1-year-old, male white-tailed deer (Odocoileus virginianus).Tissues are from 1 of 20 white-tailed deer being restrained in a drop-floor chute located outside. Deer were being restrained to obtain skin biopsies of tuberculin skin test sites, as part of an on-going project. Handling and restraint began in early morning when ambient temperatures were cooler, but by the end of the exercise ambient conditions were hot and humid. This deer was the last of the 20 deer to be processed through the chute. Upon entering the chute, the deer showed markedly increased respiration (panting), frothy saliva around the mouth, and was hyperthermic to the touch, although a body temperature was not recorded. The deer was doused profusely with cool water and given several cool water enemas. Respirations slowed toward normal, but the animal remained subjectively hyperthermic. The deer was moved to an interior, cooler location. Several hours later the deer was in sternal recumbency, alert, but did not rise when approached. Eighteen hours after restraint, although alert, the animal was unable to rise and was euthanized.
The deer was in adequate nutritional status. The forestomachs contained moderate amounts of dry ingesta. Multifocal areas of both pallor and hemorrhage were present in muscles of the hindlimbs, forelimbs, epaxial and sublumbar muscles as well as the diaphragm. Lesions were bilateral but not symmetrical. Affected muscles appeared drier than normal. The heart was grossly unaffected. Bilaterally the kidneys were characterized by focally extensive black discoloration extending superficially through the cortex and involving as much as 75% of the cortical surface. The bladder contained a moderate amount of red-brown colored urine.
The cross-section of skeletal muscle is characterized by focally extensive myofiber degeneration and necrosis. Slides vary with 20-60% of myofibers affected. Myofibers have lost visible cross-striations and vary greatly in size, many being large and swollen with flocculent, pale eosinophilic cytoplasm while others are smaller with hyalinized eosinophilic cytoplasm. Affected myofibers have pyknotic or karryorhectic nuclei. Within some myofibers there is basophilic, punctate to granular staining interpreted as mineralization. Endomysial and perimysial spaces are mildly expanded due to edema and a cellular infiltrate composed of low numbers of both neutrophils and macrophages.
Skeletal muscle: degeneration and necrosis, focally extensive, with mineralization, white-tailed deer (Odocoileus virginianus).
Capture myopathy (exertional myopathy, exertional rhabdomyolysis) is characterized by damage to skeletal muscle, and sometimes cardiac muscle, and is commonly observed after capture, immobilization (chemical or manual), and transport. It is an important cause of morbidity and mortality in captured and handled wild animals, including birds, and should always be considered in planning and designing wildlife capture and handling events.(4) All ages and sexes are susceptible and warm environmental temperatures, such as those in the present case, predispose animals to the condition.
Animals with capture myopathy may die suddenly or develop clinical signs hours, days or weeks later. Capture myopathy has been diagnosed up to a month after capture. Clinical syndromes of capture myopathy have been described based on time until onset of clinical signs as hyperacute, acute, subacute and chronic (reviewed in 4). More recently, other authors have based the classification of clinical syndromes on pathophysiology; capture shock syndrome, ataxic and myoglobinuric syndrome, ruptured muscle syndrome and a rare, poorly characterized delayed-peracute syndrome.(2) The ataxic and myoglobinuric syndrome is the most common, and is consistent with the present case.
Under normal conditions wild animals are not subjected to prolonged, maximal muscular exertion. However, during pursuit and capture such conditions may exist. Therefore, the earliest clinical signs of capture myopathy are similar to those of maximal exertion, increased respiratory and cardiac rates. Body temperature is usually elevated. Other early clinical signs may include depression, weakness, ataxia, muscle stiffness, and muscle tremors. Death may occur immediately post-capture due to marked metabolic acidosis, shock and circulatory collapse.
Animals surviving hours or even days may continue to show signs of depression, hyperthermia, tachypnea, tachycardia, weakness, and ataxia. Difficulty standing may progress to recumbency. Dark colored urine due to myoglobinuria may be seen. For weeks survivors may continue to show lameness, ataxia, muscle stiffness, and weight loss. Occasionally rupture of damaged muscle groups may occur. The gastrocnemius muscle is especially prone to rupture under such conditions.
The pathophysiology of capture myopathy is related to both shock and metabolic acidosis. The stress of pursuit and capture results in strong and prolonged sympathetic stimulation of microvasculature and eventual exhaustion of sympathetic vascular tone. Lack of vascular tone leads to visceral pooling of blood, decreased venous return, decreased cardiac output, hypotension, and hypoxia. In spite of hypoxia, tissue metabolism continues, relying on anaerobic glycolysis and resulting in increased levels of intracellular pyruvic and lactic acid. Lactic acid diffuses into the blood at levels that overwhelm the capacity of the liver, heart and other tissues to convert lactic acid to useable energy and lactic acidosis develops.
