Sprain injuries have been recognized in the veterinary literature for over a century.(2,3,5,8-10,13,15,16,18,20,22,23) They have been identified in virtually all of the domestic species but are most prevalent in the dog and horsed Although generally believed to be an "athletic-type" injury, sprains are common among household pets and occur in a wide variety of circumstances.(8,9)
Sprains are defined generally as direct or indirect trauma to a joint. Specific classification schemes focus on the qualitative aspects of associated ligamentous injury. First degree sprain injury involves minimal tearing of a ligament and fibers; second-degree, the partial tearing of a ligament; and third-degree, the complete tearing of a ligament (Fig. 69-1). All of these injuries are characterized as having a strong tendency to recurrence and aggravation, often leading to persistent instability of the joint and frequently favoring the development of secondary osteoarthritis. (11)
Sprains are a relatively common injury in the dog, particularly in the carpal region, and are sustained under a variety of circumstances.(1,8-10,22,23) Slipping and sliding, falling out of a window and landing on the forefeet, and tumbling over the side of a chair, bed, or step constitute only a brief list of potential sprain situations for the household pet. The field or hunting dog often incurs carpal sprain in the course of hurdling natural obstacles such as fallen tree limbs, gullies, and the like, especially following periods of hard and sustained exercise when fatigue levels are at their highest. It is perhaps noteworthy to mention that among track athletes, distance runners are more prone to sprain injury than their more glamorous counterparts, the sprinters.(11)
Somewhat paradoxically, sprains are probably the most poorly managed musculoskeletal disorder in the dog. The expression "it's just a sprain" should be condemned and recognized for what it is, an admission of medical ignorance. Sometimes it appears to be a statement of relief when clinical examination of an injured limb has failed to reveal instability and the radiographic examination shows no sign of fracture. However, as far as a favorable prognosis is concerned, it may be better in some instances to have a fracture injury (if not associated with significant ligamentous damage) than a second-degree sprain.
The existing attitudes toward sprain injury, apparently shared by many veterinarians, may have their origin in six principal sources: an inadequate appreciation of the pathology of a sprain; ignorance of the specific anatomy of the ligaments supporting the joints; failure to correlate clinical and radiographic information; poor understanding of the radiographic signs associated with sprain, particularly those related to the soft tissues; lack of awareness of the importance of stress radiography in the diagnosis of sprain; and failure of many teaching institutions to deal with the problem of sprain injury in pet animals in more than cursory fashion.
Sprains are recognized on physical examination by the facts that until substantial swelling has occurred, tenderness is fairly well localized to the area where the ligament has been sprained, and that movement of the joint in a direction that puts tension on the ligament will produce pain in the area of injury unless rupture is complete. Usually, if the latter is the case, the part is obviously unstable, although often relatively pain free. Table 69-1 illustrates the qualitative aspects of carpal sprain injury. Radiographic examination of a suspected sprain injury is recommended not only for the purpose of ruling out fracture complication, particularly of the avulsive variety, but to aid in the qualitative evaluation of the soft tissue injury. As indicated above, the data obtained from both the physical findings and the radiographic analysis are then integrated diagnostically.
|FIG. 69-1 Sprain classification schemes generally focus on the qualitative aspects of the ligamentous injury. First-degree sprain injury involves minimal tearing of ligament and associated fibers, as well as a varying degree of internal hemorrhage (A). Second-degree sprain usually results in definite structural breakdown as a result of partial tearing. Hemorrhage is both internal and periligamentous, with moderately extensive inflammatory edema (B). Third-degree sprain is most severe and often involves complete rupture of the ligament body (C). Avulsion at the points of origin or insertion usually results in one or more small bone fragments, which may often be identified radiographically (D).|
|TABLE 69-1 Characteristic Findings in Sprain Injury in the Dog.|
Prior to discussing the pathology of sprain injury, it seems wise to review the basic function of ligaments. Like tendons, ligaments are dense, stiff, very stable bands of fibrous tissue (Fig 69-2). The major difference between the two is in their functions. Whereas tendons attach muscle to bone, ligaments attach one bone to another. Ligaments effectively maintain proper osseous spatial relationships by providing limit to a given range of motion.(6,17) They are more flexible than tendons, hence a certain amount of motion can occur at their connecting joints, but at the same time they have, like tendons, relatively little elasticity. They therefore can be stretched only to a limited degree before they rupture or "tear." In the process of tearing of some of the fibers of the ligament, an elongation takes place, and the ligament so lengthened does not return to its normal length; thus, its cross-sectional strength in the area where the tearing occurred is permanently weakened.(7) Healing is often a protracted proposition that can require months to be completed. It takes place, not by the formation of new ligament, but by the replacement of the torn portion by fibrous connective tissue. The greater the distance between the intact fibers, the more of this scar tissue will be formed, and hence the weaker the healed ligament.(11,19)
|FIG. 69-2 A ligament is a band of relatively nonelastic tissue that unites two or more bones and is composed predominantly of long parallel collagenous fibers.|
At the gross level, the acute sprain injury is most often expressed as variable degrees of point tenderness, swelling, heat, and pain.(8,9) Instability is liable to accompany the more severe injury. The inflammatory concomitants of acute sprain relate qualitatively to the degree of ligamentous trauma as well as to the extent of damage sustained by the joint capsule and associated synovium. Figure 69-3 illustrates the gross and microscopic mechanisms of acute sprain injury.
