Following anesthesia, horses may develop severe muscle pain and weakness in one or more muscle groups. Hypoperfusion of compressed muscle groups with resultant high intracompartmental pressure is the most important causative factor for focal muscle involvement. The dependent triceps muscle is most commonly affected after anesthesia in lateral recumbency, whereas the longissimus dorsi and gluteal muscles are usually affected in horses that have been in dorsal recumbency. Generalized myopathies may develop in horses that were hypotensive during anesthesia. The longer the duration of anesthesia, the higher is the risk.
Signs are evident when horses try to stand or may be delayed for up to 2 hr. A dropped elbow stance typical of radial nerve paralysis characterizes triceps myopathy. Gluteal myopathy results in unwillingness to bear weight on the hindlimbs. Horses may appear distressed, with profuse sweating, tachycardia, and tachypnea. The degree of distress depends on the severity of the muscle damage. Affected muscles may feel very hard and show localized swelling. Serum CK may be normal immediately after the horse stands but will rise substantially and peak ~4 hr after anesthesia. Pain relief is provided by sedation with detomidine, combined with opiate analgesics and NSAID. Constant rate infusions of detomidine or butorphanol may be beneficial for pain control in severe cases. Fluid therapy helps maintain renal perfusion and urine output and ensure adequate muscle perfusion. The prognosis for unilateral myopathy is usually good, although with severe damage there may be residual muscle fibrosis, which may compromise function. The prognosis for generalized myopathy is more guarded.
Prevention requires minimizing the time under general anesthesia, careful positioning of the horse on the operating table, and maintenance of arterial blood pressure above 60 mm Hg using fluid therapy and inotropic agents such as dobutamine (1–5 μg/kg/min).
The ryanodine receptor gene (RYR1) mutation in Quarter horses described above (see Chronic Exertional Rhabdomyolysis) can cause fatal reactions under general anesthesia that are characterized by marked hyperthermia, acidosis, electrolyte derangements, and muscle necrosis. Unfortunately, once a fulminant episode is underway it is difficult to prevent cardiac arrest. Diagnosis is by clinical signs and genetic testing. Pretreatment with oral dantrolene (4 mg/kg) 30–60 min prior to anesthesia is the only potential means to prevent an episode.
Fibrotic myopathy describes a classic gait abnormality that develops when horses injure their semitendinosus and semimembranosus muscles at the point of a tendinous insertion during exercise that requires abrupt turns and sliding stops. Trauma (eg, catching a foot in a fence), IM injections, and a congenital form are other potential causes of fibrotic myopathy. Affected muscles in acute cases are warm and painful on deep palpation. Chronically, hardened areas within the muscle may represent fibrosis and ossification. The associated gait abnormality is usually most apparent at the walk and is characterized by an abrupt cessation of the anterior phase of the stride of the affected limb, causing the leg to jerk suddenly to the ground rather than continue its forward motion. The stride has a short anterior phase with a characteristic hoof-slapping gait. The gait reflects a mechanical hindlimb lameness that restricts normal function. Pain is usually not a feature of chronic fibrotic myopathy. Serum CK and AST are usually only mildly elevated. In addition to palpation, diagnosis can be confirmed by ultrasonography, thermography, or scintigraphy. Light microscopic evaluation of muscle biopsies is frequently normal in acute cases. Chronically, fibrous replacement of muscle fibers is apparent. Acute cases may benefit from rest and cold therapy followed by deep heating ultrasound and controlled stretching. Chronic cases may require surgical excision or transection of the fibrotic part of the muscle or tenotomy of the tibial insertion of the semimembranosus tendon.
Last full review/revision March 2012 by Stephanie J. Valberg, DVM, PhD, DACVIM