Skeletal Muscle


Skeletal Muscle


Normal Skeletal Muscle

Understanding the normal structure and function of muscle, including gross, histologic, biochemical, physiologic, electrophysiologic, and ultrastructural features, is critical to understanding of muscle disease.

Structure of Myofibers

Structural and physiologic features of skeletal muscle determine much of its response to injury. Although muscle cells are frequently called muscle fibers or myofibers, they are in fact multinucleated cells of considerable length, which in some animals may approach 1 m. Myonuclei are located peripherally in the cylindrical myofiber (Fig. 15-1) and direct the physiologic processes of the cellular constituents in their area through a process known as nuclear domains. This anatomic arrangement allows segments of the cell to react independently of other portions of the cell. Myonuclei are considered terminally differentiated, with little or no capacity for mitosis and thus for regeneration.

Associated with myofibers are the satellite cells, also known as resting myoblasts (Web Fig. 15-1). These cells are distributed along the length of the myofiber, between the plasma membrane (sarcolemma) and the basal lamina. Satellite cells in skeletal muscle are very different from cells of the same name found within the peripheral nervous system. Muscle satellite cells are fully capable of dividing, fusing, and reforming mature myofibers. Thus, under favorable conditions, muscle cells (myofibers) are able to fully restore themselves after damage. Recent studies have found that pluripotent cells derived from bone marrow can also contribute to skeletal muscle repair, albeit only to a very small degree.

Each myofiber is surrounded by a basal lamina and outside of this by the endomysium, a thin layer of connective tissue containing capillaries. Myofibers are organized into fascicles surrounded by the perimysium, a slightly more robust layer of connective tissue (Web Fig. 15-2). Entire muscles are encased in the epimysium, a protective fascia that merges with the muscle tendon. This connective tissue framework is not inert, but in fact forms an integral part of the contractile function of muscle by storing and relaying force generated by myofiber contraction.

Ultrastructural examination reveals that skeletal muscle is a highly and rigidly organized tissue, with what are perhaps the most highly structured cells in the body. Each myofiber is composed of many closely packed myofibrils containing actin and myosin filaments. The striations visible with light microscopy (Fig. 15-2) represent the sarcomeric arrangement of muscle cells, in which actin and myosin filaments attached to transverse Z bands form the framework, and other organelles and intracytoplasmic materials are interspersed within this framework (Fig. 15-3). The endoplasmic reticulum of myofibers is called the sarcoplasmic reticulum and is modified to contain terminal cisternae that sequester the calcium ions necessary to initiate actin and myosin interaction and thus contraction. Sarcolemmal invaginations that traverse the cell, the T (for transverse) tubules, allow rapid dispersion of a sarcolemmal action potential to all portions of the myofiber. The terminal cisternae of two adjacent sarcomeres and the T tubule form what is called the triad (Fig. 15-3, A).

Neuromuscular junctions can only be visualized using electron microscopy or other specialized procedures (Fig. 15-4). Neuromuscular junctions occur only in specific zones within the muscle, usually forming an irregular circumferential “band” midway between myofiber origin and insertion.

Types of Myofibers

Mammalian muscles are composed of muscle fibers of different contractile properties. A common classification of these fibers is based on three major physiologic features: (1) rates of contraction (fast or slow), (2) rates of fatigue (fast or slow), and (3) types of metabolism (oxidative, glycolytic, or mixed). These physiologic differences form the basis of histochemical methods that demonstrate fiber types. There are several fiber-type classifications. Classification of fibers into type 1, type 2A, and type 2B (Table 15-1) has proved to have practical application in muscle pathology. It is the classification used in this text. Type 1 fibers are rich in mitochondria, rely heavily on oxidative metabolism, and are slow-contracting and slow-fatiguing. Type 2 fibers have fewer mitochondria and are glycolytic, fast-contracting, and more easily fatigable. In most species, type 2 fibers can be subdivided into type 2A and type 2B. Type 2B fibers are the fast-contracting, fast-fatiguing, glycolytic fibers that depend on glycogen for their energy supply. Type 2A fibers are mixed oxidative-glycolytic and therefore, although fast-contracting, are also slow-fatiguing. Thus type 2A fibers are “intermediate” in the concentration of mitochondria, fat, and glycogen between type 1 and type 2B.

