Summary
The hypothesis that equine laminitis is caused by thrombosis of vessels in the laminar corium (dermis) was investigated. Hemostatic alterations were evaluated by determining platelet count, platelet survival, platelet adhesiveness to vascular subendothelium, activated clotting time, and whole blood recalcification time. Thrombosis of vessels in the hoof wall was evaluated by scintigraphic studies of the hoof wall after administration of indium-111 (111In)-labeled platelets, contrast arteriography, and histologic examination. Platelet count remained constant before and at the onset of lameness; however, survival of 111In-labeled platelets was shortened. Scintigraphy of affected feet revealed accumulation of 111In-labeled platelets distal to the coronary band. Arteriography of disarticulated saline-perfused feet revealed marked reduction in blood supply to affected hooves. Histologic examination of the laminar dermis disclosed variable numbers of microthrombi in dermal veins of affected feet from 3 of 4 ponies with laminitis. Whole blood recalcification time was shortened at 8 hours after administration of carbohydrate and was prolonged at the onset of laminitis. Activated clotting time was prolonged at 32 hours after carbohydrate administration and at the onset of lameness. Plasma endotoxin-like activity was detected in 1 of 4 affected ponies. These data confirm that microvascular thrombosis existed at the onset of lameness in ponies with carbohydrate-induced laminitis and indicate that systemic coagulopathy may have preceded development of thrombosis.
