The musculoskeletal system

Chapter 15

The musculoskeletal system

Chapter contents




The distal (third) phalanx (P3, coffin bone)

The middle phalanx (second phalanx, short pastern bone, P2)

The proximal phalanx (first phalanx, long pastern bone, P1)

The proximal sesamoid bones

The third metacarpal/metatarsal (cannon) bone

The second and fourth metacarpal/metatarsal (splint) bones

The carpal bones

The accessory carpal bone

The radius

The ulna

The humerus

The scapula

The calcaneus (fibular tarsal bone)

The tibia (crus)

The fibula

The patella

The femur

The pelvis




Lameness directly associated with trimming and shoeing

Conditions of the hoof capsule

Infections of the foot

Hoof wall separation

Conditions of the deeper structures of the foot

Conditions of the heels



Diseases of the suspensory apparatus

Miscellaneous tendon and ligament injuries

Diseases and injuries of articular soft tissue structures

Tendon lacerations and ruptures

Tendon sheaths


Diseases of muscle



Most horses are produced and kept for athletic purposes although ambitions range from intermittent use for pleasure riding to the extreme demands placed on the elite racing Thoroughbred. Whatever the requirements, lameness is the greatest contributor to loss of performance, missed training and attrition of horses, and consequently is the single most common problem of equine practice.

Disturbances of the locomotor system have attracted research funds and initiatives such that the equine veterinary literature abounds with advances in diagnostic and treatment modalities. Understanding in this field exceeds that of other domestic species and therefore the services available to horses are similar to those provided for human athletes.

The conditions encountered daily in general veterinary practice range from ill-fitting shoes through developmental conditions to long bone fractures. Accurate diagnosis and understanding of pathophysiology are vital for appropriate early case management. These areas are therefore highlighted in this section. Emphasis is also placed on the management of common problems; more esoteric considerations can be made after additional investigation of the literature or at a referral center.

Despite advances in imaging modalities, diagnostic local analgesia remains pivotal in the investigation of equine lameness. Understanding of basic local analgesic techniques is therefore necessary for all who evaluate lame horses.


The importance of diagnostic local analgesia in the investigation of equine lameness has been well documented. Typically this involves perineural or regional analgesia and intrasynovial analgesia although epidural analgesic techniques (q.v.) are frequently used for treatment of orthopedic pain.

The judicious use of local analgesia in the investigation of equine lameness should be deferred until a thorough clinical appraisal, including assessment of the gait abnormality, limb palpation, etc., has been completed. This is particularly true when the history or performance level suggests that there may be a nondisplaced fracture or serious soft tissue injury.

Fortunately, aberrant distribution of the appendicular nervous system is uncommon in horses. There are few indications for the use of ring blocks or field blocks as diagnostic techniques because they usually produce little more than cutaneous desensitization. However, when aberrant nerve routes are suspected they may be a useful adjunct to perineural analgesia.

When possible, intrasynovial analgesia should precede perineural infiltration when involvement of a specific joint, bursa or tendon sheath is suspected, since this will not interfere adversely with the interpretation of subsequent regional blockade. The reverse is, however, not true. Moreover it is acceptable to “leapfrog” with intrasynovial techniques whereas perineural analgesia should be performed in a sequential manner beginning distally. Intrasynovial analgesia is usually specific, and periarticular structures such as ligaments and tendons usually retain sensation. There are a few notable exceptions to this generalization, including intra-articular (IA) anesthesia of the distal interphalangeal joint.

Local analgesics are salts of weak bases in aqueous solution. Penetration and diffusion in tissues is determined by their lipid solubility. These salts dissociate in neutral or alkaline areas, and are therefore not as active in acid media, e.g. infected sites. The local analgesic cation binds to anionic receptors on the nerve fiber blocking the sodium channels. As a result, sodium entry and depolarization are prevented. This is referred to as a non-depolarizing block. Since the myelin sheath of nerves is both an electrical and pharmacologic insulator, access of local analgesic to myelinated fibers is limited to the nodes of Ranvier and so a higher concentration of agent is necessary to induce anesthesia of myelinated compared with non-myelinated nerves.