Most muscles contain both type 1 and type 2 fibers, and these can be demonstrated by the myosin adenosine triphosphatase (ATPase) reaction (Fig. 15-5, A). Notice that the different fiber types are normally intermingled, forming what is called a mosaic pattern of fiber types. In most mature muscles, the staining pattern of the ATPase reaction reverses when sections are preincubated in an acid rather than an alkaline solution. There are examples of both patterns in the illustrations in this section. Acid preincubation can also be used to distinguish type 2A and type 2B fibers (Fig. 15-5, B). Regenerating fibers, classified as type 2C fibers, stain darkly in both acid and alkaline preparations, which is a distinguishing feature. In most species, oxidative enzyme reactions to demonstrate mitochondria also demonstrate fiber types to some degree (Fig. 15-6, A). Fiber typing can also be done by utilizing immunohistochemical procedures to identify specific myosin isoforms.

The percentage of each fiber type varies from muscle to muscle (Fig. 15-7). Type 1 fibers (slow-contracting, slow-fatiguing, and oxidative) are plentiful in those muscles in which the main function is slow, prolonged activity, such as those that maintain posture. Type 1 predominant postural muscles are most often located deep in the limb. Within the same muscle, the percentage of type 1 fibers often increases in the deeper portions. Muscles that contract quickly and for short periods of time, such as those designed for sprinting, contain more type 2B fibers. Only rarely are muscles composed of only one fiber type (e.g., the ovine vastus intermedius is type 1). Athletic training causes some type 2B fibers to be converted to 2A. There are also variations within breeds and differences in the same muscle in different species. For example, the dog has no type 2B purely glycolytic fibers; all canine fibers have strong oxidative capacity (see Fig. 15-6, B).

Innervation and Motor Units

The axons of the peripheral nerve trunks contain terminal branches that innervate multiple myofibers. The terminal branches form synapses with the myofibers at the neuromuscular junction. The myofibers innervated by a single axon form a motor unit, all fibers of which will contract simultaneously after stimulation. Different muscles have different sized motor units that relate to their function. For example, extraocular muscle function does not call for forceful contraction, but rather for many fine movements to smoothly move the globe. Therefore these muscles have very small motor units, with only a small number of myofibers (1 to 4) innervated by each axon. In contrast, the quadriceps muscle is not designed for fine movement, but instead is designed for generation of force, therefore motor units are quite large, with many myofibers (100 to 150 or more) innervated by a single axon.


Skeletal muscle has many functions in the body. Some obvious and major functions are maintaining posture and enabling movement, including locomotion. The rhythmic contraction of the respiratory muscles (the intercostal muscles and the diaphragm) is essential for life. In addition, muscles play a major role in whole body homeostasis and are involved in glucose metabolism and maintenance of body temperature. On a purely esthetic level, muscle contributes to pleasing body contours.

The function of skeletal muscle is intimately related to the function of the peripheral nervous system. The physiologic attributes of a muscle fiber—its rate of contraction and type of metabolism (oxidative, anaerobic, or mixed)—are determined not by the muscle cell itself but by the motor neuron responsible for its innervation (Fig. 15-8). This fact is significant in evaluating histologic changes in muscle fibers. It is possible to divide changes in muscle fibers into two major classes: neuropathic and myopathic. Neuropathic changes are those that are determined by the effect or the absence of the nerve supply (e.g., atrophy after denervation). The term myopathy should be reserved for those muscle diseases in which the primary change takes place in the muscle cell, not in the interstitial tissue and not secondary to effects from the nerve supply. The term neuromuscular disease encompasses disorders involving lower motor neurons, peripheral nerves, neuromuscular junctions, and muscles.

