Managing physeal and articular fractures (Proceedings)


Juxta-articular fractures are fractures occurring near the joint surface. They may be intra- or extra-articular.

Juxta-articular fractures are fractures occurring near the joint surface. They may be intra- or extra-articular. Intra-articular fractures include Salter III and IV fractures as well as humeral and femoral supracondylar fractures. Most juxta-articular fractures occur in skeletally immature dogs. These fractures are challenging because of the short length of one of the bone segments, the potentially small size of the bone, the relative softness of bone and because of the presence of articular surfaces near the fracture site or involved in the fracture.

Juxta-Articular fractures are fractures result in the disruption of the articular cartilage, underlying subchondral bone and usually some portion of the epiphyseal, metaphyseal or diaphyseal bone. These fractures can alter joint morphology immediately affecting joint stability, cause pain, and disrupt the effective motion of the joint. Therefore, treatment of articular fractures is aimed at anatomic reconstruction of the fracture and articular cartilage, rigid internal compression and stabilization of the fracture fragments and early mobilization of the joint. The aims in treatment are to restore joint stability and congruity, to minimize degenerative articular changes and maintain joint function.

Small bone fragment size either including or near the joint surface can limit methods of stable fixation. Recommendations for plating of a fracture include at least 6 cortices on either side of the fracture site. Juxta-articular fractures are often not amenable to conventional plating methods due to the small and inadequate number of screws that can be placed in the fracture fragment and resultant tenuous fixation. The development of L-plates and T-plates changes the configuration and placement of the screws in a fracture fragment allowing for increased screw placement and stability of the fracture fixation. These plates still require a specific fracture configuration. Other alternatives for fixation include cross-pinning with k-wires, and lag screw fixation. These repairs may also not result in a rigid fracture fixation. External skeletal fixation awards the ability to place pins are wires at different angles to maximize purchase within a small fragment. External fixators can be constructed in either a uniplanar, biplanar or bilateral fashion with connecting bars or free form when using epoxy connecting bars. Circular external fixators using small transfixation wires require minimal fragment size for stabilization.

Despite appropriate reduction, stabilization of small fragments may not be adequate to allow weight bearing and joint motion without adjunctive stabilization. This can be achieved with either external coaptation with splinting, rigid external skeletal fixation or hinged transarticular external fixation. External coaptation is relatively unexpensive and can be atraumatic. Downfalls of bandaging include weekly bandage changes, pressure sores from a slipped or inappropriately placed bandage, or wounds secondary to a wet bandage. Rigid transarticular external fixation precludes the need for weekly bandage changes and possible pressure sores, however, pin tract infections are a common sequelae to external fixators and diligent cleaning of the pin tracts is required. Both rigid fixation and splinting prevent joint range of motion which is detrimental to the health of the articular cartilage, joint range of motion, limb muscle mass and overall limb function. If adjunctive fixation is warranted, hinged transarticular external skeletal fixation is the only means of protecting the primary repair while allowing range of motion and ambulation.

Articular cartilage fractures result in disruption of the matrix and cellular components of hylaline cartilage. These changes can be irreversible. The composition of hyaline cartilage does not incite spontaneous healing due to its complexity and inability for chondrocytes to migrate to the site of injury, the overall low number of chondrocytes present within the hyaline cartilage matrix, and the lack of vascularity of hyaline cartilage which results in an absence of an inflammatory response and induction of healing. Although chondrocytes close to the site of injury will replicate and increase matrix formation, their response is limited and insufficient to restore the defect to its pre-injury condition.

Defects in articular cartilage and damage to the underlying subchondral bone induces hematoma formation and a reparative matrix produced by chondrocytes close to the site of injury and undifferentiated mesenchymal cells derived from the underlying bone. The hematoma formation and resulting cellular infiltrate organizes into a fibrin clot apposing the cartilage wound edges. This reparative fibrous tissue differs from the original cartilage in its predilection for cartilage type I collagen formation rather than type II collagen formation found in hyaline cartilage. This fibrocartilage has ineffectual bonds between water and the proteoglycans compared to the original hyaline cartilage, fibrocartilage lacks the mechanical properties and durability of hyaline cartilage and will eventually degenerate.

