She could possibly have injured the leg causing some nerve damage, but I would also be worried that she could have curled toe paralysis from a riboflavin deficiency, or possibly Mareks disease. I would immediately put her on chick vitamins including riboflavin, or some BComplex ground into her food or water. She may need to be placed in a crate with food and water, near the other chickens if they continue to pester her. Here is some reading about riboflavin deficiency and Mareks disease:
RIBOFLAVIN DEFICIENCY Merck Veterinary Manual
Many tissues may be affected by riboflavin deficiency, although the epithelium and the myelin sheaths of some of the main nerves are major targets. Changes in the sciatic nerves produce “curled-toe” paralysis in growing chickens. Egg production is affected, and riboflavin-deficient eggs do not hatch. When the diet is inadvertently devoid of the entire spectrum of vitamins, it is signs of riboflavin deficiency that first appear. When chicks are fed a diet deficient in riboflavin, their appetite is fairly good but they grow slowly, become weak and emaciated, and develop diarrhea between the first and second weeks. Deficient chicks are reluctant to move unless forced and then frequently walk on their hocks with the aid of their wings. The leg muscles are atrophied and flabby, and the skin is dry and harsh. In advanced stages of deficiency, the chicks lie prostrate with their legs extended, sometimes in opposite directions. The characteristic sign of riboflavin deficiency is a marked enlargement of the sciatic and brachial nerve sheaths; sciatic nerves usually show the most pronounced effects. Histologic examination of the affected nerves shows degenerative changes in the myelin sheaths that, when severe, pinch the nerve. This produces a permanent stimulus, which causes the curled-toe paralysis.
Signs of riboflavin deficiency in hens are decreased egg production, increased embryonic mortality, and an increase in size and fat content of the liver. Hatchability declines within 2 wk when hens are fed a riboflavin-deficient diet but returns to near normal when riboflavin is restored. Affected embryos are dwarfed and show characteristically defective “clubbed” down. The nervous system of these embryos shows degenerative changes much like those described in riboflavin-deficient chicks. Clubbed down is periodically seen in cases of poor hatchability, when the “reject” chicks or dead embryos show this condition, even though the breeder diet is apparently adequate in riboflavin. Anecdotal evidence suggests greater occurrence of this clubbed-down condition in farms that select “floor-eggs” for incubation.
Signs of riboflavin deficiency first appear at 10 days of incubation, when embryos become hypoglycemic and accumulate intermediates of fatty acid oxidation. Although flavin-dependent enzymes are depressed with riboflavin deficiency, the main effect seems to be impaired fatty acid oxidation, which is a critical function in the developing embryo. An autosomal recessive trait blocks the formation of the riboflavin-binding protein needed for transport of riboflavin to the egg. Although the adults appear normal, their eggs fail to hatch regardless of dietary riboflavin content. As eggs become deficient in riboflavin, the egg albumen loses its characteristic yellow color. In fact, albumen color score has been used to assess riboflavin status of birds.
Chicks receiving diets only partially deficient in riboflavin may recover spontaneously, indicating that the requirement rapidly decreases with age. A 100-mcg dose should be sufficient for treatment of riboflavin-deficient chicks, followed by incorporation of an adequate level in the diet. However, when the curled-toe deformity is longstanding, irreparable damage occurs in the sciatic nerve, and the administration of riboflavin is no longer curative.
Most diets contain up to 10 mg of riboflavin/kg. Treatment can be given as two sequential daily 100-mcg doses for chicks or poults, followed by an adequate amount of riboflavin in feed.