A standardized injury of the nail cuticle of normal, factor VII and factor VIII deficient dogs was used to study the evolution of the morphological changes occurring within the forming and formed haemostatic plug at the site of vascular injury. The morphological changes occurring were documented by light and transmission electron microscopy (TEM). Randomized measurements were made of the distances between adjacent platelets as a function of platelet interdigitation or compaction and the degree of dilatation of the open canalicular system (OCS) was used as an indicator of the degree of platelet activation. Fibrin deposition was noted both in terms of its location and the point in time at which it first appeared. TEM demonstrated major differences between the factor VIII deficient and the normal and factor VII deficient groups. In the normal animals the intermembrane distance showed noticeable changes with the platelets becoming tightly interdigitated at the time bleeding stopped. During the same period the OCS became dilated. These changes, which were not seen in the factor VIII deficient animals, continued until many platelets lost their intracellular content and became balloon cells or ghosts and fibrinous transformation became prominent. Although those events did occur in the factor VII deficient state, each was delayed and resulted in significant differences between the factor VII and normal animals suggesting that the extrinsic pathway may play an important role in initiating the changes noted. The results suggested that the generation of thrombin and/or factor Xa is essential to promote the initial stabilization of the platelet plug as well as initiating its subsequent consolidation by fibrinous transformation.