Chapter 83Skeletal Muscle and Lameness
A history of stiffness, muscle cramping, pain, muscle fasciculations, exercise intolerance, undiagnosed lameness, weakness, or muscle atrophy may all indicate a muscle disorder. Further characterization requires a detailed account of the horse’s performance level, exercise schedule, previous lameness, diet, vaccination history, signs of respiratory disease, duration, severity and frequency of muscle problem, any factors that initiate the muscle problem, and all medications with which the horse is being treated.
A detailed evaluation of the muscular system includes inspection of the horse for symmetry of muscle mass while standing with forelimbs and hindlimbs exactly square. Any evidence of fine tremors or fasciculations should be noted before palpating the horse. Horses originating in the southwestern United States that have muscle pain and fasciculations should have their ears examined with an otoscope for ear ticks (Otobius megnini).1 The entire muscle mass of the horse should be palpated for heat, pain, swelling, or atrophy comparing contralateral muscle groups. Firm, deep palpation of the lumbar, gluteal, and semimembranosus and semitendinosus muscles may reveal pain, cramps, or fibrosis. The triceps, pectoral, gluteal, and semitendinosus muscles should be tapped with a fist or percussion hammer and observed for a prolonged contracture suggestive of myotonia. Running a blunt instrument such as artery forceps, a needle cap, or a pen over the lumbar and gluteal muscles should illicit extension (swayback), followed by flexion (hogback) in healthy horses. Guarding against movement may reflect abnormalities in the pelvic or thoracolumbar muscles, or pain associated with the thoracolumbar spine (see Chapter 52) or sacroiliac joints (see Chapter 51). The horse should be observed at the walk and the trot for any gait abnormalities, and some horses should be ridden.
Skeletal muscle necrosis may be identified by determining the activity in blood of serum enzymes or proteins that are normally present in high concentration within intact muscle cells but leak out into the bloodstream following cell damage. Three enzymes are used routinely to assess muscle necrosis: creatine kinase (CK), aspartate transaminase (AST), and lactate dehydrogenase (LDH). Serum myoglobin has also been used as a marker of acute muscle necrosis.2,3 The permeability of the muscle cell membrane, rate of enzyme production, alternate tissue sources of the enzyme, and rate of enzyme excretion/degradation may also influence serum enzyme activities.
Isoforms of CK are found in skeletal muscle (MM), cardiac muscle (MB), and nervous tissue (BB). CK is a relatively low-molecular-weight protein (80,000 Da) that is intimately involved in energy production within the cell cytoplasm. It is liberated within hours of muscle damage, or increased cell membrane permeability, into the extracellular fluid and usually peaks at 4 to 6 hours after muscle injury (half-life  is 108 min).4 A threefold to fivefold increase in serum CK from normal values is believed to represent necrosis of approximately 20 g of muscle tissue.5 Rhabdomyolysis results in a proportionately greater increase in the MM isoform than the MB isoform, although some investigators disagree with the tissue specificity of serum CK isoforms in the horse.6 Limited elevations in CK (<1000 U/L; high range of normal value = 380 U/L ) may accompany training or transport.7 Extreme fatiguing exercise (e.g., endurance rides or the cross-country phase of a Three Day Event) may result in CK activities being increased to more than 1000 U/L, but usually less than 5000 U/L. Under these circumstances, serum CK activities rapidly return to baseline (i.e., <350 U/L in 24 to 48 hours). Recumbent horses also may have slightly elevated CK activities that are usually less than 3000 U/L. In contrast, more substantial elevations (from several thousand to hundreds of thousands of units per liter) in the activity of this enzyme may occur with rhabdomyolysis.3
Serum AST, previously known as serum glutamic-oxaloacetic acid and aspartate aminotransferase, is a larger-molecular-weight protein that has high activity in skeletal and cardiac muscle and also in liver, red blood cells, and other tissues. Elevations in AST are not specific for myonecrosis, and increases could be the result of hemolysis, muscle, liver, or other organ damage. AST activity increases more slowly in response to myonecrosis than does CK, often peaking between 12 and 24 hours after the insult. In addition, AST is cleared slowly by the reticuloendothelial system and may persist for 2 to 3 weeks after rhabdomyolysis ( is 7 to 10 days).4,8
By comparing serial activities of CK and AST, information concerning the progression of myonecrosis or muscle cell membrane permeability may be derived. Elevations in CK and AST reflect relatively recent or active myonecrosis or muscle cell stress; persistently elevated serum CK indicates that myonecrosis or muscle stress is likely ongoing. Elevated AST activity accompanied by decreasing or normal CK activity indicates that myonecrosis has ceased. The degree of elevation of CK and AST does not necessarily reflect the severity of clinical signs.