The articular surface is comprised of hyaline cartilage matrix which is constantly undergoing a hemostasis of degradative and reparative processes. Proteoglycans, a constituent of the cartilage matrix, is produced by chondrocytes and degraded by enzymes released by the chondrocytes. Type II collagen, another component of the cartilage matrix is also produced by chondrocytes, but is only degraded in the presence of disease or injury by the subsequent formation of inflammatory mediators produced by the underlying bone and synovial membrane. Injury offsets the hemostatic mechanisms of the joint resulting in increased proteoglycan degradation relative to production, which exposes the collagen fibrils to the joint fluid and inflammatory mediators resulting in a disruption of the structural integrity of the collagen and collagen fibrillation. This is a self perpetuating process that eventually leads to the degradation of the articular cartilage.

Physeal fractures can be either intra-articular or juxta-articular fractures. In immature animals, the physis is the weakest point of the long bone-ligament construct which forms the limbs and joints. The strength of the ligaments and fibrous joint capsule is two to five times greater than that of the metaphyseal-epiphyseal junction. Therefore, trauma to a limb in a young animal is more likely to result in a physeal injury than a strain or sprain injury.

The physis is divided into different zones based on function including the zone of resting cartilage, the zone of proliferation, the zone of maturation, and the zone of calcification. The zone of resting cartilage lies near the epiphysis. The zone is not responsible for growth, but serves to anchor the physis to the epiphysis and has capillaries to nourish the physis. The zone of proliferation provides a new course of cells to replace the ones that become calcified and are replaced by osseous tissue. The chondrocytes in this zone are thin and stacked in straight rows parallel to the long axis of the bone. The zone of maturation is also referred as the transitional zone or zone of hypertrophy. In the proximal portion of this zone, the chondrocytes are similar to those of young proliferating cartilage, and in the distal portion the chondrocytes show signs of maturity and evidence of degeneration. The zone of calcification is only a few cells and joins directly to the metaphysis where new boney trabeculae are being formed. The zone of hypertrophy or maturation represents a region with poor structural support and therefore is a natural potential cleavage plane.

In growing dogs, physeal injuries account for up to 30% of long bone fractures. In the long bones of dogs, the proximal and distal physis contribute unequally to long bone growth. In general, the most frequently injured physis is the one which is contributing most actively to the bone length at the time of injury. This may be due to the more active physis being more susceptible to injury or this may be a result of the difficulty diagnosing Type V physeal injuries if there is little remaining growth potential.

The Salter-Harris system has been developed to assess physeal fractures radiographically and to classify them according to the probability of the injury causing growth retardation. This is based on the expectation of stem cell integrity and vascular disruption as a result of the injury and aids in prognosis. There are five classifications (I-V) in order of increasing chance of growth retardation. Type I describes a fracture through the physis alone (femoral capital physeal fractures). Type II, describes a fracture through the physis and metaphysis (distal femoral physis, distal tibial physis). Type III describes a fracture through the epiphysis and the physis (relatively rare, distal femoral physis). Type IV describes a fracture through the metaphysis, physis and epiphysis (distal humeral physis). Type V described a compression injury to the physis. Salter-Harris fracture I-IV are the result of shearing or avulsion forces to the physis whereas Type V results from a severe crushing force (distal radius and ulna). The latter is difficult to diagnose as it may cause pain and swelling with no radiographic evidence of displacement and may not become apparent until the manifestation of the sequelae of growth arrest.

The principles of treating physeal fractures are simple. Treatment should be performed as soon as possible to facilitation reduction, prevent further growth plate injury from fracture fragment movement and abrasion, and to prevent contracture. Anatomic reduction is essential to minimize the likelihood of physeal closure and in the case of Types III and IV to ensure there are no steps of gaps in the articular surface. Reduction must be performed carefully to prevent damage to the physis as a result of manipulation. These fracture, once reduced, are relatively stable due to the growth plate interdigitation, and also heal rapidly. For this reason, stabilization implants need not be rigid. The most common means of stabilizing Type I and II physeal fractures are the use of Kirschner wires or small intramedullary pins as cross pins. When this is performed, the pins should enter a non-articular portion of the epiphysis, be as close to a 90 degree angle to the physis as possible as they traverse the growth plate, cross within the metaphysis and engage the cortical bone of the distal diaphysis. This ensures that the pins are minimally affecting the physis and should not cause physeal closure while still providing stability. The use of screws or plates across the physis will compress the growth plate resulting in premature closure. In fracture Types III and IV a lag screw is often placed parallel to the physis to reconstruct the epiphysis and one or more pins inserted across the physis into the metaphysis to resist rotational forces. This results in rigid stabilization to maintain joint surface congruity while not risking additional injury to the physis.

