The rapid strides that have characterized the developments in the treatment of peripheral vascular disease during the past decade have been due in the main to a more rational comprehension of the disease process. Whereas previously studies were based on the apparent anatomic-pathologic changes, the recent concept emphasizes the less obvious alterations in physiologic function. The recognition of the associated fundamental physiologic derangement has permitted an approach toward accuracy in prognosis and efficacy in therapeusis. Peripheral vascular disease signifies simply a disturbance or actual diminution in the normal amount of circulating blood to a part. This is usually due to a decrease in the intraluminary volume of the peripheral vessels and may be caused by two factors operating either singly or together, depending on the type and stage of disease: (1) obliterative structural change in the vessels and (2) abnormal vessel spasticity. Whereas the former is an unalterable pathologic lesion,
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Ochsner et al. (1939) studied this question.
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