LDH is a tetramer made up of combinations of the M and H subunits, with five isoenzyme forms found in various organs within the body. Electrophoretic separation suggests that the M4 (LDH5) and M3H (LDH4) isoforms are found predominantly in skeletal muscle. Elevations in LDH may be detected in horses with rhabdomyolysis, myocardial necrosis, and/or hepatic necrosis.7 Therefore concurrent measurement of serum CK is necessary to establish that rhabdomyolysis is present.
Elevation in plasma/serum myoglobin concentrations indicates acute muscle damage. Myoglobin is a low-molecular-weight protein (16,500 Da) that leaks into plasma immediately after muscle damage and is rapidly cleared in the urine by the kidney. Approximately 200 g or more of muscle must be damaged before it is detectable in the urine in people.9 Normal serum concentrations in resting horses have been determined by nephelometry (range, 0 to 9 mcg/L), with measured concentrations with rhabdomyolysis ranging from 10,000 to 800,000 mcg/L.2,3
Diagnosing chronic exertional rhabdomyolysis (ER) may be problematic in horses that do not have acute clinical signs and have normal serum AST and CK at rest. In such horses, an exercise challenge can be helpful to detect subclinical ER. In addition, quantifying the extent of rhabdomyolysis during mild exercise is helpful in deciding how rapidly to put a horse back into training. Blood samples should be taken before exercise and 4 to 6 hours after exercise to evaluate peak changes in CK. Serum CK activity measured immediately postexercise will not reflect the amount of damage occurring during the exercise test. Small fluctuations in serum CK activity may occur with exercise from enhanced muscle membrane permeability, particularly if exercise is prolonged or strenuous and the horse is untrained.10 A submaximal exercise test is often valuable for detecting rhabdomyolysis because it provides more consistent evidence of subclinical rhabdomyolysis than maximal exercise tests.3,11 Fifteen minutes of trotting is often sufficient to produce subclinical muscle damage in horses prone to chronic exertional myopathies.12 If signs of stiffness develop before this, exercise should be concluded. A normal response would be less than a threefold to fourfold increase from basal CK.
Thermography may be useful for identification of superficial abnormal temperature changes from muscle damage but has little value in horses with deeper injuries. However, there are many potentially confusing issues such as recent removal of a rug or tack. Careful comparisons of the left and right sides should be made. Muscle inflammation is seen as an area of increased temperature in the skin directly overlying the affected muscle. The most common sites of muscle strain identified thermographically include the longissimus dorsi, the origin or body of the middle gluteal, the insertion of the gluteals on the greater and third trochanters of the femur, biceps femoris, semitendinosus, semimembranosus, and adductor muscles.13
Nuclear scintigraphy is useful for identification of some forms of muscle damage and may alert the clinician to an area of deep muscle damage that had not been suspected based on clinical examination. In human athletes, technetium-99m stannous pyrophosphate has been used to assess the degree of skeletal muscle damage and to delineate areas of damage.14,15 It is thought that abnormal uptake of the radiopharmaceutical reflects an early stage of muscle damage from episodic ischemia, which is reversible in some fibers but may lead to muscle necrosis in others.14
Technetium-99m–methylene diphosphonate (MDP) is taken up in some damaged muscle in the horse and is best seen in the bone (delayed) phase images, that is, 3 hours after injection. Scintigraphy has been used most commonly in horses with a history of poor performance, with or without stiffness after exercise, to confirm a diagnosis of equine rhabdomyolysis.16 The mechanism of MDP binding is unknown, but the release of large amounts of calcium from damaged muscle or the exposure of calcium binding sites on protein macromolecules in the damaged muscle may be responsible. Diffuse linear areas of increased radiopharmaceutical uptake (IRU) are commonly seen in the caudal epaxial muscles and the muscles of the hindquarters and thigh in some but not all horses with ER (Figure 83-5). Less commonly there is IRU in the triceps and latissimus dorsi muscles.