Although transmission in all nerve fibers can be blocked by local anesthetics, there is generally a difference in susceptibility of various types of nerves. Sensations disappear in order from pain, cold, warmth, light touch, joint proprioception to deep pressure, and return in the reverse order. As a result, when desensitizing a peripheral nerve, differential blockade may be produced—pain may be overcome completely (i.e. type A-δ and C fibers are blocked) but motor function and touch (type A-α and A-β fibers) can remain unaffected.

Once the local anesthetic agent has been deposited around a nerve it diffuses from outside toward the center. Small diameter nerve trunks are therefore more susceptible to blockade than large nerves. In addition, since the most distal limb elements supplied by a particular nerve are the core fibers, and therefore blocked last, the most pertinent tests of efficacy are performed as far distal to the site of infusion as possible.

Following vascular removal from a site, agents are detoxified by liver and plasma pseudocholinesterases (principally the former) and metabolites are excreted by the kidneys.

The three most suitable local analgesic agents are:

Two per cent mepivacaine hydrochloride is widely used and demonstrates reduced local tissue reaction in equines, particularly with IA infusion. Systemic toxicity is unlikely to be a problem at dose rates up to 10 mg/kg in local infiltration. However, both systemic and local reactions can occur with repeated doses, and inadvertent rapid IV injections can produce initial excitement followed by CNS depression. Intravenous barbiturate is the treatment of choice if an overdose is suspected.

All local anesthetic agents (with the exception of cocaine) cause peripheral vasodilatation, thereby enhancing vascular absorption, although the intensity of response varies with the site of injection, dosage and between individual agents. The duration of action of mepivacaine and lidocaine is reported to be as short as 45–60 min. However, clinical experience suggests that these times are frequently exceeded and there are reports that effects persist for up to 3 h. Bupivacaine has a duration of action of up to 6 h and is therefore a useful agent when sedation is required for administration of a diagnostic block.

The duration of action of all agents is prolonged by the addition of a vasoconstrictor, e.g. epinephrine/adrenaline hydrochloride. Systemic toxicity is also reduced but at a price, since prolonged local exposure will increase the effects of tissue irritation at the site of injection. Epinephrine/adrenaline at 1 in 50000 dilution results in local tissue ischemia and necrosis. Generally 1 in 100000 or 1 in 200000 is adequate and will almost double the duration of local anesthetic action, but even at these concentrations the subsequent production of white hairs at nerve block sites can be a problem, and epinephrine/adrenaline is generally avoided.

Clean injection techniques are essential when performing perineural local analgesia, and aseptic technique is mandatory for IA procedures or for performing regional nerve blocks that can inadvertently enter a synovial cavity. Appropriate aseptic technique requires full surgical skin preparation, and wearing sterile surgical gloves. Studies have shown that it is not necessary to clip the hair over the injection site, but with a heavy haircoat or gross contamination of the area it may be advisable to do so. Many experienced practitioners still routinely clip before synovial injection.

A new vial of local anesthetic should be used for intrasynovial analgesic administration.

Many of the inflammatory reactions that occur following local analgesic techniques are probably due to poor technique including iatrogenic contamination. While antibiotics are not usually necessary when intrasynovial analgesia is undertaken, if conditions are less than ideal or repeated injections are required, they can be added. It is important to select antibiotics that do not precipitate when mixed with the local anesthetic agent (i.e. 2% lidocaine mixed with penicillin or ampicillin). The aminoglycosides gentamicin (300 mg) and amikacin (250 mg) can be mixed with local anesthetics without precipitating and they maintain their antibiotic efficacy in the mixture. Consequently, they are used regularly, particularly when there is a concern about potential contamination or when sepsis is already present.



The minimal amount of restraint conducive to good technique and personal safety is recommended. When the technique in question is most easily performed with the limb weight bearing then an assistant lifting another leg is often the most effective option. A twitch can be employed when necessary and in some circumstances sedation may be required.

There are obvious difficulties in interpretation of local analgesia of a sedated animal, and a sedative with a shorter duration of action than the local anesthetic should be utilized. Intravenous xylazine (q.v.) is often the drug of choice, although almost any sedative or sedative combination can be employed if bupivacaine is used. When xylazine or another α2-agnoist is used, the sedation can also be reversed with an appropriate antagonist such as atipamezole or yohimbine to allow for earlier re-evaluation. Nervous horses can be sedated with low doses of acetylpromazine (0.02 mg/kg IV or 0.04 mg/kg IM). The drug should be administered before evaluating the horse’s baseline lameness, as the sedation can actually facilitate the examination and augment lameness.