Chronic sprain injury, while appearing outwardly similar, is inwardly much different. (11,19) The regional soft tissues are rarely tender and they lack the inflammatory characteristics seen in the acute sprain. The joint capsule is markedly thickened as a result of long-standing hyperplastic/hypertrophic activity stimulated by chronic instability. Villous hypertrophy is frequently present and associated with excessive quantities of cytologically abnormal synovial fluid. Secondary osteoarthritis impingement exostoses, avulsion fractures, and spatial derangements are often present in various combinations.
|FIG. 69-3 Mechanisms of sprain injury.|
The radiographic diagnosis of sprain injury is frequently a passive process. That is to say, if fracture injury is not identified and the patient is obviously lame, the inference is made that the injury must be of an occult variety, that is, soft tissue involvement only. This method of reasoning is obviously vulnerable and may not be expected to withstand critical examination. Moreover, it lacks a sense of diagnostic confidence that comes only from an active analytical process grounded upon expectation as well as appreciation of specific radiographic signs indicative of sprain injury, a basic understanding of the pathophysiologic alterations of sprain injury, and an accurate patient data base composed of both physical and historical information. Fundamental knowledge of bone and soft tissue anatomy is an obvious prerequisite to the diagnostic exercised An understanding of functional morphology is also extremely useful, especially in regard to prognosis.(24)
Radiographically, the acute sprain injury is evaluated best in qualitative terms. The analysis is carried out primarily on the basis of regional soft tissue alterations. In cases of suspected instability, stress radiographs are often useful. Severe forms of injury are frequently associated with avulsion fracture and subluxation. Table 69-1 describes the radiographic signs associated with varying degrees of sprain injury, while Figures 69-4 through 69-8 provide radiographic examples.
|FIG. 69-4 Hyperflexed stress radiograph of a feline carpus shows subluxation of the radiocarpal joint consistent with a third-degree sprain injury. The abnormal spatial relationship between the radius and proximal carpal row was not apparent on conventional views.|
|FIG. 69-5 Lateral stress radiograph of a canine stifle joint shows cranial subluxation of the tibia (cranial drawer sign) consistent with a third-degree sprain injury.|
|FIG. 69-6 Lateral stress radiograph of an immature canine stifle joint shows a sprain fracture luxation injury complex involving the epiphyses of the proximal tibia. Although considerable bony injury exists, the ligamentous tissues have likely sustained only a minor degree of damage (first-degree sprain). This injury emphasizes the fact that ligaments are often stronger than bone and invariably stronger than the cartilaginous growth plates in immature animals.|
|FIG. 69-7 Fulcrum-assisted craniocaudal stress radiograph of a canine stifle joint shows luxation secondary to a complete rupture of the medial collateral and cranial cruciate ligaments (third-degree sprains). The lateral collateral and caudal cruciate ligaments were partially torn (second degree sprains).|
|FIG. 69-8 Fulcrum-assisted dorsopalmar radiograph of a canine tarsus shows subluxation of the talocrural joint consistent with a third-degree sprain injury.|
Sprain injuries of intermediate and long-standing duration are often represented radiographically by osteoarthritic alterations. These changes stem from the instability resulting from the ligamentous damage incurred at the time of original injury. Focal new-bone development (exostoses) in the periarticular location may be associated with mechanical impingement of one joint member upon another as a result of chronic laxity. The most frequent types develop anteriorly at the contact points between the distal radius and radial carpal bone and between the articular elements of the distal carpal tier and the proximal metacarpus. These exostoses vary in size from small to large and can lead in extreme cases to carpal deformity (Fig. 69-9). Pathologically, impingement exostoses resemble the marginal exostoses of osteoarthritis. The dynamic implications of the impingement process are often verifiable with stress radiography (9,10,12)
Abnormal ligament healing frequently associated with second- and third-degree carpal sprain injury often results in extension instability (Fig. 69-10). This form of spatial derangement is best demonstrated with stress radiographs, particularly the fulcum-associated hyperextension maneuver in lateral recumbency, and the standing lateral projection using a horizontal x-ray beam. These methods, along with other useful stress techniques, are illustrated in Figure 69-11.
