The horse quickly became recumbent and unable to rise and was euthanized due to a poor prognosis. At necropsy, severe bilateral guttural pouch empyema was observed, as well as numerous well-demarcated areas of pallor within the skeletal muscles of all major muscle groups. Polymerase chain reaction testing of the guttural pouch exudate confirmed an infection with Streptococcus equi subsp. This report briefly discusses the various etiologies that should be considered in cases of equine myopathy, and it demonstrates the complexity of these poorly understood muscular disorders.

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Exertional myopathy in horses is a syndrome of muscle fatigue, pain, or cramping associated with exercise. Less common exertional myopathies that cause exercise intolerance without muscle necrosis include mitochondrial myopathies and forms of polysaccharide storage myopathy in Warmblood horses.

Most commonly, exertional myopathies produce necrosis of striated skeletal muscle and are termed exertional rhabdomyolysis. Although exertional rhabdomyolysis was previously considered a single disease described as azoturia, tying-up, or cording up, it is now known to comprise several different myopathies, which, despite similarities in clinical presentation, differ significantly in etiopathology.

Clinical signs usually are seen shortly after onset of exercise. Excessive sweating, tachypnea, tachycardia, muscle fasciculations, reluctance or refusal to move, and firm, painful lumbar and gluteal musculature are common signs. Episodes range from subclinical to severe muscle necrosis with recumbency and myoglobinuric renal failure.

The severity varies extensively between individuals and to some degree within the same individual. A diagnosis of exertional rhabdomyolysis is based on demonstration of abnormal increases in serum CK, lactate dehydrogenase, and AST.

Exertional rhabdomyolysis can be either sporadic, with single or very infrequent episodes of exercise-induced muscle necrosis, or chronic, with repeated episodes of rhabdomyolysis and increased serum CK or AST with mild exertion. All breeds of horses are susceptible to sporadic exertional rhabdomyolysis. The incidence of muscle stiffness also has been found to increase during an outbreak of respiratory disease.

Dietary deficiencies of sodium, vitamin E, selenium , or a calcium:phosphorus imbalance may also be contributory factors. A diagnosis of sporadic exertional rhabdomyolysis is made on the basis of a horse with no previous history, or a brief history, of exertional rhabdomyolysis, signs of muscle cramping and stiffness after exercise, and moderate to marked increases in serum CK and AST.

Immediately on detection of signs of exertional rhabdomyolysis, exercise should stop and the horse should be moved to a well-bedded stall with access to fresh water. The objectives of treatment are to relieve anxiety and muscle pain and to correct fluid and acid-base deficits. Tranquilizers or opioids may be given. NSAIDs can be given to a well-hydrated horse. Most horses are relatively pain free within 18—24 hr. Severe rhabdomyolysis can lead to renal compromise due to ischemia and the combined nephrotoxic effects of myoglobinuria, dehydration, and NSAID therapy.

The first priority in horses with hemoconcentration or myoglobinuria is to reestablish fluid balance and induce diuresis. Diuretics are contraindicated in the absence of IV fluid therapy and are indicated if the horse is in oliguric renal failure.

Horses should be stall rested on a hay diet with a dietary vitamin and mineral ration balancer supplement for a few days. For horses with sporadic forms of exertional rhabdomyolysis, rest with regular access to a paddock should continue until serum muscle enzyme concentrations are normal.

Because the inciting cause is usually temporary, most horses respond to rest, a gradual increase in training, and dietary adjustment.

Endurance horses should be encouraged to drink electrolyte-supplemented water during an endurance ride and monitored particularly closely during hot, humid conditions. Some horses have recurrent episodes of rhabdomyolysis, even with light exercise. Four forms of chronic tying-up have been identified using muscle biopsies or genetic testing: type 1 polysaccharide storage myopathy PSSM , type 2 PSSM, malignant hyperthermia, and recurrent exertional rhabdomyolysis. Type 1 polysaccharide storage myopathy is seen frequently in Quarter horse—related breeds especially halter and Western pleasure horses , Morgans, and draft horses but is also present in at least 20 other horse breeds.

It is caused by a dominantly inherited mutation in the glycogen synthase 1 GYS1 gene. A diagnosis can be made by genetic testing of blood or hair samples. Quarter horse—related breeds and other crossbred or light breeds of horses with type 1 PSSM often develop episodes of rhabdomyolysis at a young age with little exercise.

Rest for a few days before exercise is a common triggering factor. Episodes are characterized by a tucked-up abdomen, a camped-out stance, muscle fasciculations, sweating, gait asymmetry, hindlimb stiffness, and reluctance to move. Some horses paw or roll, resembling colic. Clinical signs in draft horses may include loss of muscle mass, progressive weakness, and recumbency. CK and AST may be normal in draft horses with this syndrome. When draft horses develop rhabdomyolysis, CK and AST may be markedly increased, and horses can become myoglobinuric, weak, and reluctant to rise.

Type 2 polysaccharide storage myopathy occurs in light breeds such as Arabians, Morgans, Thoroughbreds, a variety of Warmblood breeds and some Quarter horses.

A diagnosis is made by identifying an abnormal pattern of glycogen storage in muscle biopsies in a horse with a negative GYS1 genetic test. Chronic episodes of muscle stiffness, soreness, and muscle atrophy with normal to modest increases in serum CK are common in horses with type 2 PSSM.

The most common presentation of this disorder in Warmbloods is a gait abnormality, exercise intolerance, and loss of muscle mass when out of work that is not necessarily accompanied by a concomitant rise in serum CK.

