Lower extremity ulcers are a late complication of connective tissue diseases and occur more commonly in patients with this disease than in the general population. Although these lesions have historically been attributed to vasculitis, it is now recognized that inflammatory vessel injury accounts for fewer than 20% of ulcers in connective tissue disease. The pathogenesis of these lesions is complex, and often several processes act synergistically to initiate and perpetuate tissue injury. We review the evidence for antiphospholipid antibodies and prothrombotic states contributing to a vasculopathy in patients with connective tissue disease, precipitating ulceration and impairing healing.