Surgical Treatment of Joint Disease

Surgical Treatment of Joint Disease

CHAPTER Surgical Treatment of Joint Disease David D. Frisbie Over the last decade, significant advancements have been made in the understanding of m...

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CHAPTER

Surgical Treatment of Joint Disease David D. Frisbie

Over the last decade, significant advancements have been made in the understanding of medical and surgical treatment of equine joint disease. Many of these advances originally were aimed at helping humans, but the principles have been adapted for use in the horse. Advances in understanding pathophysiology, novel surgical techniques, improved surgical equipment, and more-sophisticated imaging modalities have led to improved treatment of joint disease. It is important to focus on the two main treatments for joint disease: the relief of pain to regain functional use of the diseased joint and the arrest of disease progression. In many cases, generalized osteoarthritis (OA) is treated using medical management and exercise protocols, whereas full-thickness articular cartilage damage usually involves some surgical intervention.

SURGICAL TREATMENT Diagnostic and Surgical Arthroscopy Equine arthroscopy was first described as a diagnostic tool to visualize lesions that were undetectable using radiography or other routine imaging procedures, but it was soon employed for therapeutic purposes, such as surgical removal of osteochondral fragments. Arthroscopy is now considered part of routine equine surgery and has, for the most part, replaced arthrotomy. It allows better visualization of the joint anatomy and inflicts less damage to the joint capsule and surrounding tissues, leading to quicker return to use and a more favorable outcome for the horse.1 Since the 1980s, various publications have described arthroscopy in the horse; many of the early publications only described various techniques and approaches to joints, with more detailed outcomes and prognoses for specific pathologies following in subsequent publications. Most of the published work has been compiled in equine-specific texts.1,2 The equipment used for arthroscopy and the surgical technique is discussed in Chapter 13. Arthroscopy has a diagnostic and a therapeutic function in joint disease. Even with modern imaging modalities, it is still considered the gold standard for diagnosing equine joint problems. The cost and availability of arthroscopic equipment, along with arthroscopy’s specificity and sensitivity when compared to more-complex imaging modalities such as computed tomography (CT) and magnetic resonance imaging (MRI), and the expertise needed to perform definitive joint ultrasonography, will likely keep arthroscopy in the forefront of diagnostics for equine joint disease for many years. This is especially true in cases that show no demonstrable or questionable joint lesions using traditional imaging modalities, even though the horse has localized clinical pain based on diagnostic analgesia. In recent years, additional joint pathology, such as meniscal and cruciate lesions, has been described. This may be because diagnostic arthroscopy, especially in the stifle joint, has become more accepted. Therefore, these types of lesions, which are not detectable using radiography, are being recognized more often. With an increased awareness of how often these types of lesions

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occur, further work is being focused on therapeutic treatments. This is especially true in the field of cartilage resurfacing and meniscal pathology, with many of the therapeutic avenues pursued in equine practice representing the current state of the art in human medicine. Another advantage of the use of arthroscopy is the potential benefit of lavage. Arthroscopy is often performed using fluid to distend the joint for better visualization. The accompanying egress of joint fluid, which potentially contains cytokines and cartilage wear particles, may be therapeutically beneficial, even when lavage is performed as a sole treatment in cases of osteoarthritis. However, the benefit of lavage is controversial, and it does not work in cases with significant definable disease such as meniscal tears. Research also has shown that when lavage is performed with large-gauge needles (14 gauge), it is not as effective as using arthroscopic cannulas.3-5 Distention of the joint can be accomplished using inert gas, which can be especially helpful if bleeding of intrasynovial tissues impairs visualization when a fluid medium is being used. In general, arthroscopy is of more therapeutic benefit in acute than in chronic cases. For example, removing a freshly detached osteochondral fragment before OA can develop typically produces a better outcome than waiting until after OA has developed to remove an osteochondral fragment that has been present for some time. However, there are some indications that specific chronic pathologies, such as osteonecrosis and cartilage fibrillation of the third carpal bone, can be successfully managed using arthroscopy. Another consideration regarding arthroscopic surgery is the documentation of the surgical procedure. Since the 1990s, reduction in cost and increase in availability of video and still-capture devices have allowed real-time documentation of arthroscopic surgery to be made and kept as part of the medical record. This real-time information is embraced by trainers and owners as a means of understanding the pathology and treatment procedures, as well as providing more specific information about the surgery.

