Veterinary Clinics of North America-Equine Practice最新文献

Although horses most commonly develop exertional rhabdomyolysis, there are numerous causes for nonexertional rhabdomyolysis (nonER) that pose a serious health threat to horses. Their etiologies can be broadly categorized as toxic, genetic, inflammatory/infectious, nutritional, and traumatic and a variety of diagnostic tests are available to discern among them. This study discusses causes of nonER as well as diagnostics and treatments that are specific to each etiology. General treatment of acute rhabdomyolysis is covered in detail in the study in this issue on sporadic and recurrent exertional rhabdomyolysis.

The equine muscle system is complex and prone to a large range of hereditary and acquired diseases that often have overlapping clinical signs with orthopedic, neurologic, and other disorders. Obtaining a clinical history that fully outlines the client concerns and any known information about the disorder and following with a comprehensive physical examination and screening clinical pathology tests are fundamental to achieve definitive diagnosis. A methodical and comprehensive approach aids accurate diagnosis and development of an optimal treatment and management plan. This article describes the clinical examination approach and clinical pathology relevant to evaluating muscle disease in horses.

Type 1 Polysaccharide Storage Myopathy (PSSM1) is an autosomal dominant glycogen storage disorder affecting more than 20 breeds of horses that can present with a variety of signs, including exertional rhabdomyolysis (ER). It is diagnosed by genetic testing or muscle biopsies containing muscle fibers with abnormal amylase-resistant polysaccharide. Type 2 PSSM has recently been subdivided. PSSM2-ER is a glycogen storage disorder identified in Quarter Horses that causes ER and is diagnosed by muscle biopsy as its genetic basis is unknown. Both PSSM1 and PSSM2-ER respond well to a low nonstructural carbohydrate, high fat diet combined with regular exercise. These forms of PSSM are discussed in this article.

Successful rehabilitation of muscle injury requires a comprehensive understanding of the injury process, healing phases, and resources to be employed. The initial phase is characterized by acute inflammatory signs, followed by the regenerative and remodeling phases. Therapeutic exercises can be utilized in all 3 phases, progressing from isometric exercises to aquatic therapies. The classification and phase of injury and the individual response to the applied therapies will guide the progression of the therapeutic exercises through the rehabilitation program.

Traumatic muscle injuries are likely to be frequent in athletic horses yet are often overlooked. These injuries usually involve internal (intrinsic) trauma, and particularly occur in athletic horses exercising at higher intensities, at unaccustomed workloads, or performing work requiring sudden acceleration, deceleration, and/or direction changes. These injuries can present with signs ranging from acute pain and lameness in a localized region to unexplained elevations of muscle enzymes on routine blood tests with or without poor performance. They include exercise-induced muscle damage such as delayed-onset muscle soreness and muscle injury such as muscle tears.

Nutritional deficiencies of vitamin E and selenium can occur alone or concurrently. Prolonged and sustained deficiency of either or both nutrients can lead to profound clinical disease. Selenium deficiency can also result in signs of cardiac disease, upper gastrointestinal dysfunction, and abortion or the birth of weak foals. Deficiencies can usually be readily established by evaluating the dietary intake of individuals and by measurement of blood concentrations of these nutrients. Treatment of clinical disease is not always successful and prolonged morbidity and mortality can be encountered; hence, prevention is of the utmost importance.

Muscle disease has various clinical manifestations that range from exertional and non-exertional rhabdomyolysis, fasciculations, weakness, rigidity, stiffness, gait abnormalities, poor performance, and alterations in muscle mass and tone. Neurogenic disorders and non-neurogenic disorders such as primary muscle disease can cause muscle atrophy and changes in muscle tone. Myotonic disorders can have a genetic (eg, inherited channelopathies) or acquired (eg, electrolyte derangements) origin. Normal muscle enzyme activities do not rule out a myopathic disorder as the underlying cause of muscle atrophy and changes in muscle tone. Genetic testing to facilitate responsible breeding practices is recommended.

Horses are particularly susceptible to developing exertional rhabdomyolysis (ER) characterized by muscle stiffness, pain, and reluctance to move. Diagnosis requires establishing abnormal increases in serum creatine kinase activity when horses exhibit clinical signs. The 2 main categories of ER include sporadic ER arising from extrinsic causes and chronic ER that arises from intrinsic continuous or episodic abnormalities in muscle function. This article focuses on treatment of acute ER and causes and management of sporadic ER. Differential diagnoses for chronic ER as well as the pathophysiology, diagnosis, and management of recurrent ER, and malignant hyperthermia are also discussed in this article.

In the field of equine muscle disorders, many conditions have a genetic basis. Therefore, genetic testing is an important part of the diagnostic evaluation. Validated genetic tests are currently available for 5 equine muscle disorders: hyperkalemic periodic paralysis, malignant hyperthermia, glycogen branching enzyme disease, type 1 polysaccharide storage myopathy, and myosin heavy chain myopathy. These diseases should be tested for in the appropriate breeds with clinical signs of disease or as part of breeding management. Genetic testing in veterinary medicine is not regulated, and therefore, any new genetic test offered in horses should be carefully evaluated and confirmed to be a valid test before use.

Several inflammatory myopathies have an infectious or immune-mediated basis in the horse. Myosin heavy chain myopathy is caused by a codominant missense variant in MYH1 and has 3 clinical presentations: immune-mediated myositis, calciphylaxis, and nonexertional rhabdomyolysis in Quarter Horse-related breeds. An infarctive form of purpura hemorrhagica affects numerous breeds, presenting with focal firm, painful muscle swelling, and subsequent infarction of multiple tissues. While Streptococcus equi equi is often the inciting cause, anaplasmosis, sarcocystis, piroplasmosis, viruses, and vaccines can also be inciting agents. This article describes the diagnosis, pathophysiology, and treatment of these inflammatory myopathies.