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Nutrition: nutritional myopathy

ISSN 2398-2977


Synonym(s): Muscular dystrophy, white muscle disease, nutritional myodegeneration, Zenker's necrosis

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.
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Presenting signs

  • Subacute syndrome with weakness, stiffness, recumbency, dysphagia   Foal: neonatal regurgitation  .
  • Post-excessive exercise.
  • Tachycardia, arrhythmias.
  • Elevated respiratory rate.
  • Brown urine.
  • Peracute syndrome with sudden death.

Geographic incidence

  • Selenium deficient soil areas, eg USA - NE, E and NW States.

Age predisposition

Cost considerations

  • Loss of animal.
  • Treatment.

Special risks

  • Cardiac form of disease.
  • Hyperkalemia.

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

General
  • 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

Presenting problems

Client history

  • Usually foals <2 months of age.
  • Subacute syndrome with slow onset of signs:
    • Occasionally groups of animals are affected.
    • Failure to suckle and/or dysphagia.
    • Muscle weakness or stiffness.
    • Trembling +/- recumbency.
  • Known vitamin E deficiency +/- selenium deficient soils/feeds.
  • Often post-exercise.
  • Peracute syndrome with sudden death sometimes following 1-2 h of severe illness.
  • In adults the subacute syndrome   →  
    • Depression.
    • Inability to eat.
    • Swollen head and neck.
    • Stiffness.
    • Ataxia.

Clinical signs

  • Variable depending on distribution of muscular lesions and extent of damage.
Peracute
  • Sudden onset and rapid progression.
  • Sudden death immediately or within a few hours of onset of severe illness.
  • Damage to myocardium, diaphragm and respiratory muscles   →  
    • Heart failure.
    • Dyspnea.
    • Pulmonary edema.
  • Difficulty in standing.
  • Painful subcutaneous swellings over rump, ventral abdominal wall and nuchal crest - usually older foals.
  • Older animals - sudden post-exercise recumbency, cf "tying-up", rhabdomyolysis   Muscle: myopathy - exertional rhabdomyolysis  .

Subacute

  • Weakness, stiffness and lethargy.
  • Muscle trembling.
  • Inappetence.
  • Inability to eat (dysphagia):
    • Tongue, pharyngeal and masticatory muscle involvement.
    • Possible secondary aspiration pneumonia.
    • Starvation.
  • Swollen and sore muscles, especially in the hindlimbs.
  • Variable body temperature.
  • Recumbency.
  • Cardiac involvement   →  
    • Tachycardia.
    • Arrhythmias.
    • Systolic murmurs.
    • Respiratory distress.
  • Myoglobinuria   Urine: myoglobinuria  .

Diagnostic investigation

Biochemistry
  • Glutathione peroxidase (GTHPx):
    • Use of RBC levels.
    • Low levels reported in affected foals but also in normal animals.
    • Stabled animals/normal balanced diet: >30 IU/ml RBC.
    • Grazing animals: >25 IU/ml RBC.
    • Deficient intake of selenium: <20 IU/ml RBC.
  • Vitamin E  Vitamin E  :
    • Serum values >1.5-5 ug/ml have been reported as normal.
    • Adipose tissue contains large amounts (10-60 ug/g) not prone to the short-term fluctuation characteristic of blood levels.
    • Clinically normal animals have been reported with lower levels.
    • High variability in values between and within animals.
    • Reference values vary between laboratories.

    Collect samples carefully as rubber may interfere with analysis.

Confirmation of diagnosis

Discriminatory diagnostic features

  • History and clinical signs.
  • Dietary analysis.

Definitive diagnostic features

Gross autopsy findings

Peracute
  • Few findings.
  • Pale muscles with streaking (necrosis):
    • Bilateral, symmetric.
    • Pelvic, thoracic limb, cervical muscles.
    • Muscles of mastication, diaphragm, tongue, pharynx.

Subacute

  • Yellow-white streaks in heart and muscle (calcification).
  • Steatitis, yellow fat deposits and fat necrosis.

Histopathology findings

  • First few days: extensive follicular, granular and severe hyaline degeneration of myofibers.
  • After a week: phagocytosis of necrotic tissue with endomysial thickening (mononuclear infiltration, edema and fibroblast proliferation).
  • By 2 weeks: epimyseal connective tissue proliferation, myodegeneration and early regenerating fibers.
  • Coagulative necrosis of the muscle bundles.
  • Muscle thickening and fragmentation with some mineralization of muscle fibers.
  • Macrophage and mononuclear cell infiltration.
  • Renal tubular nephrosis secondary to myoglobinuria.

