Nutritional Myodegeneration

Young, rapidly growing foals born to dams that consumed selenium deficient diets during gestation can develop nutritional myodegeneration (NMD; see Myopathies in Ruminants and Pigs: Nutritional Myodegeneration). Selenium deficiency has also been implicated in masseter muscle myopathy and occasionally non-exertional 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 marked elevated 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 extra-cellular and intracellular compartments is destroyed by massive tissue necrosis. Selenium-dependent glutathione peroxidase formed in RBC 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 administration of antibiotics to combat secondary pneumonia and feeding via nasogastric tube, provision of adequate energy intake, and attention to the fluid and electrolyte balance.

Last full review/revision March 2012 by Stephanie J. Valberg, DVM, PhD, DACVIM