Metabolism and Ionic Homeostasis

Myofibers require a great deal of energy in the form of adenosine triphosphate (ATP) to generate force and movement. Type 1 oxidative and type 2A oxidative-glycolytic fibers use aerobic metabolism of glucose, stored in the muscle as glycogen, and fat. Type 2B glycolytic fibers rely primarily on anaerobic metabolism of glycogen for energy. Inherent or acquired metabolic defects that reduce skeletal muscle energy production can result in severe muscle dysfunction. A commonly encountered postmortem change, rigor mortis, illustrates the importance of ATP generation within skeletal muscle. The muscle contractile apparatus is still active immediately after death. ATP is necessary for the release of actin from myosin, the interaction that results in the sliding of myofilaments and contraction of muscle. After death, the absence of adequate ATP production causes the muscle fibers to undergo sustained contraction, which is known as rigor mortis. Rigor mortis eventually disappears because of muscle structural breakdown caused by autolysis or putrefaction (bacterial decomposition). The period of time for onset and release of rigor mortis varies, depending on physiologic (glycogen stores at the time of death) and environmental factors such as the environmental temperature (see Chapter 1).

Skeletal muscle is also excitable tissue, similar to that of the nervous system. Maintenance of proper ionic gradients across the sarcolemma is essential for initiation of the action potential. Internal ionic gradients, especially of calcium ions, are critical for initiation and termination of contraction. Alterations of ionic fluxes across the sarcolemma, or within the sarcoplasmic reticulum, can have a serious negative impact on myofiber function.

Examination of Muscle: Clinical, Gross, and Microscopic

The decision to closely examine muscle, either by a biopsy or at necropsy, relies on recognition of indicators of neuromuscular dysfunction.

Clinical Findings

Clinical signs of muscular disease are variable (Box 15-1). The most common manifestations are alteration in muscle size, muscle weakness, and abnormal gait. Depending on the nature of the disorder, clinical signs can be localized, multifocal, or generalized.

Alteration in muscle size is readily detected with careful physical examination. Unilateral atrophy is best appreciated by comparing muscles on both sides of the body. In cases of generalized atrophy, it is important to bear in mind the normal muscling of the breed. For example, the muscling of dairy cattle is less prominent than that of beef cattle, and mild generalized muscle atrophy in a draft horse breed is more difficult to detect than in a light horse breed.

Weakness can be obvious, as in an animal that is unable to rise or prefers to remain recumbent, or can be manifested primarily as exercise intolerance. Special attention should be paid to gait analysis. The gait of an animal with generalized weakness caused by muscle or peripheral nerve dysfunction will have a short stride and often be stiff, and all four legs are often positioned well under the body for support while standing. The abnormal gait of an animal with neuromuscular disease must be distinguished from a similar gait that can occur because of musculoskeletal disease (which is a misnomer, as these disorders affect bone and joint not muscle). Muscle or peripheral nerve dysfunction in the horse, with this species’ unique biomechanics of the pelvic limb, can result in mechanical lameness that can be mistaken for neurologic disease. Odd equine hindlimb gaits designated with such terms as shivers, stringhalt, and fibrotic myopathy are caused by muscle or peripheral nerve disorders. A fibrotic myopathy-like condition also occurs less commonly in the dog and can involve the forelimb. Severe denervating or progressive myopathic conditions that begin in utero or at an early age can cause joint contractures and limb deviation (see Fig. 15-44).

Animals with myotonia often exhibit a stiff gait and develop episodic muscle spasms that can lead to collapse. Percussion of muscle groups can cause a persistent muscle contraction known as dimpling.

In dogs, horses, and ruminants, the esophagus contains a large percentage of skeletal muscle. In dogs and camelids, myopathic, neuropathic, and neuromuscular junction disorders can involve these muscles, causing esophageal dysfunction and megaesophagus. Denervation can also contribute to esophageal dysfunction in cattle with vagal indigestion.