For injection around deep nerve trunks, e.g. median nerve or tibial nerve, and for difficult intrasynovial infusions or fractious horses, a small SC bleb of local anesthetic greatly facilitates the procedure. Eliminating patient movement increases the accuracy of placement and reduces iatrogenic damage.

During intrasynovial techniques, accuracy of placement can be ensured by aspirating synovial fluid before infusion although this is not possible in all locations. It is not necessary to withdraw the same volume of synovial fluid as of the local analgesic agent to be infused. When synovial fluid cannot be aspirated, careful movement of the needle can also be used to confirm IA or intrasynovial placement. This can usually be supported by observation of the site as injection proceeds. Ultrasound can also be invaluable in guiding difficult intrasynovial injections, e.g. the coxofemoral joint.

There is general agreement that approximately 5–10 min should be allowed for regional blockade to be effective and 15–30 min for intrasynovial analgesia. However, there is significant variation in these times between sites and between individual patients, e.g. some intrasynovial techniques have shown responses in <5 min and some proximal (large) perineural blocks may take >30 min for full effect. During this time the horse is usually walked quietly to become accustomed to the desensitized area and to provide diffusion of intrasynovial anesthetic agents before reassessing the animal’s gait and, where appropriate, the quality of the block.

Evaluation of the efficacy of perineural local analgesia requires knowledge of the zones of cutaneous innervation provided by individual nerves together with the deeper structures supplied. Whenever possible both should be evaluated.

Individual techniques

Details of forelimb and hindlimb regional and intrasynovial analgesia are given in Table 15.1.



Four major functions of bone can be identified. The tissue provides:

To function as a skeleton, the bones must be stiff, and bone is one of the hardest substances in the body.

Bone derives from the embryonic mesenchyme, developing either by endochondral ossification or by intramembranous ossification. Long bones have specialized sites of endochondral ossification—the growth plates. In both types of ossification the method of bone deposition is the same. Under the influence of increased vascularity, mesenchymal cells differentiate and become osteoblasts. These cells line the surfaces on which bone matrix is being deposited. Osteoid is the organic portion of bone that is laid down first and later becomes mineralized. Both the production and mineralization of osteoid seams are functions of the osteoblast. The matrix of mature bone is approximately one third organic (mainly osteocollagenous fibers) and two thirds inorganic (hydroxyapatite crystals of calcium phosphate).

Early in its formation bone is described as woven because the collagen fibers are entwined in a haphazard fashion. Fetal bone and the first bone produced at sites of fracture repair have a high woven component. In certain specialized localities, such as dental alveoli or osseous labyrinths, woven bone persists into maturity. However, woven bone is usually gradually replaced by lamellar bone in which the collagen fibers are organized into layers.

According to the density of lamellae, bone may be classified as compact (cortical, dense) or spongy (cancellous, trabecular). Lamellae may be piled in one plane, but more typically they are ordered according to the Haversian system in which between 4 and 20 layers of bone describe concentric rings around a central canal containing blood vessels. Each Haversian unit is called an osteon. The principal cell of mature bone is the osteocyte. Osteocytes function to preserve the integrity of bone matrix. They respond to certain stimuli to release calcium and are also capable of bone destruction. The specialized cell for bone destruction is, however, the osteoclast.

The external, non-articular surfaces of bones are covered by periosteum consisting of an outer fibrous layer permeated by blood vessels and nerves and an inner osteogenic layer. Periosteum derives from the periosteal bone collar, which supplies osteoblasts to the periphery of developing bones. At that stage it is a highly vascular structure, but in adulthood it is a relatively loose covering of connective tissue containing mostly venules and capillaries. Nonetheless the periosteum retains osteogenic potential if injured. At certain sites, e.g. ligament, tendon or capsular insertions, modified periosteal fibers called Sharpey’s fibers penetrate cortices providing firm anchorage. Endosteum is similar to periosteum, but is thinner and lines the medullary cavity of the bone.

