (?3.4 pm), and 9.6 p m ( t 3.4 pm), respectively. Statistical difference between the atherosclerotic patients and nonsmoker controls was significant at P < 0.02; the difference between the atherosclerotic patients and smoker controls was significant at P < 0.001. Statistical difference between the two control groups was not significant.These data indicate that atherosclerotic lesions elicit chronic dilation of distal cutaneous capillaries in patients who are smokers. However, comparison of these patients with tobacco smokers who are asymptomatic for atherosclerosis suggest that capillary dilation in atherosclerosis is attributable to the disease process itself and not to the effects ofcigarette smoking. This dilation of cutaneous capillaries in the atherosclerotic toe nail fold may be caused by angiogenic factors released secondary to chronic ischemia.
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