The use of scintigraphy for the diagnosis of other muscle injuries has not been documented in the horse, but in one author’s experience (SJD) it can be helpful in some horses with either proximal forelimb or hindlimb muscle injuries. Uptake of the radiopharmaceutical tends to be much more focal and much less intense than in horses with rhabdomyolysis. In some, but not all, horses the region of IRU has correlated with a region of increased echogenicity identified ultrasonographically.
Diagnostic ultrasonography is potentially useful for identification of muscle trauma and fibrosis, provided that there is physical disruption of the muscle and assuming that one knows where to look. Muscles have a rather typical striated echogenic pattern,17,18 but this varies according to the muscle group, and careful comparisons must be made between similar sites in contralateral limbs, in both transverse and longitudinal images. The appearance of muscle is also sensitive to the way the horse is standing and whether the muscle is under tension; therefore it is important that the horse is standing squarely and bearing weight evenly. Muscle fascia appears as well-defined relatively echogenic bands. Care must be taken in identifying large vessels and artifacts created by them.
In an acute injury, muscle fiber disruption is seen as relatively hypoechoic areas within muscle, with loss of the normal muscle fiber striation. The jagged edge of the margin of the torn muscle may be increased in echogenicity. Tears in the muscle fascia may be identified. The muscle defect may be filled by a loculated hematoma that is slowly replaced by hypoechogenic granulation tissue. With muscle fiber repair there is a progressive increase in echogenicity. Relatively hyperechogenic regions may develop as a result of fibrous scarring, which may result in long-term gait abnormalities. Hyperechogenic regions causing shadowing artifacts reflect mineralization.
The routine examination of muscle biopsies has resulted in the identification of a number of specific equine myopathies. To fully characterize a neuromuscular disorder and its rate of progression, muscle fiber sizes, shapes, and fiber type distribution, mitochondrial distribution, polysaccharide staining pattern, neuromuscular junctions, nerve branches, connective tissue, and blood vessels should be examined in frozen sections using a battery of tinctorial and histochemical stains.19
A number of basic pathological responses of muscle can be identified in formalin-fixed, paraffin-embedded sections. These include inflammation, muscle fiber necrosis, muscle fiber regeneration, variations in muscle fiber sizes and shapes, alterations in the number of cell nuclei, vacuolar change, and proliferation of connective tissue. However, there are many pathological alterations that cannot be detected in formalin-fixed tissue but can readily be seen in histochemical stains of fresh-frozen biopsy samples.20 Histochemical stains of frozen tissue allow muscle fiber types to be distinguished, differentiation between neurogenic and myogenic atrophy, characterization of vacuolar storage material, characterization of inclusion bodies, and assessment of mitochondrial density. In addition, frozen samples may be used for biochemical analysis of substrate concentrations and enzyme activities, as well as DNA isolation.
