Treatment and Prevention:
After stabilizing the animal with fluids, oxygen, and blood products as necessary, removal of the source of zinc as early as possible is paramount. This often requires surgery or endoscopy. Inducing emesis to remove chronic gastric zinc foreign bodies is typically not rewarding because zinc objects often adhere to the gastric mucosa.
Diuresis with a balanced crystalloid solution is indicated to promote renal excretion of zinc and prevent hemoglobinuric nephrosis.
There is debate regarding the necessity of chelation therapy in cases of zinc toxicosis. Animals can recover from zinc intoxication following only supportive care and removal of the source. However, chelation therapy enhances elimination of zinc and thus may accelerate recovery. Calcium disodium ethylenediaminetetraacetate (Ca-EDTA) successfully chelates zinc when given at 100 mg/kg/day IV or SC for 3 days (diluted and divided into 4 doses), but may exacerbate zinc-induced nephrotoxicity. Although they have been used to treat animals with zinc toxicity, d-penicillamine and dimercaprol (British antilewisite) have not been specifically validated for this purpose. Reported doses are 110 mg/kg/day for 7-14 days for d-penicillamine, and 3-6 mg/kg tid for 3-5 days for dimercaprol. Chelation therapy with any of these agents should be monitored with serial serum zinc levels to help determine the appropriate duration of treatment.
If diagnosed early and treated aggressively, the outcome is often favorable for animals with zinc toxicosis. Eliminating sources of zinc from the environment is essential in preventing recurrence.