Vascularity of bone is maintained through a medullary and periosteal blood supply, and the blood supply to bone differs between mature and immature states. Generally the blood supply to immature bone is more extensive. In developing bones with active growth plates the epiphysis and metaphysis have separate supplies because most vessels do not traverse the cartilaginous plate. There are transphyseal vessels in large epiphyses. The epiphysis is supplied by a network of vessels entering at articular margins circumferentially—an arrangement particularly vulnerable to trauma. The metaphyseal side of the growth plate is supplied by a similar arborization of vessels entering via numerous foramina. These anastomose with branches of the nutrient artery before coursing perpendicular to the active growth plate. Periosteal vessels supply the outer third of forming cortical bone of the diaphysis. In mature bone significant periosteal supply persists only at sites of firm fibrous attachments.

The principal supply to long bones is via a main nutrient artery which enters the diaphyseal cortex at a fascial attachment, passes through the cortex to the medulla and then divides into ascending and descending branches. These subdivide to supply intramedullary bone, sites of hematopoietic marrow plus the inner two thirds of all cortical bone. The metaphyseal ends of long bones are supplied by the proximal and distal metaphyseal arteries that persist from the immature state. Blood flow through cortical bone is mainly centrifugal, i.e. from medullary cavity to periosteum, with an intravascular pressure gradient between vessels at the two sites. Blood supply to flat and irregular bones is much more diverse than that to long bones, with multiple afferent and efferent points.

Marrow is the term used to describe the soft substance occupying the intertrabecular spaces of spongy bone. Marrow in the fetus and neonate is primarily hematopoietic (red). In the adult the marrow of long bones becomes primarily fatty (yellow) but does contain primordial stem cells. In the mid-shaft of some long bones the medulla has no spongy bone present and is termed the medullary cavity.


Bone is a unique material that can change shape as it grows in a process called modeling. It can also regenerate itself through remodeling, in which the bone is activated and areas are resorbed and reformed. Bone responds readily to the complex forces on the skeletal system that cause small deformation of the bone, but superimposed on the mechanical requirements of bone is the need for it to fulfill its metabolic role, specifically in calcium homeostasis. Bone is therefore subject to adaptive activity in response to a wide range of biochemical influences, principally hormonally mediated. There are three major hormones (q.v.) that affect the activity of bone cells:

1. Parathyroid hormone (PTH) is secreted by the parathyroid glands from cells highly sensitive to the calcium concentration in blood. PTH (q.v.) is the principal hormone regulating plasma calcium levels. Its action on bone is to increase resorption thus elevating blood calcium.

2. Calcitonin is secreted by C cells of the thyroid gland, which are also sensitive to plasma calcium concentration. Calcitonin (q.v.) is inhibitory to PTH and disables osteoclasts, therefore acting to decrease blood calcium levels.

3. Cholecalciferol (vitamin D3) is both ingested and, catalyzed by ultraviolet radiation, synthesized in the epidermis. The principal purpose of vitamin D3 (q.v.) is to provide sufficient extracellular calcium and phosphorus for mineralization to take place, and its chief role is increasing intestinal absorption of these.

The interactions of these three hormones are complex. In addition, their effects on bone cells can be modified or overridden by many other factors including the effects of other hormones, age, nutritional status, pathologic processes and biomechanical influences.

Although the basic blueprint for their overall structure is genetically predetermined, bones will model and remodel according to the use to which they are put or as a result of disease processes. In the course of normal activity a bone is intermittently loaded causing intermittent deformations of its structure. This physical property is at least part of the stimulus enabling bones to maintain mechanical competence. Excessive strains, either absolute or relative to the state of the bone under load, can be the cause of structural deterioration and ultimate failure.

The end stage of the modeling/remodeling adaptation is a function of antagonistic processes: resorption of existing bone and formation of new. In normal bone, equilibrated with its environment, there is still a constant need to replace damaged tissue. In compact bone, osteoclasts bore through existing Haversian systems, which become filled in by secondary osteons. In cancellous bone, the same occurs in large trabeculae but the smaller ones ossify by appositional deposition on their surfaces. With a decrease in customary strain levels, osteonal replacement rate increases but more bone is resorbed than is laid down. Consequently, cortices become porotic and can also become progressively thinner due to endosteal resorption.

Excessive strain levels cause damage to bone matrix, which stimulates replacement. The first phase of this involves bone resorption, further weakening the structure. If activity levels persistently outstrip the ability of a bone, or area of a bone, to remodel then defects in structure may progress to failure. This is the phenomenon sometimes referred to as exercise/stress adaptation mismatch or stress fracture. Candidates for such injuries are immature animals subjected to physiologically abnormal levels of exercise, perhaps with inappropriate training, or high performance athletes that undergo a change in training regimen for which they were unprepared. A series of studies at the University of Pennsylvania has provided an excellent example of the failure of bone remodeling to keep pace with athletic training.