As far as can be determined by clinical evaluation and extrapolation from similar conditions in other species, most neuromuscular disorders in animals are not associated with pain. Muscle cramps, caused by either primary myopathy or partial denervation, and muscle swelling are exceptions to this rule.

Clinicopathologic Findings

If the plasma membrane of the myofiber is damaged or a segment of the myofiber becomes necrotic, some of the contents of the muscle cell will “leak out” and be taken up into the blood. The concentrations of some of these components in serum are used as an index of the extent of myofiber damage. The most commonly used is creatine kinase (CK), formerly called creatine phosphokinase (CPK). Aspartate aminotransferase (AST), formerly known as serum glutamic-oxaloacetic transaminase (SGOT), and lactic dehydrogenase (LDH) are also released but are not as specific an indicator of muscle damage because they are also present in other tissues. Because CK has a low renal threshold, it is quickly excreted in the urine. The half-life of circulating CK varies somewhat between species but is generally about 6 to 12 hours. The half-life of AST and LDH in the serum is much longer, and serum AST and LDH concentrations remain elevated for several days after muscle injury. Serum concentration of alanine aminotransferase (ALT) will also increase in all species from severe muscle cell necrosis. Other serum indicators of skeletal muscle injury include carbonic anhydrase III and fatty acid binding protein, but these latter proteins are not part of a routine serum chemistry panel. It has been speculated that the sarcolemma can become “leaky,” leading to release of CK and other enzymes, without the affected segment becoming overtly necrotic. This possibility is very hard to prove or disprove.

Although the laboratory testing for CK and AST is relatively standardized, laboratory normal ranges may vary considerably within and among laboratories. Determining the normal range of blood values for animals is a difficult task. Normal serum CK concentration in animals is generally less than 500 U/L. Normal serum concentrations of AST, ALT, and LDH vary greatly between species. Tests included in chemistry panels also vary in different laboratories. Some laboratories do not include CK in small animal chemistry panels, which can result in a misdiagnosis of hepatic disease in a dog or cat with a persistent increase in serum AST and ALT concentrations because of degenerative muscle disease. For the purposes of discussion in this chapter, a mild increase in CK or AST is considered to be up to 2 to 3 times normal, a moderate increase is 4 to 10 times normal, and a severe increase is 10 times normal or more.

It should be emphasized that myofibers can be dysfunctional without undergoing necrosis. Myopathic and neuropathic conditions resulting in atrophy, weakness, spasm, stiffness, or myotonia rarely result in significant increase in serum muscle enzyme concentrations. At this time there is no biochemical parameter that will assess muscle fiber function; only morphologic or structural muscle fiber integrity can be assessed.


Electromyography (EMG) can be a valuable tool when evaluating patients with suspected neuromuscular disease. Concentric needle EMG studies look for abnormal spontaneous activity generated by myofibers. In contrast to other electrodiagnostic studies, a flat line generated by a noncontracting muscle indicates a healthy muscle. Abnormal spontaneous activity includes wave forms designated as positive sharp waves, fibrillations, and myotonic bursts. These abnormal spontaneous electrical events are associated with characteristic sounds emitted by the EMG machine. Abnormal spontaneous activity, typically dense and sustained fibrillations and sharp waves, is generated in denervated muscle because of alteration in sodium channel activity in the membrane of denervated fibers. Spontaneous activity in degenerative myopathies, usually scattered fibrillations, positive sharp waves, and myotonic bursts, is likely related to ionic disturbances associated with fiber degeneration and regeneration; functional denervation after segmental necrosis of the segment containing the neuromuscular junction is also possible. Myotonic conditions result in notably abnormal ionic fluxes leading to waxing and waning of spontaneous potentials with a characteristic “dive bomber” sound. Severe denervating and degenerative disorders and canine cushingoid myotonia can be accompanied by myotonic bursts that start and stop abruptly, characteristic of pseudomyotonia.

