Abstract
Although Marchal de Cavi clearly described diabetic neuropathy and its relationship
to diabetics in 1864 and in 1887, T. Davis Pryce assigned ‘‘ . . . considerable share [of
the blame for a perforating foot ulcer] to diabetes and vascular disease.’’ Until the
1930s, diabetes was only credited with causing the painful, dry, or senile gangrene
of the foot. Rose and Carless in 1933 recognized in younger diabetic patients a
wet gangrene with hot swollen painful foot ulcers under callosities. The link between
neuropathies and the deformities as summarized by Charcot was recognized by
Lambrinidi in 1937. D.H. Lawrence, himself a diabetic and among the first to use
insulin, requested a wedge resection of his metatarsalphalangeal joint and toe leading
to the so-called ray amputation, whose healing confirmed the lack of an arteriosclerotic basis for wet gangrene.