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SYNOPSISThe structure of 50 small thrombi in femoral valve pockets and the microscopic contents of 35 apparently empty pockets were studied in an attempt to ascertain the nature of the microscopic nidi from which thrombi form and their manner of growth to visible thrombi. Sixteen thrombi had little or no cellular invasion. Most of these recent structures had two main regions, red areas restricted distally in the pocket by the vein wall, and larger white regions comprising most of the thrombus length and often covering the red areas. Red areas are the early sites of cellular adhesion and invasion and the likely sites of origin of most thrombi. They were usually dominated by red cells and fibrin. White zones, which represent propagation growth, are characterized by many foci of platelets with fibrin borders (platelet-fibrin units). Some red areas also contained platelet-fibrin units but they were few and tiny; platelets were not seen in others and one small wholly red thrombus was devoid of platelets. Degenerative changes in platelet-fibrin units were observed, and it is postulated that many become purely fibrin structures. There was no significant evidence of preceding intimal damage in the vein wall. Therefore nidi are laid down on normal endothelium probably on the vein wall near the apex of the pocket. Some pockets, empty of thrombi, contained condensed foci of red cells or tiny fibrin fragments surfaced by endothelial cells and considered to be the remnants of aborted thrombi; a few contained clumps of platelets or leucocytes. It is postulated that any of these may represent the nidi from which thrombi grow. Several thrombi also incorporated large fat droplets, numerous in two. Fat embolic globules derived from fractures are their likely source.Small isolated thrombi in valve pockets (valve sinuses) are not infrequent in major deep veins of the thigh (fig 1) and calf, especially in middle-aged and elderly subjects at bed rest

1. At necropsy the arterial distribution within the head and neck of the femur was investigated by arteriographic injection in fifty-seven uninjured hips of mostly elderly subjects. 2. Before injection all vessels to the head except for one or more particular groups were divided. 3. The superior retinacular arteries were found to be the most important arterial supply to the head. Through the widely distributed branches of their lateral epiphysial vessels (superior capital) they supplied the superior, medial, central and usually the lateral parts of the head: through anastomoses they could also supply the anterior and posterior segments, the subfovea and the inferior sector, which receive separate contributions. Sometimes the inferior or the lateral connections were defective. 4. The arteries in the ligamentum teres were either absent or unimportant for the head in most subjects. Either the vessels in the ligament never reached the head or they supplied only a limited subfoveal zone. In only one out of sixteen specimens was the whole head injected through the vessels of the ligamentum teres. 5. The inferior retinacular arteries were found to be of subsidiary importance and generally supplied a variable infero-lateral part of the head, particularly posteriorly. In a small number there was an anastomotic supply to other parts of the head, but only in two out of sixteen specimens was nearly all the head injected through these vessels. 6. The regular anastomotic supply from the superior retinacular arteries to the subfovea and to the inferior part of the head was in curious contrast to the infrequent anastomotic filling of the lateral epiphysial arteries from the inferior retinacular or ligamentum teres arteries. 7. Vessels within the femoral neck sometimes supplied the lateral part of the head but never the medial three-quarters. 8. The neck of the femur received important branches from the superior retinacular arteries but only in a small number (15 per cent) was part of it entirely dependent on this supply.

SYNOPSIS Serial changes in coagulation and fibrinolysis studied among 42 patients admitted to hospital with a wide variety of injuries are reported. The first hours after trauma are dominated by an acceleration of fibrinolysis (clot lysis) and clotting time which are often followed by an abrupt rebound to prolonged fibrinolysis and normal clotting. Evidence is presented that acceleration of fibrinolysis is due to flooding of the circulation by plasminogen activator and that prolongation is probably due to an inhibitor. A prolonged prothrombin time, increased prothrombin consumption index, an acceleration of the heparin-retarded clotting time, and a fall in the platelet count are also frequent during the first hours after injury. There is evidence also of an early deficiency in factor V and the onset of a fall in factor VII and prothrombin.The following days are characterized by continued prolongation of fibrinolysis, a lengthening of clotting time, and an increased prothrombin consumption index suggestive of a defect in thromboplastin generation. Subsequent periods of prolonged fibrinolysis may develop. Prothrombin time often continues prolonged for one to three weeks and may vary phasically; plasma prothrombin and factor VII are reduced but there is now little change in factor V. The platelet count continues to fall for one to three days, then a thrombocytosis develops, often with abnormally high platelet levels, a week or so later. Plasma fibrinogen rises within 24 hours to reach a plateau maximum a few days later and levels remain high for prolonged periods in the severely injured. Various changes are related to or influenced by the severity of trauma. Mechanisms are discussed, including thrombosis in vivo, and reference is made to homeostatic significance and its possible breakdown.

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