Abstract
A review of the literature would seem to indicate that ischemic necrosis of the femoral head (INFH) is growing in importance as a clinical entity. In 1962, Mankin and Brower found only 22 cases in the English literature, to which they added five of their own. Since then, series with more than 100 cases have been reported (Ficat et al. 1971; Merle d’Aubigne et al. 1965). In 1948, Chandler postulated that blockage of the posterolateral retinacular artery leads to infarction and eventual collapse of the anterolateral area of the femoral head. The typical X-ray picture supported that hypothesis in what appeared to be a wedge-shaped bone infarct (Fig. 1). This concept of “coronary disease of the hip” seemed almost self-evident and was widely accepted. Although this might be the case for post-traumatic INFH, a wide variety of other apparent etiologic associations, including alcohol abuse (18), both endogenous and exogenous steroid excess (Cruess et al. 1968; Edstrom 1971; Harrington et al. 1971; Soloman 1973), connective tissues diseases, especially systemic lupus erythematosis (Dubois 1960; Zizic et al. 1980), gout, Gaucher’s disease, and hemoglobinopathy (Dubois 1960), all have a similar morphological localization which would seem to transcend the simple mechanical involvement of a single artery. The mechanisms by which these diverse presumed etiologic associations produce such a similar clinical pattern have been the source of considerable controversy.
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Hungerford, D.S. (1981). Early Diagnosis and Treatment of Ischemic Necrosis of the Femoral Head. In: Weil, U.H. (eds) Segmental Idiopathic Necrosis of the Femoral Head. Progress in Orthopaedic Surgery, vol 5. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-68049-6_3
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DOI: https://doi.org/10.1007/978-3-642-68049-6_3
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