Other indications of chronic sprain injury may include regional heterotopic bone formation, osteochondral fracture, osteoporosis, and, on rare occasion, focal bone necrosis.
|FIG. 69-9 Lateral radiograph of a canine carpus shows extensive impingement exostoses in the periarticular region of the dorsoproximal metacarpus (large arrow). These changes have developed subsequent to a long-standing third-degree sprain injury to the intercarpal joint.|
|FIG. 69-10 Standing lateral stress radiograph of a canine carpus employing a horizontal x-ray beam demonstrates an abnormal degree of hyperextension. This abnormal weight-bearing posture is indicative of a third-degree sprain injury involving the palmar intercarpal ligaments flexor carpi ulnaris tendon, and palmar fibrocartilage.|
|FIG. 69-11 basic techniques by which stress radiographs may be obtained.|
Sprain injury shares many of its physical features with other musculoskeletal disorders. These include contusion, strain, fracture, infection, and circulatory disorders. Thorough physical examination combined with radiographic analysis usually narrows considerably the number of diagnostic possibilities.
Since descriptions of fracture, infection, and circulatory disorders appear elsewhere in this text, this discussion will focus on the less frequently published disorders, strain and contusion.
There are important fundamental differences between strain and sprain injuries. The term strain should be applied only to injury involving the muscle-tendon unit. Sprain is the appropriate term for discussing ligamentous injury. These terms are not interchangeable, although both forms of injury may exist concurrently.
Strain may be defined more exactly as damage to some part of a muscle-tendon unit (muscle, tendon, or associated attachment sites) resulting from unaccustomed activity. Strain in the dog may be either chronic, as a result of repeated "stretching" of the involved muscle-tendon unit, or acute, as occasioned by a single, sudden hyperextensive or hyperflexive action.
In either case, accepted classification schemes focus on the qualitative aspects of the strain injury: mild (first-degree), moderate (second-degree), and severe (third-degree). The point of damage commonly occurs at the weakest link of the muscle-tendon unit at the time of injury. Under a given stress the tendon may rupture, the muscle-tendon junction may give way, the muscle itself may be damaged, or the attachment sites may avulse.
The pathophysiology of strain injury is deceptively simple. Structural alterations in the muscle-tendon unit will obviously vary with the degree of injury. In any case, it is the attendant inflammatory changes that produce pain, discomfort, and concomitant lameness. The pathophysiological picture clouds, however, when the temporal aspects of the patient's pain profile are considered. Interestingly, and most importantly from the standpoints of history taking and, ultimately, client education, the lameness and associated discomfort are usually most pronounced on the second or third day following the onset of signs. The specific reasons for this unusual pain profile are unknown, although general belief holds that the primary cause is likely to be some form of biochemical injury that probably requires some finite period of time in order to reach maximal effect. It further appears that a similar period of time is necessary for these "chemical" offenders to be dissipated from the affected tissues.
There is little in the clinical profile of the strain patient that might be considered etiospecific, with the possible exception of the history, which may provide circumstantial evidence of strain, as well as some indication of whether or not the injury is likely to be chronic or acute.
The acute form of strain injury is more easily recognized than its chronic counterpart. The characteristic findings upon physical and radiology examination are presented in Table 69-2 as part of an integrative diagnostic approach that has been advocated in any clinical context employing radiologic input.(9)
Differential diagnosis should include moderate to severe contusive injury, sprain, and the milder forms of fracture. Aggravation of preexisting, compensated skeletal disorders, such as hip dysplasia and primary or secondary osteoarthrosis, should also be considered, especially in the geriatric patient.
|TABLE 69-2 Characteristic Findings in Strain Injury in the Dog|
A contusion (bruise) may be defined as a direct blow against the integument causing damage to the skin and underlying tissues. This results in capillary rupture and an infiltrative form of hemorrhage followed by edema and inflammatory reaction. The result is local swelling, which may be superficial or deep depending upon the nature of the object striking the blow and the location involved.(3) For example, a dog that is struck by an automobile and hurled headlong into the roadway catches the skin between two hard objects. The result is damage to the skin and subcutaneous regions and possibly to the cranium and brain. Conversely, a steel bumper striking the thigh region will trap the lateral musculature between the bumper and the femur. The resultant damage in this instance is to the muscle, since the underlying soft tissue protects the skin. The fundamental pathologic disorder is the same in either instance. Contusive injury is seen most frequently in cases of road accidents, although it may be present in any form of major or minor trauma, either in combination with other injury forms or as a separate entity. It may be recognized visually as a partial or complete defect in the hair coat or as a discoloration, abrasion, or discontinuity of the skin. On the other hand, contusion may appear as little more than a focal area of increased sensitivity, which may or may not be accompanied by additional diagnostic signs. The absence of skin discoloration, considered by most to be the hallmark of contusive injury, should not dissuade the clinician from the diagnosis of contusion. The blue black appearance of extravasated blood may develop more slowly in some animals than in others (minutes to days), while in many deep contusions there are neither initial nor subsequent skin manifestations, even though extensive underlying injuries may be present. Clearly, the presentation of all proposed contusive injuries will not be straightforward; on the contrary, many may be quite ambivalent. In such circumstances, it is well to recognize that even the most severely contused patient should be free of major pain and discomfort 7 to 10 days following injury. If this is not the case, the initial diagnosis must obviously be reconsidered.