Young Thoroughbred racehorses exercising at speed often develop a syndrome of bucked shins (q.v.) due to repetitive motion injury associated with high-strain cyclic fatigue of the third metacarpal bone, and can develop a stress fracture up to a year after the original injury. Adaptive exercise programs (q.v.) involving high-speed exercise in small doses can change the geometric properties of the bone and reduce the incidence of fatigue failure by changing the shape and substance of the bone.

Grooves and prominences on the outer surfaces of bones develop in adaptation to the pressure from overlying muscle bellies or tendons and the pull from soft tissue attachments, respectively. Mature periosteum can be reactivated by increased vascularity to form new bone at, or close to, sites of injury. Subchondral bone is also subject to remodeling in the face of repetitive functional overloading. This reduces its compressibility, undermining its ability to absorb shock, and so contributes to the vicious circle of osteoarthritis (q.v.).

The ultimate mechanical failure of bone is exemplified by fracture. The immediate response at a fracture site is an acute inflammatory reaction (q.v.) to soft tissue disruption and periosteal tearing, and to the necrosis caused by vascular compromise of the fracture ends. The inflammatory phase is succeeded by the reparative phase during which the initial hematoma is invaded by capillary buds (the process of granulation) that deliver mesenchymal cells enabling organization to occur. A callus is formed comprising fibrous tissue, cartilage and immature woven bone. The proportion of bone increases steadily, and with it the stability of the fracture site improves. The final step in healing of bone is the remodeling phase during which, through osteoclastic and osteoblastic activity, mature lamellar bone is produced. On occasion, fracture ends can be rigidly stabilized, permitting primary bone formation in which cutting cones of osteoclasts traverse the fracture gap and filling takes place via Haversian remodeling, bypassing the fibrocartilaginous callus stage.


Bone infection can cause periosteitis, osteitis or osteomyelitis, depending on the depth of involvement. When the infection is initiated in the periosteum and outer cortex the term osteitis or osteoperiostitis is used, and when the infection begins in or extends into the medullary cavity the term osteomyelitis is more appropriate. An acute inflammatory process is provoked leading to edema, thrombosis and ischemic bone necrosis. Infective material travels through the Haversian and Volkmann’s canals, spreading the process. Extension into epiphyses and joints is possible because of the communication between metaphyseal and epiphyseal vessels.

As the disease progresses, scar tissue forms. Necrotic bone is sequestrated by osteoclastic activity and becomes encapsulated by dense sclerotic bone (involucrum). Inflamed periosteum lays down new bone. If the process is not arrested then pathologic fractures may result from physiologic loads applied to bone with a compromised infrastructure.


Clinical signs can be highly suggestive but radiography is the definitive diagnostic procedure. Osteomyelitis may however be radiographically silent in the early stages and optimal radiographic definition is necessary to maximize diagnostic sensitivity. The first signs are typically mottling within the trabecular pattern, which progresses to areas of distinct radiolucency within the bone. Lesions are frequently discrete and with chronicity become surrounded by the radiodense involucrum. Sequestra are separated from the parent bone by radiolucent halos and they may increase in radiodensity. Periosteum adjacent to a site of bone infection may lift off the surface and produce palisading new bone.

Ultrasonography can also be valuable in identifying osteomyelitis and sequestrum formation. Ultrasound is particularly valuable for early identification of periosteal inflammation and subperiosteal fluid accumulation associated with infection or for evaluating areas that are difficult to evaluate radiographically such as the scapula.

Osteomyelitis has an intense uptake pattern with standard nuclear scintigraphy, and specialized nuclear imaging techniques including white blood cell labeling and radiolabeled ciprofloxacin can also be used to identify bone infection in difficult cases such a vertebral osteomyelitis. Computed tomography (CT) can also provide improved localization of osteitis lesions by eliminating superimposition in cross-sectional images. Magnetic resonance imaging has been found to be more sensitive for osteomyelitis than CT or radiography.

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Jul 8, 2016 | Posted by in EQUINE MEDICINE | Comments Off on The musculoskeletal system
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