When considering collection of muscle biopsies, some general guidelines are applicable. Preferably, samples should be collected from what is considered abnormal/diseased muscle. A 6-mm outer diameter (Jorgen KRUUSE A/S, Langeskov, Denmark) percutaneous needle biopsy technique can be used to obtain small muscle samples through a 1.5-cm skin incision using a local anesthetic solution subcutaneously. If this technique is used, enough muscle should be obtained to form a 1.5-cm2 sample at a minimum. However, these samples do not tolerate well shipment to an outside laboratory. The optimum biopsy for shipment of histopathological tissues to a laboratory is collected using surgical or open techniques and performed under local analgesia. Care must be exercised to infiltrate only the subcutaneous tissues, not the muscle, with the local anesthetic solution. The objective is to obtain approximately 2-cm3 of tissue; hence a suitably long skin incision is required. Subsequently two parallel incisions 2 cm apart should be made longitudinal to the muscle fibers with a scalpel. The muscle should only be handled in one corner using forceps, and care should be taken not to crush the tissue. The muscle sample is then excised by transverse incisions 2 cm apart, and the tissue is fixed appropriately.
Samples submitted for routine histopathology can be placed in formalin. Samples for histochemical analysis require fixation in isopentane (methylbutane) chilled in liquid nitrogen to ensure rapid freezing and minimization of freeze artifact. In the field, where freezing is not possible, fresh samples wrapped in gauze slightly moistened with saline can be shipped in a water-tight hard container on icepacks to specialized laboratories. Samples that potentially may be used for biochemical analysis should be immediately frozen in liquid nitrogen. Samples for electron microscopy (EM) require appropriate fixation in glutaraldehyde preparations. Ideally, thin sections of muscle for EM should be clamped in vivo to maintain fibers at a resting length before they are excised. However, if pathology other than the alignment of thick and thin myofilaments is to be investigated, small muscle pieces can be excised and placed directly in appropriate EM fixative.
Responses of strips of fresh muscle to stimuli such as caffeine, halothane, and a variety of other agents can be performed on site by specialized laboratories, but these tests are largely research tools.21,22
A specific diagnosis of the cause of muscle atrophy, muscle fasciculations, or myotonic dimpling after tapping the muscle can be aided by performing electromyography (EMG). EMG of normal skeletal muscle shows a brief burst of electrical activity when the needle is inserted in muscle and then quiescence, unless motor units are recruited (motor unit action potentials), or the needle is very close to a motor endplate (miniature endplate potentials). Normal muscle shows little spontaneous electrical activity unless the muscle contracts or the horse moves. Motor unit action potentials can be evaluated to assess amplitude, duration, phase, and number of phases. Myopathic changes include a decrease in duration and amplitude of motor unit action potentials.23,24 Horses with abnormalities in the electrical conduction system of muscle, or denervation of motor units, show abnormal spontaneous electrical activity in the form of fibrillation potentials, positive sharp waves, myotonic discharges, or complex repetitive discharges.
Based on the information obtained on neuromuscular examination and muscle biopsy, a diagnosis can usually be obtained. The following classification system may be helpful to narrow down rule-outs for muscle disease in horses:
The role of muscle pain and injury in lameness and poor performance in the horse is rather poorly recognized. In human athletes, muscle fatigue, muscle stiffness, and muscle soreness are well-recognized entities, although the pathological processes in the absence of detectable structural abnormalities are not completely understood. Increased intramuscular pressure may be associated with muscle pain after prolonged vigorous exercise in human athletes.14
Delayed-onset muscular stiffness or soreness (DOMS) is recognized in people as pain that develops 24 to 48 hours after unaccustomed use of certain muscles and usually resolves spontaneously, assuming the muscles are not overworked again.25 Continued overstress may result in structural damage to myofilaments. However, specific training involving the activity that provoked the original DOMS decreases the amount of soreness associated with that condition over time.
Muscle soreness in the pectoral region after repeated jumping efforts is commonly recognized, especially in event horses several hours after completing the cross-country phase of a Three Day Event.26 It seems to improve with massage.
Muscle fiber tearing and hemorrhage can result in acute muscular pain in human athletes. A palpable defect or swelling can be detected in superficial muscles. For deeper muscles, ultrasonography is required for accurate diagnosis.
Muscle fibrosis and mineralization have been well documented in the horse following tearing of the semimembranosus and semitendinosus muscles (see Fibrotic Myopathy section, page 558), but acute lesions here and elsewhere in the limbs have been poorly documented.27-29 The use of diagnostic ultrasonography17,18 has helped in the diagnosis of both acute and more chronic muscle lesions, but diagnosis often remains a challenge because of the deep location of some affected muscles and the lack of localizing clinical signs.