Collateral ligaments are found medial and lateral to all major appendicular joints except the shoulder. Often in extremes of varus, valgus, rotation, or trauma the structure will tear (a third-degree sprain).
Collateral ligaments are short, relatively inelastic structures that may be difficult to repair. Many methods for repair have been devised and are discussed below.
External fixation of a joint in its midrange position may encourage healing. This usually requires very rigid fixation for a minimum of 6 to 8 weeks. At best, this technique is 25% successful. Success requires healing and scarring of the torn ligament.
Inadequate external fixation will result in failure of healing and probably sufficient joint instability to begin the process of degenerative joint disease.
Surgical reconstruction of collateral ligaments rarely involves primary suture of the torn ligaments, since most have been shredded beyond repair.
Collateral avulsions that have torn with a bony fragment may be reconstructed by interfragmentary screw fixation of the bone fragment. If the fragment is too small to accommodate a hole for the screw, the ligament can be trapped into its normal location using a spiked washers The reconstruction must be as anatomical as possible if normal joint function is to result.
Collateral ligament tears are usually reconstructed by supporting the joint using wire or nylon to mimic the collateral function; then, if possible, the torn ends are sutured. The most basic technique requires placing a cortical screw at each attachment point of the collateral ligament and connecting the screws with orthopaedic wire or nylon suture(4) (Fig. 69-12). If screws are unavailable, orthopaedic staples may be used or holes can be drilled through the attachment points as points of wire attachment.
The wire should be tightened sufficiently to give a stable joint but not so tight as to crush the opposing cartilage surface. It is generally agreed that in time the wire or nylon prosthesis will break and probably require removal. Prior to breakage, however, the collateral ligament scars and results in a stable repair. A few anatomical variations may require alteration in these techniques. Specifically, the very prominent medial malleolus makes wire placement difficult at the hock; therefore, a technique in which holes are placed through the malleolus allowing nylon to mimic collateral function may prove more useful.(14)
|FIG. 69-12 Technique for a repair of a collateral ligament using two cortical screws and a figure-of-eight orthopaedic wire. The screws must be placed as near as possible to the anatomical points of attachment of the ligament being reconstructed This figure illustrates use of the technique to reconstruct the medial collateral ligament of the stifle.|
Prolonged postoperative external immobilization will lead to joint stiffness. A supportive external bandage may be helpful for 7 to 10 days but should not remain longer. Following removal, exercise should be restricted to leash walking for an additional 2 to 4 weeks.
Complications can occur if excessive early activity is permitted. Should the wire or nylon prosthesis break prior to collateral scarring, the repair will fail. Likewise, surgical contamination or wound dehiscence leading to infection of the repair will result in failure.
The patellar ligament can be torn if the knee is severely flexed while the quadriceps is contracted. This may result in avulsion from the tibial tuberosity or tear through the ligament. Laceration due to automobile trauma or glass cuts is common.
Diagnosis of patellar ligament rupture is made by palpation. On flexion of the knee, there remains laxity of the patellar ligament. Radiographically the patella will be located more proximally than normal.
Repair requires removing tension from the ligament, followed by primary fixation. Surgical intervention is necessary. To remove tension from the patellar ligament, a tension band wire should be affixed between the patella and the tibial tuberosity. The patellar attachment may be accomplished by drilling a transverse hole through the patella or by looping the wire over the top of the patella (Fig. 69-13). The distal attachment is through a transverse hole in the tibial tuberosity. The tension band wire should be tightened until the patellar ligament ends lie in apposition. The ligamentous repair may be by a large tension suture and simple interrupted pattern at the cut ends. In instances of severe ligamentous loss, strips of dense fascia lata may be sutured into the defect.
Postoperative care is similar to aftercare of collateral ligament injuries: soft supportive bandage for 7 to 10 days, followed by 2 to 4 weeks of restricted activity. The wire will break and probably necessitate removal at a later date. Wire breakage is usually accompanied by acute lameness.
|FIG. 69-13 Technique to remove tension from a severed patellar ligament to allow suture The proximal point of purchase of the tension band wire is the proximal pole of the patella The wire is over the patella and through the quadriceps muscle insertion.|
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