Nerve conduction velocity studies evaluate the integrity and function of the peripheral nervous system. Primary demyelinating disorders result in severe reduction of nerve conduction velocity, but axons are intact and muscles are still technically innervated; therefore spontaneous activity does not occur. Repetitive nerve stimulation tests the function of the neuromuscular junctions.

Methods of Gross and Microscopic Examination of Muscle

A variety of examination techniques are often necessary to best appreciate changes occurring in muscle.

Gross Pathology and Muscle Sampling

Gross examination includes evaluation of changes in size (atrophied, hypertrophied, or normal), color, and texture. The gross pathologic appearance of skeletal muscle can be quite deceiving. What appear to be mild changes in muscle on gross examination often can be severe on microscopic examination, and what appear to be severe changes on gross examination can turn out to be artefact. Subjective evaluation of size can be highly unreliable unless control muscles (e.g., from normal animals or from the opposite sides) are available for weighing and measuring.

Color changes are common. The intensity of the red color of muscle varies, depending on the type of muscle, the age and species of animal, and the extent of blood perfusion. Pale muscle can indicate necrosis (Fig. 15-9, A and B; see Figs. 15-26; 15-34, A; 15-36, A; and 15-40) or denervation (Fig. 15-9, C; see Fig. 15-37) but is also common in young animals and anemic animals. Pale streaking of muscle most often reflects myofiber necrosis and mineralization (see Fig. 15-9, A and B) or infiltration by collagen or fat (see Fig. 15-9, C and D), and is one of the more reliable indicators of gross pathologic changes. Muscle parasites can be grossly visible as discrete, round to oval, pale and slightly firm zones (see Figs. 15-41 and 15-42, A). Dark red mottling of skeletal muscle can indicate congestion, hemorrhage, hemorrhagic necrosis (see Figs. 15-32, A, and 15-38), inflammation, or myoglobin staining after massive muscle damage (see Fig. 15-36, A) or can simply reflect vascular stasis (hypostatic congestion) after death. Hemorrhagic streaks within the diaphragm often accompany death caused by acute exsanguination. A green discoloration can indicate either eosinophilic inflammation (Fig. 15-10) or severe putrefaction. Lipofuscin accumulation in old animals, especially cattle, can cause a tan-brown discoloration of muscle. Black discoloration of the fascia occurs in calves with melanosis as an incidental finding and in older gray horses with metastasis of dermal melanoma to muscle fascia.

Evaluation of texture is also important. Severely thickened and often calcified fascia occurs in cats with fibrodysplasia ossificans progressiva. Fat infiltration or necrosis can result in abnormally soft muscle. Decreased or increased muscle tone can be caused by denervation. Decreased tone can also occur as a result of a lack of muscle conditioning or postmortem autolysis.

Careful microscopic examination of multiple muscles is often required to detect lesions. In cases of suspected neuromuscular disease, multiple muscle samples should include active muscle (tongue, diaphragm, intercostals, and masticatory muscles), proximal muscle (lateral triceps, biceps femoris, semimembranosus, semitendinosus, and gluteal), and distal muscle (extensor carpi radialis, cranial tibial). For purposes of a biopsy, certain muscles (e.g., lateral triceps, biceps femoris, cranial tibial, semimembranosus, and semitendinosus) are easier to sample because of their parallel myofiber orientation. The ideal samples will also vary, depending on the suspected disorder, such as a type 1 predominant postural muscle for diagnosis of equine motor neuron disease; a type 2 predominant locomotory muscle for diagnosis of equine polysaccharide storage myopathy (EPSSM); and temporal or masseter muscle for diagnosis of masticatory myositis in dogs and masseter myopathy in horses. Short fibers, such as those in the intercostal muscle, are preferred for physiologic studies in which intact muscle fibers are necessary and for studies of neuromuscular junction zones.

