Nutritional Myopathies in Horses

Young, rapidly growing foals born to dams that consumed selenium-deficient diets during gestation can develop 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 nutritional myodegeneration.

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 occur. Aspiration pneumonia is a frequent complication.

Diagnosis is based on finding moderate to markedly increased serum CK and AST activities, combined with low whole blood selenium (< 0.07 mcg/mL) or vitamin E (< 2 mcg/mL) concentrations. 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 selenium (0.055–0.067 mg/kg, IM, once) and vitamin E (0.5–1.5 U/kg, IM, IV, or PO, repeated as needed at 5- to 10-day intervals). Supportive treatment includes administering antimicrobials to combat secondary pneumonia, feeding via nasogastric tube, providing adequate energy intake, and maintaining fluid and electrolyte balance.