In one author’s (SJD) experience, the most commonly recognized muscle injury sites in the forelimb include biceps brachii, brachiocephalicus, the pectorals, and the musculotendonous junction of the superficial digital flexor (Figures 83-1 to 83-4). In the hindlimb, semimembranosus and semitendinosus, adductor, gracilis, gluteal, and gastrocnemius muscle injuries have been recognized most frequently. Acute muscle tearing and hemorrhage can result in severe pain and lameness and other clinical signs mimicking colic. Swelling around the damaged muscle, assuming it is superficial, may not appear until 24 to 48 hours later.
Fig. 83-1 A and B, Longitudinal ultrasonographic images of the muscles at the base of the neck on the left and right sides of an advanced-level event horse with restricted forelimb gait (left images indicate left side; right images indicate right side). The horse had severe pain and tension in the strap muscles at the base of the neck on the left side and slight muscle atrophy. Note the increased echogenicity of the deeper muscle on the left side compared with the right. The horse was treated by H-wave stimulation that resulted in progressive relief of the muscle spasm and clinically significant improvement in gait and ability to jump.
Fig. 83-2 Transverse ultrasonographic images of the right (left) and left (right) gracilis muscles of a 12-year-old Thoroughbred cross event horse with acute-onset right hindlimb lameness of 6 days’ duration, with slight swelling of the muscle, pain on palpation, and diffuse edematous swelling in the crus. At the time of lameness onset, the horse showed signs attributed to colic. A focal region of increased echogenicity in the right gracilis muscle is caused by muscle fiber tearing and hemorrhage.
Fig. 83-3 Transverse ultrasonographic image of the left brachiocephalicus muscle of a Grand Prix dressage horse that showed left forelimb lameness only when performing lateral movements, such as half pass. The lameness was not altered by any local analgesic technique. There is a focal area of increased echogenicity, caused by muscle fibrosis, resulting in acoustic shadowing.
Fig. 83-4 Longitudinal ultrasonographic image of the cranial aspect of the antebrachium of a 7-year-old hunter. The horse had developed acute-onset lameness 3 months previously, associated with substantial soft tissue swelling on the cranial aspect of the antebrachium. The extensor carpi radialis muscle is enlarged greatly and has hypoechoic and hyperechoic regions, with little normal muscle architecture.
Muscle tension and spasm in the thoracolumbar region are well-documented sources of pain contributing to poor performance in association with primary hindlimb lameness, but primary muscle pain in this region has often tended to be overlooked by many veterinarians, although recognized by physiotherapists. Localized muscle soreness and the interpretation of abnormal sensitivity of acupuncture points are potentially confusing. Protective muscle spasm may also develop secondary to a primary lesion of either the thoracolumbar spine or the sacroiliac region (see Chapters 49 to 52).
Jeffcott et al30 demonstrated that injection of lactic acid into the left longissimus dorsi muscles could significantly diminish performance of Standardbred (STB) trotters worked at speed on a treadmill, although changes in gait were subtle.
One author (SJD) has seen a number of horses that had suddenly lost performance during competition or training, either following a particularly extravagant jump or after an awkward jump. The horses had subsequently become reluctant either to jump or to gallop downhill. Clinical examination revealed intense muscle spasm in the caudal thoracic and lumbar regions, with associated pain. Manipulation to release muscle spasm resulted in relief of pain and rapid restoration of normal performance. Acute back muscle pain may also be induced by a fall.
Localized back muscle soreness is readily induced by a poorly fitting saddle. It may also be caused by a rider who either sits crookedly or is unable to ride completely in balance with the horse. This may be because of the ineptitude of the rider or the shape of the saddle and the way in which it sits on a particular horse and thus positions the rider. Such muscle pain is usually localized to the saddle area and may be associated with slight soft tissue swelling. Thermographic examination may be helpful to demonstrate to an owner the associated localized inflammation. Pressure measurements can also be used (see Figure 117-6), although there is some variability in the accuracy of different commercially available systems.
