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Nutritional Myopathies in Horses


Stephanie J. Valberg

, DVM, PhD, DACVIM, ACVSMR, McPhail Equine Performance Center, Michigan State University

Last full review/revision Feb 2014 | Content last modified Feb 2014

Nutritional Myodegeneration

Young, rapidly growing foals born to dams that consumed selenium-deficient diets during gestation can develop nutritional myodegeneration (NMD; see Nutritional Myodegeneration). 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.

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