Avascular necrosis of bone

Abstract

1. Disturbance of the vascularity of bone by trauma, emboli, inflammatory, or neoplastic changes may result in avascular necrosis of the affected bone. 2. Avascular necrosis becomes associated with osteoporosis of the adjacent bone and the phenomena known as osteochondritis, although it is not always a recognizable factor in the latter condition. 3. Roentgenograms may show evidence of disturbance of the vascularity of a fragment of bone within six weeks of the application of the causal factor. If the signs of osteochondritis develop in association with avascular necrosis, the necrotic fragment will be recognizable by its relative density throughout the whole period of reorganization, — for upwards of four years. 4. It is the long period of bone plasticity in osteochondritis (one to four years) to which the clinician should give due attention, for disregard of this is responsible for the deformities caused by stresses and strains on the inadequately immobilized joint surfaces. Avascular necrotic bone undergoing substitution displays a plasticity which persists over a similar period. 5. Osteochondritis presents a characteristic roentgenographic time table. If the affected part is spared from stresses and strains during plasticity, regeneration is perfect. 6. The roentgenographic changes of Legg's disease and those following surgical trauma in reducing congenital dislocation of the femoral head, dislocation of the femoral head, fractures of the femoral neck, and displacement of the femoral diaphysis from its capital epiphysis are not identical; they vary from complete restoration to complete destruction of the joint, although avascular necrosis may occur in many of these conditions. 7. Roentgenograms do show evidence of pathological changes in the metaphysis of the upper femur in some cases before disintegration and displacement produce the lesion known as slipped epiphysis. Due attention to this roentgenographic finding and the prompt institution of protective measures may prevent the displacement and the consequences of avascular necrosis of the epiphysis. 8. Osteochondritis dissecans produces symptoms when the fragment becomes necrotic or displaced; the lesion may be recognized roentgenographically several years before. 9. Temporary retention of calcium by a fragment of bone does not indicate that the fragment is necrotic; it may fuse without any of the secondary changes characteristic of necrotic bone. 10. Avascular necrosis of bone can be detected roentgenographically by the greater density of a fragment which may exhibit friability associated with decalcification of adjacent bone and by the serial roentgenographic changes which show gradual absorption of the dense and apparently structureless fragment. Hypercalcification of bone is not in itself an indication of avascular necrosis. 11. As long as the necrotic bone is present, decalcification and plasticity of adjacent bone will exist; hence, the indication is that necrotic bone in traumatic cases should be removed as soon as detected, if for any reason the part cannot be efficiently immobilized until complete restoration can be detected roentgenographically. 12. The destructive changes in the hip joint, due to avascular necrosis following internal splintage (pinning, etc.), are worse than after any form of external immobilization. The pin gives a false sense of security, which lessens the period of freedom from weight-bearing; the latter and, possibly, added vascular damage by the pin probably account for these disasters. 13. No sign of avascular necrosis can be detected during the first month after the trauma; this latent period will be extended to many months if the femoral neck is pinned and the limb is allowed to bear weight. 14. The recognition of avascular necrosis and, thereby, prevention of its important complications would be facilitated if, after pinning, the patient rested in bed with the limb immobilized for three months. 15. The clinical signs and symptoms of disease usually disappear (at any rate for a time) long before the plasticity of the bone. Treatment must, therefore, be regulated by the roentgenographic appearances and not by the absence of clinical signs or symptoms. The plasticity of the bone can be judged by the roentgenographic appearances only; therefore, rest of the affected bone should be enforced as long as the roentgenograms suggest plasticity.