Introduction

• Cause: controversial pathogenesis but vitamin E and selenium deficiencies are very likely to play a part. Increased physical activity and other initiating factors may lead to increased free radical release, toxic cellular reaction and myodegeneration.
• Signs: peracute and subacute clinical syndromes; usually foals <2 months old with peracute, sudden death syndrome; or subacute type with weakness, stiffness and dysphagia often associated with vascular disorders.
• Diagnosis: clinical signs, elevated aspartate transferase, elevated creatinine kinase, hyperkalemia, hyponatremia, hypocalcemia and hyperphosphatemia.
• Treatment: reduced physical activity, supportive care and vitamin E/selenium supplementation.
• Prognosis: guarded to hopeless depending on clinical syndrome.

Pathogenesis

Etiology

• Dietary deficiencies in selenium   Selenium   or vitamin E   Vitamin E  , particularly during pregnancy and lactation results in insufficient amounts reaching the foal.
• Colostrum contains particularly high concentrations of vitamin and selenium, so lack of colostrum intake (failure of passive transfer)   Foal: failure of passive transfer (IgG)   may increase risk.
• Presence of other dietary factors.
• Stress.
• Increased physical activity, cf rhabdomyolysis   Muscle: myopathy - exertional rhabdomyolysis  .

Predisposing factors

• Stress, including management and environment.
• Increased physical activity.
• Exercise increases urinary selenium.

Specific

• Vitamin E deficiency:
  • Rancid feed.
  • Addition of fish/plant oil to feed, especially poor quality fat.
  • Prolonged storage of grain.
  • Poor quality hay.
  • Lush pastures.
• Selenium deficiency:
  • Acid, poorly aerated soils.
  • Soils with high sulfur content.
  • Volcanic rock.
  • Low plant selenium (<0.05 ppm).
  • Interference to availability by high, non-toxic levels of copper, silver, tellurium and zinc.

Dietary levels are misleading due to unknown bioavailability of various types of selenium.

• Selenium enriched yeast (amino acid bound selenium) has been found to be absorbed more efficiently than sodium selenite, or selenate, which is typically included in horse feeds and supplements.

Pathophysiology

• Some controversy regarding exact mechanism.
• Vitamin E   Vitamin E  and selenium   Selenium  deficiency are very likely to play a part.
• Other factors include: stress, unaccustomed exercise.
• Toxic cellular reaction   →   myodegeneration.
• Free radicals are produced by the reduction of molecular oxygen and during normal oxidative processes as the by-product of normal cellular metabolism.
• Under controlled conditions they are necessary for life, but when this control is lost they result in a number of degenerative disease processes by causing irreversible denaturation of essential cellular proteins, eg polyunsaturated fatty acids within phospholipid cell membrane can be attacked and disrupted releasing further hydroperoxides and yellowing of depot fat (steatitis).
• A system of natural anti-oxidant defences is present in the body including glutathione peroxidase (of which selenium is an integral component), vitamins C and E, and chelators.
• A similar myopathy has been reported in foals (particularly in geographic regions with selenium deficiency and low vitamin E intake) and possibly in adults (? maxillary myositis, polymyositis, dystrophic myodegeneration). There is controversy over this role of vitamin E and selenium in these adult conditions.
• Strenuous exercise may   →   excessive free radical production exceeding the cells' natural defence mechanisms.
• All muscles are affected, including cardiac and respiratory muscles.
• Foals may die from cardiac arrest secondary to heart muscle degeneration or from hyperkalemia.
• Death may also be due to failure of the respiratory muscles.

Diagnosis

Treatment

Prevention

Outcomes