Differential diagnosis

Treatment

Standard treatment

  • Reduce physical activity.
  • Early administration of vitamin E   Vitamin E  and selenium   Selenium  :
    • NOT intravenously.
    • Deep intramuscular.
    • May   →   soreness/abscess formation.
    • Toxicity is possible: foals >/= 200 ug/kg BW.
    • 0.05-0.06 mg/kg BW selenium + additional vitamin E to compensate for low levels in vitamin E/selenium combinations.
  • Supportive care:
    • Nasogastric feeding in dysphagic, anorectic or recumbent foals.
    • Fluid therapy   Fluid therapy: overview  to: combat electrolyte and fluid disturbances   Fluid therapy: electrolyte abnormalities  ; maintain renal function and urine output; prevent myoglobin-associated renal damage - 0.9% NaCl solution with added calcium.
  • Anti-inflammatory agents   Therapeutics: anti-inflammatory drugs  to reduce pain and swelling - flunixin meglumine   Flunixin meglumine  0.5 mg/kg.

Beware ulcerogenic properties.

Great care with feeding subsequent to antibiotic treatment - give probiotics   Nutrition: probiotics  .

  • Foals with severe hyperkalemia may benefit from 5% dextrose   Glucose   and insulin therapy.
  • Sodium bicarbonate   Sodium bicarbonate   may be useful in foals with acidosis.

Monitoring

  • Clinical signs.
  • Biochemistry: GTHPx increases in 2-3 weeks.
  • CK and AST should be monitored to check for a response to the vitamin E/selenium supplementation.
  • Renal parameters should be check for acute renal failure.
  • Acid base and electrolyte levels.

Prevention

Prophylaxis

  • Conduct analysis of pasture and hay to identify any deficiencies.
  • Source hay from non-selenium deficient areas.
  • Vitamin E and selenium supplementation, especially in pregnant and lactating mare (only limited placental transfer of selenium but greater lactogenic):
    • Oral or by intramuscular injection.
    • Preferably constant daily oral supplementation: alpha-tocopherol acetate: 1.5-4.4 mg/kg BW daily for adults or 100 IU/kg/DM intake/day.
    • Feed good quality, properly stored hay and grain.
    • Allow access to good quality green forage.
    • Feeding 1 mg/day oral selenium is said to maintain blood levels - organic form is better: fed as free access; as salt licks 15-30 ppm selenium; feed ration (up to 0.2 ppm selenium).
  • Selenium should be provided in the diet to all individuals if compund feeds are used at manufacturers guidelines, additional selenium supplementation should not be necessary other than in deficient geographical locations.

Selenium may be terratogenic in early pregnancy and should be fed with caution.

Toxicity is recorded.

Over-supplementation can pollute the environment.

Outcomes

Prognosis

  • Guarded if recumbent or treatment delayed.
  • Poor in cases with secondary problems such as electrolyte/acid-base changes.
  • Hopeless in cardiac form.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Valberg S J (2002) A review of the diagnosis and treatment of rhabdomyolysis in foals. AAEP Proc 48, 117-121 VetMedResource.
  • Valberg S J (1999) Spinal muscle pathology. Vet Clin North Am Equine Pract 15 (1), 87-96 PubMed.
  • Perkins G, Valberg S J, Madigan J M, Carlson G P & Jones S L (1998) Electrolyte disturbances in foals with severe rhabdomyolysis. J Vet Intern Med 12 (3), 173-177 PubMed.
  • Freestone J F et al (1991) Muscle disorders in the horse - a restrospective study. Equine Vet J 23 (2), 86-90 PubMed.
  • Moore R M (1991) Nutritional muscular dystrophy in foals. Comp Cont Educ Pract Vet 13 (3), 476-481 VetMedResource.
  • Step D L et al (1991) Severe masseter myonecrosis in a horse. JAVMA 198 (1), 117-119 PubMed.
  • Hosie B D et al (1986) Acute myopathy in horses at grass in east and south east England. Vet Rec 119 (18), 444-449 PubMed.
  • Dill S G & Rehbun W C (1985) White muscle disease in foals. Comp Cont Educ Pract Vet (11), 627-635 VetMedResource.
  • Wilson T M et al (1976) Myodegeneration and suspected selenium/vitamin E deficiency in horses. JAVMA 169 (2), 213-217 PubMed.

Other sources of information

  • Paradis M R (2006) Aspiration pneumonia secondary to dysphagia. In: Equine Neonatal Medicine: A Case Based Approach. Ed: Paradis M R. Elsevier, USA. pp 148-156.
  • Frape D (2004) Equine Nutrition and Feeding. 3rd edn. Blackwell Publishing Ltd, UK. ISBN: 1405105984.