Prolonged hypoxia and acidosis result in generalized tissue deterioration. Active transport of sodium and potassium is reduced due to low intracellular pH. Intracellular sodium and chloride levels rise as do extracellular potassium levels. Mitochondrial activity decreases, lysosomes rupture, releasing damaging enzymes. Tissue necrosis ensues, especially in skeletal muscle, heart, liver and lung. Renal lesions of capture myopathy are characterized by moderate to severe tubular epithelial cell degeneration and necrosis with protein (myoglobin) and cellular casts. Renal lesions are primarily the result of renal ischemia.
Hyperthermia exacerbates tissue necrosis. Heat is generated from muscle myofilament action, glycolysis, recovery heat production as metabolic processes attempt to restore muscle to a resting equilibrium, and the environment. Heat from the environment can be transferred to muscle cells during exertion.(1)
Capture myopathy is similar to march myoglobinuria or extertional rhabdomyolysis in untrained athletes or military recruits following heavy exercise at high ambient temperatures.(2)
Skeletal muscle: Myocyte degeneration and necrosis, focally extensive, moderate, with mineralization and edema.
The contributor provides an outstanding review of the entity. Although skeletal muscle is a remarkably plastic tissue capable of a variety of responses to injury (e.g. necrosis, degeneration, regeneration, atrophy, hypertrophy, splitting, and fiber-type conversion), segmental necrosis and regeneration is a common result of a number of causes that merit inclusion in the differential diagnosis, and definitive determination of the underlying etiology is often difficult based solely on gross and microscopic lesions.(3) Conference participants considered nutritional myopathy due to selenium and vitamin E deficiency or imbalance, toxic myopathy (e.g. ionophore toxicosis), and other types of exertional myopathies (e.g. polysaccharide storage myopathy) which could produce identical microscopic lesions, but strongly suspected capture myopathy based on the signalment. Characterizing the distribution and duration of the lesions, and in particular, classifying necrotic skeletal muscle lesions as monophasic or polyphasic, is sometimes helpful in narrowing the differential diagnosis. For instance, monophasic necrosis, as in the present case, is more consistent with an exertional or acute toxic myopathy, while polyphasic necrosis is more consistent with muscular dystrophy, selenium deficiency, or ongoing intoxication.(3)
Participants reviewed the basic stages of skeletal muscle necrosis, repair, and regeneration. Because myofibers are multinucleate, these changes can occur segmentally and are initially characterized by hyalinization of the sarcoplasm with loss of cross striations, followed by sarcoplasmic fragmentation often with mineralization. Effective skeletal muscle regeneration depends on the presence of an adequate blood supply, an intact basal lamina, and viable satellite cells. In the presence of adequate blood supply, macrophages derived from blood monocytes, with or without other leukocytes, are quickly recruited to the site of necrosis, traverse the basal lamina, and clear cytoplasmic debris. Simultaneously, satellite cells, juxtaposed between the sarcolemma and basal lamina, are activated and begin division into myoblasts in support of the regenerative effort. The remaining intact basal lamina forms a scaffold, i.e. sarcolemmal tube, which excludes fibroblasts and guides proliferating myoblasts, which then fuse end-to-end to form myotubes that eventually produce thick and thin filaments and mature into myofibers. By contrast, if large numbers of satellite cells are killed, even with persistence of the basal lamina, healing occurs by fibrosis rather than regeneration. In cases typified by loss or disruption of the basal lamina, even with persistence of viable satellite cells, regeneration is ineffective and healing is characterized by the formation of muscle giant cells (large, bizarre multinucleated giant cells) accompanied by fibrosis.(3)
1. Spraker T: Pathophysiology associated with capture of wild animals. In: Pathology of Zoo Animals, eds. Montali RJ, Migaki G. pp. 403-414. Smithsonian Institution Press, Washington, DC, 1980
2. Spraker T: Stress and capture myopathy in artiodactylids. In: Zoo and Wildlife Medicine Current Therapy 3, ed. Fowler M, pp. 481-488. W.B. Saunders, Philadelphia, PA, 1993
3. Valentine BA, McGavin MD: Skeletal muscle. In: Pathologic Basis of Veterinary Diseases, ed. McGavin MD, Zachary JF, 4th ed., p9. 985-989, Mosby Elsevier, St. Louis, MO, 2007
4. Williams E, Thorne E: Exertional myopathy (capture myopathy ). In: Noninfectious Diseases of Wildlife, eds. Fairbrother A, Locke L, Hoff G, 2nd ed., pp. 181-193. Iowa State University Press, Ames, IA, 1996