7 Degenerative/necrotizing myopathies

Although degeneration and necrosis are a feature of a number of different myopathies, this section describes myopathies that do not have a congenital, nutritional, toxic, or infectious etiology.

7.1 Exertional myopathies

An exertional myopathy is defined as myofiber damage occuring as the direct result of exercise.

7.1.1 Equine exertional rhabdomyolysis

Synonyms: blackwater, Monday morning disease, set fast, paralytic myoglobinuria, azoturia, tying-up

Exertional rhabdomyolosis is a significant disease of horses. It is often worse in heavy, draft breeds as compared to light breeds, and female horses are predisposed. The pathogenesis of the condition is not completely known. The current accepted theory is that muscle damage is most often due to underlying metabolic abnormalities, possibly a post-exercise hypokalemia, and not management factors. Interestingly, although diet is not considered to be the underlying cause of exertional rhabdomyolysis, virtually all horses suffering from the condition respond favourably to a diet high in fat and fiber and low in starches.

Exertional rhabdomyolysis presents as a sudden onset of weakness, pain, and discomfort, sometimes with tremors or sweating, during or after periods of exercise. The exercise does not have to be overly strenuous or exhaustive. Severe cases may progress to recumbency. Type 2 glycolytic myofibers are most severely affected. Cardiac muscle is spared, and mineralization is not a feature. Grossly, affected muscles (particularly the gluteal, femoral, and lumbar muscles) may be swollen and dark red, with streaks of pale pallor present in severe cases. Histologically there is necrosis of type 2 fibers. Fibrosis and atrophy will be present in chronic cases. Myoglobinuria is a common feature, and can lead to myglobinuric nephrosis.

There is evidence that horses with PSSM are predisposed, but the exact mechanism is unclear.

7.1.2 Canine exertional rhabdyomyolysis

As one might expect, this syndrome appears most frequently in racing dogs, namely Greyhounds and sled dogs. It is not particularly well understood, but thought that separate mechanisms cause the syndrome in sprinting versus endurance racing. In Greyhounds, clinical signs and symptoms are similar to those noted for horses, while in sled dogs may present with sudden death.

7.1.3 Capture myopathy

This is a syndrome seen both in free and captive wildlife. The stress of capture, which is usually preceeded by a chase and/or struggle in these animals, results in a combined massive release of catecholamines and overexertion that is frequently fatal. Muscles may be pale and edematous or may show pale streaks with hemorrhage. Degeneration and necrosis is frequently observed histologically. This condition is extremely important in zoological collections, and as such great care is often taken when tranquilizing or restraining animals for examination.