Removal of Osteochondral Fragments In most instances, osteochondral fragments are removed when they are diagnosed in conjunction with clinical lameness. Some fragments are considered relatively benign, and removal is not indicated without clinical lameness.1,6,7 The routine use of arthroscopy has improved the outcome of osteochondral fragment removal as compared to removal using arthrotomy. Outcomes related to osteochondral fragment removal are presented in Table 80-1, and specific anatomic landmarks relating to arthroscopic approaches to the different joints can be found detailed in this text and in published references.1 In general, diagnostic visualization of the entire joint cavity is performed before fragment removal (Figure 80-1). When multiple fragments are present, typically the smaller fragments are removed first. This postpones the need to increase the size of the instrument portal and delays the potential for subsequent 1123

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TABLE 80-1.  Prognosis* for Racing or Athletic Soundness Given by Various Authors for Intra-Articular Osteochondral (Chip) Fractures† in Various Locations and Joints Fracture Location

Treatment‡

Prognosis

Reference

Extensor process of P3

M or Sa M or Sa M or Sa Sa Sa M or Sa Sa (displaced) M (nondisplaced) Sa — Sb Sa Sa Sb Sb M Sa Sb Sb M Sa M or Sa Sb Sb M or Sa Sb M Sa Sa Sb Sa Sa Sb Sb Sa Sa Sb Sb Sa Sb Sa

Guarded Poor Good Guarded to good§ Guarded Poor Good Good Excellent Good Excellent Excellent Good Excellent Good Guarded Excellent Excellent Good Poor Good S better than M Good Good Guarded Guarded Guarded HR = 1¶ Guarded to good§ Good Good HR = 2¶ Good Good Guarded HR = 1¶ Guarded Good Guarded to good§ Guarded HR = 1¶

8, 9, 10 11 12 13, 14 11, 15, 16 11 17 17 18 19 16, 20, 21 22 23 12 24 22 25 12, 26 27 28 28, 29 30 31, 32 33 34, 35 36 12 34 37 20 37 20, 38 20 20 37, 35 38 35, 20 20 36, 39 36, 39 20, 38

P2 (not involving DIP joint) P2 (involving DIP joint) Dorsal frontal P1 Proximodorsal P1 Plantar P1

Palmar P1

Apical sesamoid

Abaxial sesamoid Basilar sesamoid Distal radius

Proximal RC Proximal IC Distal RC Distal IC C3

*The prognoses have been graded as excellent (80% to 90% chance of athletic soundness), good (60% to 80%), guarded (40% to 60%), and poor (<40%) and usually refer to the ability to race after injury. These are approximate percentages extrapolated from the literature because these categories are not always used by each author and a definition of these categories is not usually given. “Favorable” has been graded with “good.” In general, the prognosis given is for horses with no radiographic signs of osteoarthritis (i.e., the horse is given its best chance of recovery). † These fractures do not cause major joint instability. ‡ a, Arthrotomy; b, arthroscopy. § Guarded to good used when the percentages spanned 2 ranges. ¶ HR, Hazard ratio was used to compare the racing performance of the treated with that of a control group, taken from the race horse registry for the same period. A hazard ratio of approximately 1 means that the same number of treated horses dropped out of racing as the controls. A hazard ratio of 2 means that twice as many treated horses were lost as the controls. C3, Third carpal bone; DIP, distal interphalangeal; HR, hazard ratio; IC, intermediate carpal bone; M, medical; P, phalanx; RC, radial carpal bone; S, surgical. Adapted from Caron JP: In Auer JA, Stick J (eds): Equine Surgery. 2nd Ed. Saunders, Philadelphia, 1999.

reduced visualization until the end of the surgery. Very large fragments can be broken into smaller pieces using a rongeur or osteotome to prevent the need for excessive portal size. Hand curettes are typically used to débride the parent bone down to the appropriate level as well as to smooth any edges that might traumatize opposing joint surfaces postoperatively. Before

finishing arthroscopic surgery, typically the joints are lavaged with fluids while a final inspection of the joint is completed to ensure all debris has been removed. Debris often accumulates in certain locations within a specific joint, and knowledge of these locations often aids in finding debris that has inadvertently escaped removal by lavage alone.