To ensure proper fixation and orientation of sections prepared from fixed specimens, the sample should be a strip of muscle no more than 1 cm in diameter, with myofibers running lengthwise. Muscle maintains the ability to contract for some time after death, with the time varying, depending on the physiologic state.

Contraction of muscle after contact with fixative is the most common cause of an artefact called contraction band artefact. Contraction can be prevented or at least minimized by use of a specially designed muscle clamp (Web Fig. 15-3, A) or by placing the sample on a rigid surface, such as a portion of a tongue depressor, and fixing the ends with sutures, staples, or clamps before submersion in the fixative (Web Fig. 15-3, B).


Web Fig. 15-3 Techniques for collection of muscle samples for histologic examination.
Clamps are used to prevent contraction of a fresh muscle specimen when it is immersed in 10% neutral-buffered formalin or EM fixative. A, Types of muscle clamps (from left to right): disposable plastic clamps (open and closed), stainless steel clamps (open and closed), a gallbladder clamp (unmodified), and a modified gallbladder clamp. The stainless steel clamps are autoclavable, the best but expensive. A suitable and economical clamp (not shown), can be made by welding a bar approximately 1 cm long, 3 to 5 mm wide, and 3 mm thick between the lower jaws of two small hemostats. B, Final excision stage. Initially two longitudinal incisions, approximately 5 mm apart and 15 mm long are made into the muscle in the direction of the myofibers. A horizontal cut is made 3 to 4 mm below the surface to undermine a piece of muscle. One jaw of the clamp is inserted under the muscle until its tip just exits on the other side. The clamp is lifted several mm above the surface of the muscle to ensure that the muscle fibers are tense and then the jaws are clamped. The clamped piece of muscle is excised by cutting at each end adjacent to the clamp as shown above. The muscle sample, still in the clamps, is placed in the fixative, usually 10% BNF for histopathologic examination and fixed overnight. For fixation for electron microscopic examination, the muscle in the clamp is placed into EM fixative for 1 to 2 hours. For histopathologic examination the muscle is trimmed by freeing the strip of muscle between the clamps by cutting immediately adjacent to the clamp jaws. Then a transverse section is cut from one end of this sample, avoiding any crushed area, and the remainder of the sample is cut longitudinally in the direction of the myofibers. Both samples are desirable for histopathologic examination. For electron microscopy, after fixation for 1 to 2 hours, slivers 0.5 to 1 mm thick are shaved from the outside of the sample. These are cut into pieces 0.2 mm in diameter and 0.5 mm long, with the longer dimension being in the direction of the myofibers. This long sample facilitates embedment so that the fibers are oriented either in cross section or longitudinally. Both sections are required for electron microscopy. C, Pinning strips of muscle onto a rigid surface, such as a piece of tongue depressor before immersion in 10% neutral-buffered formalin, will also minimize fixation artifacts but is not as effective as the clamps shown above. (A and B courtesy Dr M.D. McGavin, College of Veterinary Medicine, University of Tennessee. C courtesy Dr. B.A. Valentine, College of Veterinary Medicine, Oregon State University.)

Microscopic Examination

Frequently, lesions in muscles can be detected and evaluated only by microscopic examination. Proper microscopic examination requires evaluation of both transverse and longitudinal sections. Myofiber diameters, cytoarchitectural changes, and the percentage of abnormal myofibers are most reliably evaluated in transverse sections. Longitudinal sections reveal the length of changes such as segmental necrosis or regeneration or deposition of storage material. Improperly oriented samples, which result in sections that have obliquely oriented myofibers and thus neither longitudinal nor transverse myofibers, are difficult to evaluate. Use of a magnifying glass or dissecting microscope can aid in determining the orientation of myofibers during trimming of muscle before sectioning. Routine stains, such as hematoxylin and eosin (H&E), run the risk of offering the pathologist a “vast pink wasteland” for evaluation (Fig. 15-11, A) and are often inadequate for detecting subtle myopathic changes, lesions within intramuscular nerves, or presence of abnormal stored material. Various special stains, including reticulin, Masson trichrome, von Kossa, lipid (performed on frozen sections of fixed samples), and periodic acid–Schiff (PAS) for glycogen, are often invaluable in evaluation of routinely processed skeletal muscle (Web Table 15-1). Examples of many of these disorders can be found here in this chapter. Other valuable stains and reactions can only be performed on frozen sections of unfixed muscle samples (see Web Table 15-1).