It is important to establish whether there was a history of a fall or other traumatic event, the duration of clinical signs, whether swelling was noted, and whether the horse had exhibited lameness or had performed poorly.
The detection of muscle swelling from recent trauma or loss of muscle bulk as a result of fibrosis, chronic injury, or atrophy requires the horse to stand completely squarely, bearing weight evenly on all limbs and looking straight ahead. The horse should be appraised visually and by careful, systematic palpation, looking for defects in the muscle, muscle swelling, areas of abnormal muscle firmness from fibrosis, muscle tension, or spasm, and areas of pain.
In an acute injury resulting in muscle tearing or rupture, it may be possible to palpate a defect in the very early stages, but this will become filled with hemorrhage, inflammatory exudate, and edema. Careful palpation should enable detection of most acute superficial muscle injuries, but localization of deeper muscle injury may be more difficult. Identification of chronic muscle strain is more challenging because clinical signs are more subtle. The horse must be as relaxed as possible to assess properly the response to firm and deep palpation. If the muscle is sore, the horse may react by increasing tension in anticipation of pain or by pulling away. There may be “knots” within the area of damaged muscle.
The neck, limbs, and thoracolumbar region should be moved passively to detect any limitations in movement or pain induced by movement. The horse should be observed moving at both the walk and the trot to identify any characteristic gait abnormalities, such as an abnormal hind foot placement from fibrotic myopathy (see Chapter 48) or sinking of a front fetlock as a result of rupture at the musculotendonous junction of the superficial digital flexor (see Chapter 13). However, it must be borne in mind that muscle soreness resulting in compromise of performance may not result in overt lameness because pain may only be induced when the muscle contracts strongly or is stretched maximally. Pain associated with a brachiocephalicus muscle in a dressage horse may only be evident in particular movements such as half pass (see Figure 83-3). A show jumper with sore gluteal muscles may not push off as strongly with the affected limb, resulting in the hindquarters drifting toward the ipsilateral side as the horse jumps.
Muscle-stimulating machines can be helpful in the identification of superficial muscle injuries. Intermittent electrical stimulation of focal areas within a muscle results in muscle contraction and relaxation. The strength of stimulus can be varied. Horses vary in sensitivity and tolerance of the procedure, so careful comparisons must be made between the left and right sides. Damaged muscle tends to respond greater to lower stimulus strength, and contraction and relaxation are less smooth and may induce pain.
The aims of treatment include repair of damaged muscle, relief of both muscle spasm and pain, restoration of normal circulation, minimization of fibrous scar formation, and remobilization of muscles. The precise mode of treatment will depend on the type of muscle injury and the stage of injury and repair. Treatment modalities include laser,31,32 therapeutic ultrasound,31 H wave, transcutaneous electrical stimulation, electromagnetic therapy,33 massage,26 passive stretching combined with box rest, and a graduated, controlled exercise program. Relief of acute muscle spasm may require chiropractic manipulation. During return to work, the exercise program must be carefully moderated according to the site of the injury and to avoid overstress in the early stages of repair while encouraging a progressive increase in strength. These subjects are discussed more fully elsewhere (see Chapters 92 through 96).
Because equine muscle injuries are poorly recognized there has been little work on prevention. However, there is evidence to document the beneficial effects of warm-up before strenuous exercise.34-36 Warm-up enhances blood flow to active muscle and increases muscle temperature. This results in better oxygen delivery to exercising muscle, improved enzyme function, and increased range of motion. The best warm-up program for each type of exercise remains poorly defined; however, warm-up should aim to prepare the physiological systems, without contributing to excessive heat generation or fatigue.
