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Muscle Disease

Muscle Disease. Lab evaluation- muscle enzymes. AST (SGOT): Not muscle specific Increases more slowly than CK and has a longer half life Often used to decide ability to return to exercise CK (CPK): Fairly muscle specific Very sensitive Deflects degree of muscle damage

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Muscle Disease

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  1. Muscle Disease

  2. Lab evaluation- muscle enzymes • AST (SGOT): • Not muscle specific • Increases more slowly than CK and has a longer half life • Often used to decide ability to return to exercise • CK (CPK): • Fairly muscle specific • Very sensitive • Deflects degree of muscle damage • Increases rapidly and has a short half life • Ongoing damage

  3. Muscle enzymes cont. • LDH: • Not muscle specific • Has many isoenzymes • Has a half life in between that of CK & AST

  4. Exercise Challenge Test • 15-30min of light exercise • Rarely causes >3 fold increase in CK • Evaluate changes in CK 4-6hrs after exercise • Increases of 5X or more are indicative of exertional rhabdomyolysis

  5. Muscle Fasiculations • Myotonic Muscle Disorders: • Group of diseases that manifest delayed relaxation of muscle after mechanical stimulation or voluntary contraction • Ex: non-dystrophic myotonia in the horse, HYPP and myotonia congenita

  6. Hyperkalemic Periodic Paralysis (HYPP) Signalment, History & risk factors: • Breed predisposition: Quarter horses • Horses from “Impressive” blood line • Heavily muscled QTR horse • May be found in conjunction with spasm or paralysis of laryngeal & pharyngeal musculature

  7. HYPP • Clinical signs: • Highly variable • Depends on degree they are affected • Homozygotes (HH) or heterozygotes (HN) • Typically intermittent signs occur by 2-3yrs of age • Are normal in between episodes • Variety of stimulations may precipitate episodes • Trailering, post-exercise, fasting , stress, cold, diet change suddenly

  8. HYPP • Serum CK is unaltered in response to muscle fasiculations and weakness! • Brief myotonia • Prolapse of 3rd eyelid! (Tetanus also) • Sweating, fasiculations, tachypnea • Possibly severe cramping

  9. HYPP • Autosomal Dominant Inheritance • Gene defect in voltage gated Na+ channels of skeletal muscles • Resting potential in affected animals is closer to firing • Hyperkalemia is only seen during episode • Dx: • Positive gene test & DNA probe blood test • C.S and Hyperkalemia during an episode

  10. HYPP • Treatment: • Many attacks pass w/out need for tx • Acute episodes with severe hyperkalemia: • IV Calcium gluconate! • IV dextrose to help drive K+ intracellularly • Dextrose + sodium bicarbonate • Insulin or epinephrine

  11. HYPP • Control: • Acetazolamide: • K+ wasting diuretic • Cannot legally “show” on this drug • Management changes: • Dietary adjustments • Exercise regularly • Frequent access to large paddock or pasture

  12. Exertional Myopathy/Rhabdomyolysis • Synonyms: • Monday morning dz • Tying-up • Set-fast • Azoturia • Paralytic myoglobinuria • Chronic intermittent rhabdomyolysis • Hemoglobinemia paralytica

  13. Exertional Rhabdomyolysis • Etiology: • Environmental influence • Inadequate training- especially endurance horses in hot weather • Alteration of blood supply due to metabolic derangements (ex: fluid/electrolyte imbalance) • Genetic basis for some forms of dz

  14. ER • Classification: Class I: • Associated with limited exercise • 2-4yr old racing filly that is nervous or high strung • Often trains OK, but cannot race • Weekend riders- Monday morning dz • Associated with various other abnormalities such as PSSM and RER

  15. ER • Classification: Type II: • Associated with protracted exercise (ex: endurance horses) • Electrolyte and perfusion disturbances in the face of heavy exercise • Overexertion • Horse is not fit for expected level of demand

  16. ER • Sporadic versus chronic • Sporadic: occurring after previously normal performance, situational • Recurrent (chronic): several episodes occur, tendency to recur

