Young, rapidly growing foals born to dams that consumed selenium-deficient diets during gestation can develop nutritional myodegeneration (NMD; see Nutritional Myodegeneration Nutritional Myodegeneration Young Boer goat kid with white muscle disease. The patient can move its legs normally but is too weak to stand. CK and AST concentrations were elevated on serum biochemical evaluation. The goat... read more ). Selenium deficiency has also been implicated in masseter muscle myopathy and occasionally nonexertional rhabdomyolysis in adult horses. Selenium and vitamin E appear to be synergistic in preventing NMD. Clinical signs in foals include dyspnea; a rapid, irregular heartbeat; and sudden death in those with myocardial involvement. Dysphagia, muscle stiffness, trembling, firm muscles, difficulty rising, and myoglobinuria may also be seen. Aspiration pneumonia is a frequent complication. Diagnosis is based on finding moderate to markedly increased serum CK and AST, combined with low whole blood selenium concentrations (<0.07 ppm) or vitamin E (<2 ppm). Hyperkalemia, hyperphosphatemia, hyponatremia, hypochloremia, and hypocalcemia can occur with severe rhabdomyolysis when the normal distinction between extracellular and intracellular compartments is destroyed by massive tissue necrosis. Selenium-dependent glutathione peroxidase formed in RBCs during erythropoiesis also provides an index of body selenium status. Treatment includes IM injection of selenium (0.055–0.067 mg/kg) and either injectable or oral vitamin E (0.5–1.5 IU/kg). Supportive therapy includes administering antibiotics to combat secondary pneumonia, feeding via nasogastric tube, providing adequate energy intake, and maintaining fluid and electrolyte balance.