ER has numerous etiologies and is a common complex cause of poor performance. About 3% of exercising horses had an episode of ER in the past 12 months.37 It occurs in a variety of breeds, including draft breeds, Warmbloods, Thoroughbreds (TB), STBs, Arabians, Morgans, Quarter Horses, Appaloosa, American Paint horses, and many more.37-41 In draft breeds, ER can be particularly debilitating, and terms such as Monday morning disease, azoturia, or paralytic myoglobinuria are used.42 A milder syndrome occurs in lighter breeds, and the terms tying-up, set fast, myositis, and chronic intermittent rhabdomyolysis are used to describe muscle necrosis or muscle cell stress following any form of exercise in the lighter horse breeds.43,44 Several specific causes have been identified for ER. Otherwise successful athletic horses may have a sporadic episode of ER from extrinsic causes such as dietary imbalances, concurrent respiratory infections, and inappropriate training regimens. In horses chronically afflicted with ER there may be an intrinsic dysfunction of muscle metabolism or muscle contraction.
The most common extrinsic cause of sporadic ER is exercise that exceeds the horse’s underlying state of training.44 Horses that are advanced too quickly in training, horses that are only ridden sporadically while being continually fed full rations, and horses performing strenuous exercise such as racing or endurance riding without sufficient conditioning commonly develop rhabdomyolysis. In addition, rhabdomyolysis may be more common in horses exercising during an outbreak of respiratory disease. Both equine herpesvirus–1 and equine influenza virus have been implicated as causative agents.38,45
Classically, horses lose impulsion and develop a stiff, stilted gait, particularly involving the hindquarters during exercise. There is excessive sweating and a high respiratory rate from pain. The horse may be unable to walk forward after resting because of firm painful muscle contractures involving the back and hindquarters. Signs are most commonly seen after 15 to 30 minutes of light exercise.40,46 A horse with severe rhabdomyolysis shows signs of colic, becomes recumbent, and develops occult myoglobinuria. The urine may be discolored and has an abnormal smell. Attempts to move more severely affected animals may result in extreme pain, obvious anxiety, and exacerbation of the condition.
ER is often symmetrical, involving gluteal, biceps femoris, semitendinosus, and semimembranosus muscles. Forelimbs are less commonly overtly affected. ER may accompany the exhaustion syndrome in endurance horses with concurrent evidence of a rapid heart rate, dehydration, hyperthermia, synchronous diaphragmatic flutter, and collapse.47 Muscle contractures are not always consistent in either endurance horses or event horses with ER.
Diagnosis is usually obvious based on the clinical signs, but measurement of serum muscle enzyme activities provides an assessment of the severity of muscle damage and confirms the diagnosis. The degree of elevation of muscle enzyme activity does not necessarily reflect the severity of clinical signs.
If an attack has occurred during exercise some distance from where the horse is normally stabled, the horse should not be made to walk home. It should be transported back home or left in a nearby stable. If an attack has occurred at a competition, the horse should be treated there and should not be transported home over a long distance until at least 24 to 48 hours later.
The objectives of treatment are to relieve anxiety and muscle pain, as well as to correct fluid and acid-base deficits. Acetylpromazine (0.04 to 0.07 mg/kg), an α-adrenergic antagonist, is helpful in relieving anxiety and may increase muscle blood flow. Its use is contraindicated in dehydrated horses. Alternatively, xylazine (0.4 to 0.8 mg/kg) may provide short-term relief from anxiety. In horses with extreme pain, detomidine (0.02 to 0.04 mcg/kg) combined with butorphanol (0.01 to 0.04 mg/kg) provides excellent sedation and analgesia. Nonsteroidal antiinflammatory drugs (NSAIDs) such as ketoprofen (2.2 mg/kg), phenylbutazone (2.2 to 4.4 mg/kg), or flunixin meglumine (1.1 mg/kg) provide additional pain relief. Analgesic treatment is continued to effect, but most horses are relatively pain free within 18 to 24 hours.