Malignant hyperthermia is caused by an autosomal dominant mutation in the skeletal muscle ryanodine receptor gene RYR1. The mutation is responsible for both anesthesia-related and non-anesthesia-related causes of rhabdomyolysis in Quarter horses. A diagnosis can be made by genetic testing of blood or hair roots. Signs related to inhalation anesthesia include tachycardia, tachypnea, hyperthermia, muscle rigidity accompanied by a severe lactic acidosis, increased serum CK, and electrolyte derangements.

Exertional rhabdomyolysis in Quarter horses with malignant hyperthermia can result in sudden death. Signs are preceded by excessive sweating, tachycardia, tachypnea, hyperthermia, and muscle rigidity. Some Quarter horses have both malignant hyperthermia and PSSM, which results in more severe signs of exertional rhabdomyolysis than those seen in horses with PSSM alone.

Recurrent exertional rhabdomyolysis is seen frequently in Thoroughbreds, Standardbreds, and Arabian horses. It is likely due to abnormal regulation of intracellular calcium in skeletal muscles.

It appears there is intermittent disruption of muscle contraction, particularly when horses susceptible to the condition are fit and have a nervous temperament. In Thoroughbreds, it is likely inherited as an autosomal dominant trait. Diagnostic tests to determine the cause of chronic tying-up include a CBC, serum chemistry panel, serum vitamin E and selenium concentrations, urinalysis to determine electrolyte balance, dietary analysis, exercise testing, muscle biopsy, and genetic testing.

An exercise challenge test is useful to detect subclinical cases; serum CK is measured before and 4 hr after light exercise. In addition, quantifying the extent of exertional rhabdomyolysis during mild exercise is helpful in deciding how rapidly to reinstate training.

A diagnosis of type 2 PSSM is based on the absence of the GYS1 mutation and the presence of muscle fibers with aggregates of amylase-sensitive PAS-positive staining glycogen and occasionally small amounts of amylase-resistant PAS-positive material.

A diagnosis of recurrent exertional rhabdomyolysis is based on history, clinical signs, increases in serum CK and AST, and muscle biopsy. Horses with type 1 PSSM have constitutively active glycogen synthase that is further stimulated by increased blood insulin concentrations, resulting in high muscle glycogen concentrations. When fed a starch meal, these horses take up a higher proportion of the absorbed glucose in their muscles than healthy horses.

Horses with type 2 PSSM also have abnormal glycogen storage, but the cause of this myopathy is unknown. Thus, the ideal diet for PSSM is based on feeding forage at a rate of 1. Caloric needs should be assessed first to prevent horses becoming obese on a high-fat diet. Improvement in signs of exertional rhabdomyolysis for horses with PSSM requires both dietary changes and gradual increases in the amount of daily exercise and turn-out.

Management of recurrent exertional rhabdomyolysis is aimed at decreasing the triggering factors for excitement and pharmacologic alteration of intracellular calcium flux with contraction. Management changes that may decrease excitement include minimizing stall confinement by using turn-out or a hot walker, exercising and feeding horses with recurrent exertional rhabdomyolysis before other horses, providing compatible equine company, and the judicious use of low-dose tranquilizers during training.

A high-fat, low-starch diet is beneficial, possibly by decreasing excitement. At these high caloric intakes, specialized feeds designed for exertional rhabdomyolysis are necessary, because additional vegetable oil or rice bran cannot supply enough calories for equine athletes in intense training. Hay should be fed at 1. Phenytoin 1. However, longterm treatment with dantrolene or phenytoin is expensive. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world.

The Veterinary Manual was first published in as a service to the community. The legacy of this great resource continues in the online and mobile app versions today. This site complies with the HONcode standard for trustworthy health information: verify here. Common Veterinary Topics. Videos Figures Images Quizzes. Sporadic Exertional Rhabdomyolysis.

Chronic Exertional Rhabdomyolysis. Myopathies in Horses. Test your knowledge. The lameness examination is an important method to identify musculoskeletal abnormalities. Which of the following abnormalities is NOT observed during a physical and lameness exam?

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Identifying and Managing Acute Rhabdomyolysis in Horses

An Arabian endurance horse quits at the 25 th 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. Owners of draft teams, especially, noticed muscular distress in their horses following a full day of rest on full feed.


Exertional Rhabdomyolysis (ER)

Understanding equine acute rhabdomyolysis can help ensure affected horses receive appropriate veterinary care. At a recent veterinary conference, one researcher gave an overview of how to identify and manage episodes of "tying up. Before delving into identification and treatment, McKenzie discussed a few causes of rhabdomyolysis. McKenzie said that rhabdomyolysis can be caused by either "exertional or non-exertional phenomena. The clinical signs and treatments for rhabdomyolysis are generally influenced by the severity and root of the condition, so McKenzie stressed that identifying the initiating cause is beneficial to ensure proper therapeutic options are employed. Not surprisingly, exertional and non-exertional rhabdomyolysis may have different clinical signs to watch for, McKenzie said. When dealing with a case of exertional rhabdomyolysis, clinical signs will develop during or shortly after exercise, she said.


Exertional Myopathies in Horses

A diagnosis of RER is made on the basis of a history of recurring signs of muscle stiffness in association with high serum levels of the muscle enzymes creatine kinase CK and aspartate aminotransferase AST subsequent to muscle cell necrosis. There is strong evidence from earlier studies that RER susceptibility has an underlying genetic basis; however the genetic model and pattern of inheritance has not yet been conclusively defined. Estimations of RER heritability have been variable, which may reflect differences in RER diagnostic criteria or the contribution of many non-genetic factors. Such non-genetic risk factors include temperament, sex, age, diet, exercise routine, and the presence of lameness. Thoroughbreds with the greatest risk of developing RER are young, nervous females. We have scanned the horse genome with more than 48, single nucleotide polymorphisms SNPs in a search for genetic variants associated with RER in Thoroughbreds.

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