Equine MSK Dz ✔️

Sporadic exertional rhabdomyolysis

• caused by vigorous exercise beyond trained capacity

• any horse can get it, no predispositions

Recurrent exertional rhabdomyolysis

• genetic condition of thoroughbred racehorses

Polysaccharide storage myopathy

• glycogen storage Dz of skeletal muscle

• mutation in glycogen synthase gene (poorly mobilized glycogen stored due to poor folding)

  • severity increased by mutation in RYR1 gene

• type I heritable (autosomal dominant) & diagnosed via genetic testing, type II diagnosed via muscle biopsy

• most common in stock breeds

Clinical signs of PSSM

• repeated episodes of rhabdomyolysis induced by very mild exercise

• muscle atrophy

• weakness/stiffness/gait abnormalities

• abnormal increases in muscle enzymes 4-6 hours post-exercise (elevations >3-4x baseline)

Muscle biopsy for PSSM diagnosis

• done on semimembranosus/semitendinosus

• processed chilled & fresh

• test for accumulation of abnormal glycogen

  • PAS + & amylase-resistant

Treatment of PSSM

• IV fluids

• restricted activity

• muscle relaxants/analgesics

• diuretics/dialysis if severe

• limit stall confinement, maximize turnout time (self-directed exercise), introduce more intense exercise gradually but daily

• reduce dietary non-structural carbs to <10% (increased BG → increased abnormal glycogen formation), avoid lush pasture + cereal grains, increase dietary fat as alternate energy source

Prognosis of PSSM

• QOL excellent unless AKI occurs (may be life-limiting)

• performance prospects guarded to good w/proper management

Hyperkalemic periodic paralysis

• inherited, autosomal dominant, traceable to a singular Quarter Horse sire

  • most surviving horses are heterozygous

• caused by defect in 1 subunit of transmembrane fast sodium ion channel responsible for action potentials

  • inefficient/abnormal voltage inactivation results in persistent depolarization of skeletal muscle cells

• seen in QH, paint, Appaloosa, & crosses of those breeds (heavily muscled horses)

• commonly manifests as episodic weakness associated with elevated plasma potassium

Treatment of HYPP

• oral or IV dextrose during acute attack (increase blood glucose → increase insulin → drive potassium back into cells

  • can also give Ca, bicarb, or insulin IV

• preventative measures: potassium-wasting diuretics, regular exercise/routine, minimize dietary potassium (<1.1% of ration) & feed frequent meals w/high soluble carb content

  • avoid feeding: legume hays, molasses, kelp-based supplements

Clinical signs of rhabdomyolysis

• noted during or after vigorous exercise

• muscle stiffness/soreness

• stilted gait/reluctance to move

• firm muscles, painful on palpation

• tachypnea, tachycardia, sweating, hyperthermia

Lab results of rhabdomyolysis

• elevated CK + AST

• decreased Na, Cl, Ca

• increased K, Phos (intracellular, cytolysis causes increase)

• azotemia if recurrent or extreme (myoglobin toxic to renal epithelium)

• myoglobinuria (brown/red/black), cylindruria (granular casts later in Dz process)

Muscle enzymes

• CK relatively specific for skeletal + cardiac myocytes, peaks within 4-6 hours & clears within days

• AST less specific, peaks within 12-24 hours & clears within 2-3 weeks

Treatment for rhabdomyolysis

• fluid therapy (due to risk of pigment nephropathy)

• analgesia, muscle relaxants

• stall restriction, then gentle exercise

• gradual resumption of work