Intravenous or intragastric dimethyl sulfoxide (as a <20% solution) can be used as an antioxidant, antiinflammatory, and osmotic diuretic in severely affected horses. Corticosteroid administration is advocated by some veterinarians in the acute stage. If the horse is recumbent, methyl prednisolone succinate (2 to 4 mg/kg intravenously [IV]) should be given once. Muscle relaxants such as methocarbamol (5 to 22 mg/kg, IV slowly) seem to produce variable results, possibly depending on the dosage used. The administration of dantrium sodium (2 to 4 mg/kg orally [PO]) in severely affected horses may decrease muscle contractures and possibly prevent further activation of muscle necrosis. This can be repeated in 4 to 6 hours.
Severe ER can lead to renal compromise from ischemia and the combined nephrotoxic effects of myoglobinuria, dehydration, and NSAIDs. The first priority in horses with hemoconcentration, or myoglobinuria, is to reestablish fluid balance and induce diuresis. In horses with mild rhabdomyolysis, administration of fluids via a nasogastric tube may be adequate, but generally fluids are better given intravenously. Balanced polyionic electrolyte solutions are best. If severe ER is present, then isotonic saline or 2.5% dextrose in 0.45% saline may be necessary because horses often have hyponatremia, hypochloremia, and hyperkalemia. If hypocalcemia is present, then supplementing intravenous fluids with 100 to 200 mL of 24% calcium borogluconate is recommended, but serum calcium should not exceed a low normal range. Affected horses are usually alkalotic, making bicarbonate therapy inappropriate.48
Ten liters of fluids may be given rapidly. The total fluid replacement is based on an estimation of the degree of dehydration and the clinical response: if the horse is mildly dehydrated (5%), give 10 L fast and then 15 L over the next 4 to 6 hours; if dehydration is severe (20%), give 10 L fast and then 50 L at 4 L/h. If the horse is recumbent, consider using at least two intravenous giving sets and infusing into both the jugular and the cephalic veins. Suture the catheters in place.
Ideally, reassessment of the packed cell volume and concentrations of total plasma protein and serum electrolytes after the initial period of therapy should provide a successful guide for the therapeutic regimen. However, in the practical situation, the clinical response to therapy is usually an adequate indicator. In severely affected horses, regular monitoring of blood urea nitrogen and/or serum creatinine is advised to assess the extent of renal damage. Diuretics are usually contraindicated unless the horse is in oliguric renal failure.
Horses should be stall rested on a hay diet for a few days. Small paddock turnout in a quiet area for a few hours twice a day is then helpful. Horses may be handwalked at this time but not for more than 5 to 10 minutes at a time. For horses with extrinsic (sporadic) ER, rest with regular access to a paddock should continue until serum muscle enzyme activities are normal. Training should be resumed gradually, and a regular exercise schedule that matches the degree of exertion to the horse’s underlying state of training should be established. Avoid lunging exercise until the horse is back in normal work. If the horse has a day or several days off, the dietary energy concentrations should be reduced accordingly.
Horses that have repeated episodes of ER from a young age, or from the time of purchase, or when they are put back into training after a long period of rest may have a chronic dietary imbalance or underlying intrinsic abnormality of muscle function. Chronic forms of ER are seen in many breeds of horses, including draft horses, Warmbloods, Quarter Horses, American Paint horses, Appaloosas, TBs, Arabians, STBs, Morgans, and crossbreds.39,44,49-55 Many of the horses with intrinsic muscle defects will have repeated episodes of rhabdomyolysis with minimal exercise, even when the dietary and training recommendations for sporadic ER are followed. Three specific intrinsic causes of ER have been identified to date: recurrent exertional rhabdomyolysis (RER),56 type 1 polysaccharide storage myopathy (PSSM),57,58 and type 2 PSSM.59 It is likely that there are other specific causes that have yet to be identified (idiopathic chronic ER). In all these intrinsic forms of chronic ER, it appears that there are specific environmental stimuli that are necessary to trigger muscle necrosis in genetically susceptible animals.46,56 Horses cannot be cured of a susceptibility to this condition, but if the specific disease is identified, changes in management can be implemented to minimize episodes of rhabdomyolysis.