Type V Salter-Harris fractures present a different challenge as they are not usually diagnosed until some degree of deformity has resulted. This is also the case when dealing with any other type of physeal injury that has resulted in complete or asymmetric premature physeal closure and growth arrest. Another factor to be considered is the significant deformity that can result in a two bone unit when one bone is affected by premature growth arrest.

Two bone units such as the radius/ulna and tibia/fibula must grow in a synchronized manner to avoid growth deformities. This can result in some remarkable deformities when one of the bones in a two-bone system has premature physeal closure and growth arrest. This occurs from a tethering mechanism of the two bones, where the lack of growth of one bone of the unit will exert a bowstring effect on the bone that continues to elongate. This will introduce a varus/valgus and rotational deformity along with varying degrees of cranial/caudal bowing. The most common deformity involves the radius as a result of premature distal ulnar physeal closure. The distal ulnar growth plate is conical in shape and therefore an axial or bending force will cause both compressive and shear forces on the cells of the physis. This makes the distal ulnar physis uniquely susceptible to Type V injuries. These injuries are magnified in severity by the fact that the distal ulnar physis contributes a full 85% of ulnar growth and elongation. The shortening of the ulna exerts a tethering effect on the radius leasing to a valgus deformity with external rotation and cranial bowing. In addition, there will be varying degrees of humeroulnar joint incongruity as a result of growth retardation in the ulna and continued radial growth. Severe deformities can also occur in asymmetric or incomplete physeal closures especially when it occurs when there is abundant growth potential present.

Deformities of the distal aspect of the tibia (tarsal varus and tarsal valgus) have been attributed to premature closure of the distal fibular physis and subsequent tethering affects similar to the radius and ulna. It is interesting to note, however, that these deformities result in a simple uniplanar deformity without rotation, cranial/caudal bowing or length deficit. A retrospective study has been performed to assess the potential role of the fibula in the development of this deformity, however there was no change in physeal shape, position, or overall fibular length between those limbs affected and clinically normal. Relative to the age of dogs with carpal varus/valgus, dogs with tarsal deformities are much older (9mo compared to 6mo). It is therefore believed that these deformities are the result of an asymmetric premature closure of the distal tibial physis. The fact that this occurs in older animals supports the lack of length deficit concurrent with the deformity.

In all deformities, the goal for correction is to achieve good alignment and congruity and to avoid significant disparity in limb length. In cases of premature physeal closure, treatment is determined by the nature and severity of the deformity. The prognosis is not only based on type, mechanism and location of the injury as described in the classification system by Salter-Harris, but also on the growth potential remaining at the time of trauma and length deficit present.

Moderate deformities in animals with no remaining growth potential and minimal limb deficits can be treated by a one stage corrective osteotomy and stabilized with either external skeletal fixation or bone plate and screws. In severe deformities that have significant limb length disparity the ideal treatment is one that allows for both bone lengthening and angular and rotation correction. Circular external skeletal fixators (CESFs) provide stabilization while allowing progressive limb lengthening and angular correction using the Ilizarov technique of distraction osteogenesis. This approach utilizes distraction motors on the CESF frame that allows the bone fragments to be distracted at a specific rate multiple times a day. This stretches the fracture hematoma and soft callus and results in formation of linear bone trabeculae between the bone fragments that is later remodeled. Using this form of fixation and distraction, angulation can be either corrected acutely during surgery or progressively post-operatively. CESFs are quite versatile even correcting multiple deformities within a bone with multiple osteotomies. Results using CESFs are very good for restoring normal joint alignment and limb length even with complex deformities.

Corrective procedures for deformities are also advocated to restore the mechanical limb axis which will prevent abnormal stresses on normal cartilage resulting in degenerative joint disease of the adjacent joints. There are prolonged cases of carpus valgus/varus or tarsal varus/valgus in which the secondary degenerative changes have clinically surpassed the original deformity. In cases of chronic carpal valgus significant degenerative changes can be present in the carpus resulting in lameness and discomfort on palpation. In these cases, progressive correction with the CESFs may not be warranted at this time. Another treatment option is a pancarpal arthrodesis limiting motion and thereby pain, with concurrent correction of the deformity. This correction will restore the mechanical axis hopefully diminishing the effects on the elbow joint. It is however, preferable to correct the deformity prior to these secondary changes for the best long-term post-operative results.

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