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Equine Exertional Rhabdomyolysis
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Equine Exertional Rhabdomyolysis

  A Thoroughbred racehorse acts colicky returning to his stall after a morning workout.  An Arabian endurance horse quits at the 25th mile, trembling at the top of a hill.  A Quarter Horse ranch horse is stymied by progressive weight loss and decreased performance.  A Standardbred trotter lies sternal in his stall and is reluctant to rise.  It’s equivocal, but a Belgian draft mare seems to be showing a hind-limb lameness.

  What might all these horses have in common?

  It’s possible that all five are suffering from Exertional Rhabdomyolysis, a clinical syndrome denoting muscular pathology, whose varied etiologies are only beginning to be determined.  “Tying up”, as the condition is commonly described, has been recognized by horsemen since at least the early part of the 20th century.  Owners of draft teams, especially, noticed muscular distress in their horses following a full day of rest on full feed.  Their workhorses came out stiff the “day after” (typically Monday), leading to the term “Monday Morning Disease”.  Curiously, not all draft horses were similarly affected.  More curious still, not all affected horses were helped by a reduced diet during the rest day.  The conclusion that “tying up” was associated with both heredity and husbandry governs research on the syndrome to this day.

Clinical Signs and Diagnosis

  In general, exertional rhabdomyolysis elicits a spectrum of physical signs from mild stiffness and myalgia to recumbency and death.  Diagnosis is based on clinical signs, with concurrent increases in serum creatinine kinase (CK), aspartate amino-transferase (AST), myoglobinuria in severe cases, and distinctive lesions on muscle biopsy.  Critical consideration must be given to ruling out other diagnoses.  From the opening examples, it can be seen that rule-out diagnoses include colic, fractures, pleuritis, laminitis – anything that might cause a horse to act painful and reluctant to move.

  Serum chemistry can help determine the prognosis as well as diagnosis.  In a small study, one researcher noted that, while CK, AST, and lactate dehydrogenase (LDH) all increased immediately after onset of clinical signs, CK had the shortest half-life.  AST and/or LDH, to CK, ratios corresponded with stage of disease.  Ratios were low in acute stages, and high during recuperation.

  Most diagnostic biopsies are taken from the middle gluteal and semimembranous muscles.  These muscles are comprised largely of Type II (slow twitch or “non-oxidative”) fibers; specimens are submitted on ice or frozen, not fixed.  Histological signs of rhabdomyolysis (literally, “muscle cell loosening”) include vacuolization and fragmentation of myocytes, and macrophage infiltration.  Centrally located nuclei (indicating myocyte regeneration), fibrosis, and fatty infiltration all indicate chronic damage.


  Of the many disparate causes for “tying up”, certain ones are particular to certain breeds.  The more heavily muscled, calmer breeds (e.g. Quarter Horses, warm bloods and draft breeds) are more likely to be affected by a defect in muscular metabolism called Polysaccharide Storage Myopathy (PSSM or EPSM).  Thoroughbreds and other hot-blooded breeds, however, are thought to suffer a defect in intracellular calcium regulation.  Other proposed etiologies tend to be suggested and unsubstantiated repeatedly, and include Vitamin E deficiency, electrolyte imbalance, viral infection, and, because of an increased incidence in mares, normonal influences.

  The PSSM subset of rhabdomyolysis is named from an intramyocellular accumulation of periodic acid-Schiff-positive, abnormal mucopolysaccharide.  Increased intra-cellular glycogen levels

occur also, but are not specific to PSSM.  Muscle glycogen levels may be more than doubled in PSSM positive horses compared

to unaffected counterparts.  It was originally thought that these horses suffered from a decreased ability to use stored glycogen; however, measurement of muscle glycogen and lactate during exercise tests have shown that the abnormality lies in increased synthesis, not decreased usage, of muscle glycogen.  The role of the abnormal polysaccharide is unknown.

  Affected thoroughbreds, and other breeds which “tie up” without histologic evidence of PSSM, have been shown to have abnormal regulation of myocyte contraction.  In vitro studies compare muscle twitch responses to chemical stimuli such as caffeine and halothane.  Muscle-contracture thresholds are lower in samples from affected horses, and the theory is that abnormal calcium regulation is to blame.

  Genetic studies of affected horses have revealed different patterns of inheritance for both the PSSM and calcium related forms of exertional myopathy.  PSSM horses have been shown to be descendents of one of three stallions, with an autosomal recessive inheritance pattern.  The names of the three stallions have not been released.  In thoroughbred racehorses, pedigree analysis revealed an autosomal dominant inheritance pattern, with variable expression.  The trait seems to have first appeared in stallions in the early 20th century.

Treatment and Prevention

  Horses acutely affected with rhabdomyoysis should be moved as little as possible.  Mild cases may be walked bak to a stall, but movement will worsen the pathology in severe cases.  In this regard, treatment should be directed towards reducing pain and anxiety in these horses to keep them as quiet as possible.  Flunixin meglumine, phenylbutazone, acepromazine, and butorphanol have all been used with success.

  Correcting hydration status is crucial, especially to prevent kidney damage in cases with myoglobinuria.

  Dantrolene, a muscle relaxant which inhibits intracellular calcium release, and Phenytoin, an anti-convulsant, have been

used for both treatment and prevention.  No clinical trials have demonstrated efficacy, however, and dosing may be expensive and time consuming.  One author suggested use only in horses known to be affected with abnormal intracellular calcium regulation.

  Limited studies have shown a decreased incidence of rhabdomyolysis following a switch to high-fat, low-carbohydrate diets, based on the theory that this will decrease muscle glycogen stores.  Regular, daily exercise and turn-out are also suggested; their success in reducing episodes of rhabdomyolysis is anecdotal.

 - by Katherine Ulman, Class 2000

 - edited by Janice Lacey, DVM, ADDL Graduate Student


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