Serial arterial blood-gas analyses showed a phase of primary hypoxaemia in thirty-two out of fifty fracture patients (64 per cent) without head, chest or abdominal injury. The incidence was greater in those with shaft fractures of the femur or tibia or both, than in those with fractured hips, and was related to the severity of injury and the nature of the accident. Most affected subjects were already hypoxaemic on admission to hospital: the arterial PO2 commonly fell to between 60 and 70 millimetres of mercury, and the episode generally lasted a few days. The hypoxaemia was generally subclinical but four patients developed mild clinical fat embolism. Early hypoxaemia was not found in six patients admitted with only soft-tissue injuries. One or more subsequent attacks of subclinical hypoxaemia, each lasting a few days, occurred in half of those previously affected. Most episodes followed fracture operation or manipulation. Pulmonary thromboembolism seemed responsible in two patients, but it could be excluded in others given oral anticoagulant prophylaxis from soon after admission. Pulmonary fat embolism is the most likely explanation of the primary episodes and could account for most of the subsequent periods of hypoxaemia.
1. The processes of repair and union were studied in six fractures of the lower end of the radius, ranging in age from ten days to five and a half months. 2. The major pathway to union is medullary, through the proliferation around the fracture of vascular granulation tissue with osteogenic power. This invades and then bridges the fracture and is followed by the laying down of trabeculae of new bone. 3. Success depends on the growth of new capillaries across the fracture line, some of which mature and re-establish the meduilary circulation. 4. Indriving of the lateral cortex of the proximal fragment into the distal spongy medulla at the time of injury (in Colles's fractures) permits bridging between proximal periosteal and distal meduliary callus. Otherwise periosteal proliferation plays only a subsidiary role in union. 5. Fissure fractures of the lower articular surface were frequent and they also healed by the invasion of granulation tissue proliferating in the medulla nearby.
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 ( 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.
1 . The arterial pattern and the histological features in the femoral head and neck were studied at necropsy in twenty-five specimens with intracapsular fractures. An improved visual-arteriographic method employing barium sulphate dyed with Prussian blue was used. Twenty-three of the fractures were from a few days to twenty-four weeks old and two were seven and ten years old. Nineteen had been nailed or nail-plated. 2. The results were divided into four groups according to the state of the femoral head. In the first group, four heads were histologically viable and had a normal vascular pattern; in the second group, four showed partial avascular necrosis with part of the head retaining a normal blood supply; in the third group, ten had avascular necrosis in all or most of the head and showed little or no revasculanisation; and in the fourth group, seven showed extensive revascularisation of grossly necrotic heads. Total or subtotal capital necrosis had occurred in 64 per cent and total or partial necrosis in 84 per cent of the specimens. The results indicated that interruption of the retinacular vessels was the cause of gross necrosis; and that in most cases an intact blood supply through the ligamentum teres cannot keep more than a part of the head alive when the other vessels are cut off. Occasionally the ligamentum teres is torn by the nail, or though intact, its blood supply is interrupted. This accounts for completion of avascular necrosis in most cases with total capital necrosis. Viability of the subfoveal area from an intact supply through the ligamentum teres was the main source of revascularisation after capital necrosis. Other sources–from across a uniting fracture line, from growth of soft tissue round the head and neck and from other small viable foci in the head and neck–were much less important and the degree of revascularisation was generally limited. Revascularisation was accompanied by fibrocellular invasion of the marrow, differentiation of cells and the formation of oil cysts whereby the necrotic fat is removed; but bony reconstitution was limited. 3. Six fractures were uniting and another had united by bone making an overall union frequency of 50 per cent considering only the nailed fractures older than two weeks. Four of them (57 per cent) showed total or subtotal capital necrosis. In fractures older than two weeks the frequency of union among the eleven nailed fractures with avascular necrosis was 36 per cent, and it was 100 per cent among the three nailed ones with viable or substantially viable heads. Necrosis of the neck side of the fracture was unrelated to non-union because it soon becomes invaded by fibrovascular tissue and new bone. 4. Fibrosis was the basis of union when the head was dead but examination of older fractures at necropsy is needed to assess the long-term results of revascularisation and union. The clinical desirability or otherwise of capital revascularisation after necrosis also needs to be studied.
1. A clinico-pathological study of a patient who suffered traumatic rupture of his right popliteal artery is outlined. 2. Collateral circulation from the genicular anastomosis developed within twenty hours. 3. Ischaemic necrosis of the belly of the tibialis anterior occurred, but voluntary power began to return about twenty-one weeks after injury. 4. Biopsy of the muscle nineteen, fifty-seven and seventy-six weeks after injury showed that the muscle belly was being reconstituted by new fibres and that the ischaemic tissue remained entombed in the deepest part of the muscle. The regenerating fibres arose from small numbers of subfascial fibres which either survived the ischaemic episode or had arisen by myoblastic differentiation of connective tissue cells. Sarcoplasmic outgrowths produced new contractile substance, and new fibres were formed by amitotic fission. Many of the fibres matured and the regenerative process was still active seventy-six weeks after injury. 5. Growth of new nerve bundles containing myelinated axons accompanied the development of new muscle fibres.