  17. ER Clinical signs: • Mild cases: • Common in racing breeds • Shortly after completion of exercise • May be insidious- Poor performance • Little to no obvious muscle pathology • Slight reluctance to move • Firm, painful hindquarters are common • Urine is usually of normal color • May respond favorably to mild walking

  18. ER Severe cases: • Often begins during exercise • Stiff and stilted gait • Excessive sweating & tachypnea • Seen after 15-30min of light exercise • Reluctant to move, muscle tremors • May show signs of colic & become recumbent • Firm hind limb & back musculature- painful • Pigmenturia is often evident • ARF due to severe renal tubular damage

  19. ER Diagnosis: • History and clinical signs • Lab evaluation: • Electrolyte evaluation (fractional excretion) • Enzymes are usually elevated!! • CK & AST tend to be very elevated- depending on degree of myonecrosis • Elevated blood lactate and metabolic acidosis • Muscle biopsy: • Histopathology • Exercise test: increase in CK w/minimal exertion

  20. ER • Treatment for acute episodes: • Goal is to limit muscle damage, reduce pain, restore fluid/electrolyte balance and to reduce chances of renal impairment • Improve blood flow & perfusion to muscle • Aggressive fluid therapy (LRS) • Vasodilators like ACE if normal hydration • Improve renal perfusion by diuresis (fluids) • Relief of pain/inflammation • Sedation with ACE, Xylazine or Diazepam • Butorphanol • Bute (nephrotoxic, so make sure horse is well hydrated) • DMSO IV or per NG tube

  21. ER Tx cont: • Muscle relaxants: • Methocarbamol • Dantrolene sodium- acts intracellularly by slowing release of Ca++ form sarcoplasmic reticulum • Supportive care: • Bedding, warmth, sling

  22. ER Control (reduction of recurrence): • Dietary management • Inability to adequately use dietary CHO’s for muscle energy, so uses proteins • Feed low CHO diet with moderate fat and high protein • Need 3-6mths for results to be seen • Exercise: • Start once CK is normal again • Gradual increase in exercise, continual • Medication: • Prophylactic use of Dantrolene • In nervous fillies, can try Phenytoin (Dilantin) • Acepromazine

  23. Recurrent Exertional Rhabdomyolysis (RER) • Inherited disorder in 5% of Thoroughbreds • Heritable stress-related defect in intracellular calcium regulation • Young nervous fillies are predisposed • Higher incidence of anesthetic rxns • Muscle biopsy is best test • Management: try minimize stress • Dantrolene before racing • Avoid excessive stall resting • Low CHO diet, use fat for energy

  24. Polysaccharide Storage Myopathy in Draft (Belgians) horses • Definitive dx depends on demonstration of glycogen accumulation within skeletal muscle • QTR horses and Belgians • Deficiency in skeletal muscle glycolysis • Any age can be affected • Most likely related to exercise • Acute & chronic forms • Tx: dietary modification: give diet rich in fat and poor in CHO’s • Maintain regular exercise program

  25. Anesthetic Related Myopathies/Rhabdomyolysis • Most commonly seen with inhalant anesthesia • Large breed horses (ex: Draft) with heavy muscles are predisposed • Prolonged anesthesia (>2hrs) • Hypotension (keep MAP>60) • Inappropriate padding & positioning

  26. Anesthetic Related Myopathy • Clinical signs: • Prolonged or difficult recovery • Dog sitting • Buckling of fetlocks in the rear • Lab evaluation: • Same as with exertional rhabdomyolysis • Complications: • Fractures during recovery, renal damage, permanent muscle damage, protracted recumbency which leads to euthanasia • Tx: same as with exertional rhabdomyolysis

  27. Clostridial Myonecrosis (Inflammatory Myositis) • Rapidly infectious myositis with systemic toxemia • Most cases in the horse are associated with drug injections rather than wounds • Farms where horses are housed with cattle predispose them to this • Develop a fever of 104-106F • Rapid progression & possibly death in 48hrs • Tx: surgical fenestration of affected musculature, high doses of Penicillin IV, intensive supportive therapy

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