For many decades, myofiber typing could be done only on frozen sections using the myosin ATPase reaction. Recently, immunohistochemical staining of myosin has been developed for demonstration of myofiber types in formalin-fixed muscle. This is a major advantage because fiber-type staining is often essential for the complete evaluation of muscle. It is most useful in demonstrating preferential involvement of a fiber type and alteration of the fiber-type pattern, the result of denervation and reinnervation.

Enzyme Histochemistry and Immunohistochemistry: There is no question that frozen section histochemistry of unfixed muscle samples is the “gold standard” of muscle pathology. Skeletal muscle may be the one tissue in which the morphology of cells and cellular components is best appreciated in frozen sections (Fig. 15-11, B). Routine frozen section histochemistry on muscle includes a battery of stains applied to serial sections. Examples of many of these stains are illustrated in this chapter. Stains used include H&E, modified Gomori’s trichrome, ATPase for fiber typing, nicotinamide adenine dinucleotide dehydrogenase (NADH), succinate dehydrogenase (SDH), cytochrome oxidase, and other mitochondrial enzyme stains, PAS for glycogen, alizarin red S for calcium, alkaline phosphatase and nonspecific esterase for macrophages and denervated fibers, and lipid stains. When indicated, frozen sections also allow for immunostaining for cytoskeletal proteins, such as dystrophin (see Fig. 15-46) and the dystrophin-associated proteins. Certain abnormal structures, such as nemaline rods formed by expansion of Z bands, as seen in nemaline rod myopathy, are not visible in routine sections but are readily identified in frozen sections stained with modified Gomori’s trichrome.

The major disadvantage of frozen section histochemistry is that unless a neuromuscular disease laboratory is readily available to immediately process unfixed muscle samples, careful preparation for overnight shipping, on ice, in a moist but not overly wet environment, is necessary. Any delay in shipment or overwetting or overheating of the sample results in nondiagnostic samples. In addition, preparation of frozen sections is time and labor intensive, and in most cases only a single transverse section approximately 1 cm in diameter is examined. This can create a significant sampling error when evaluating a small sample of a large muscle in which lesions may not be evenly distributed.

Complete evaluation, which includes morphometric examination and calculation of the percentage and mean diameter of each fiber type, detects changes in the percentage of each fiber type and fiber atrophy or hypertrophy. But at this time, morphometric analysis is not routinely performed on samples submitted for diagnostic purposes.

Frozen section histochemistry is always a powerful tool for evaluation of muscle disease. But in many disorders, it is possible to obtain diagnostic sections from routinely processed muscle samples when appropriate sample selection, handling, and processing are performed, and sections are examined by a pathologist familiar with muscle pathology.

Portals of Entry

Portals of entry are summarized in Box 15-2. Injury to muscle can occur secondary to trauma or infection. Muscle lying superficially can be damaged by penetrating wounds, including those created by intramuscular injections (Fig. 15-12; see also Fig. 15-9, B), which can also allow entry of infectious agents. Muscles located deeply are often injured after bone fracture. Crush injuries from external forces cause extensive muscle damage, and excessive tension can cause muscle tearing. Muscles are endowed with an extensive vascular network that can allow entry of blood-borne pathogens, immune complexes, antibodies and toxins, and inflammatory cells.

Sep 17, 2016 | Posted by in GENERAL | Comments Off on Skeletal Muscle
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