CHAPTER 80  Surgical Treatment of Joint Disease

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A A

B Figure 80-1.  Arthroscopic image of a chip fragment off the distal radial carpal bone before (A) and after removal (B).

B Figure 80-2.  A, Arthroscopic image of a slab fracture of the third carpal

Reconstruction of Intra-Articular Fractures Once damaged, bone can be repaired so that it is indistinguishable from the original tissue. However, articular cartilage does not have the same ability to heal. Therefore correct anatomic alignment and reconstruction of the fracture gap, especially the articular component, is integral to the repair process and determines the long-term resolution of intra-articular fractures. Arthroscopic visualization during the reconstruction of the articular component of the fracture is recommended to ensure the best possible outcome in a high-motion joint. In many cases, loose debris is removed and flushed from around and in the fracture gap, allowing more anatomically correct reduction and better stabilization of the fracture. In some cases, such as with slab fractures of the third carpal bone, assessment of the articular component dictates the surgical procedure, namely repair or removal of the fracture fragment (Figure 80-2). Common intra-articular fractures encountered in equine athletes are condylar fractures of the third metacarpus (MCIII) and third metatarsus (MTIII), third carpal bone slab fractures, and

bone before reduction. B, Lateromedial radiographic view of the slab fracture seen in A after reduction and fixation using a 4.5-mm cortex screw in lag fashion.

sagittal fractures involving the proximal phalanx. Most cases of intra-articular fractures are repaired using internal fixation with screws inserted using lag technique (see Chapter 76). These fracture repairs are covered in other chapters of the text, but some treatments and outcomes are listed in Table 80-2.

Synovectomy Equine synovium is occasionally removed locally (partial synovectomy) to help arthroscopic visualization, but synovectomy can also be performed as a therapeutic treatment, most often in cases of septic arthritis. With sepsis, the synovial membrane can be laden with fibrin. Fibrin is thought to harbor bacteria; thus removal of the involved synovium is thought to aid in the treatment and potentially prevent recurrence of the septic process.

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TABLE 80-2.  Prognosis* for Racing or Athletic Soundness Given by Various Authors for Intra-Articular Fractures Fracture Location and Type

Treatment†

Prognosis

Reference

Distal phalanx (all except fractures of extensor process fractures) Distal phalanx (intra-articular, except extensor process fractures) P3 (type II) Middle phalanx (comminuted)

M

Good (horses <3 yr old)

8

S

Good (horses >3 yr old)

8

M M or S S M M or S S S M or S S S S S M or S S S M S (TB) S

Guarded Guarded Poor to guarded‡ Poor Good Good Poor Poor Good Guarded Good Good Poor Good Excellent Excellent Guarded to good‡ Guarded to good‡ Guarded Poor Good Guarded

11, 40 11 15 15 11, 17, 41, 42, 43, 44 17, 45 11, 43 34, 43 34, 46, 47 34 48 49 41 41 41 41 50 12, 51 52 53 50 12, 45

Proximal phalanx (simple, nondisplaced) Proximal phalanx (noncomminuted, displaced) Proximal phalanx (comminuted) Proximal sesamoid (midbody) MCIII/MTIII (noncomminuted) MCIII/MTIII (with comminution) MTIII (medial condyle) MCIII/MTIII (displaced) MCIII/MTIII (complete, nondisplaced) MCIII/MTIII (incomplete, nondisplaced) C3 slab (frontal)

C3 slab (sagittal)

M M or S (SB) M

*The prognoses have been graded as excellent (80% to 90% chance of athletic soundness), good (60% to 80%), guarded (40% to 60%), and poor (<40%) and usually refer to the ability to race after injury. These are approximate percentages extrapolated from the literature because these categories are not always used by each author and a definition of these categories is not usually given. Favorable has been graded with good. In general, the prognosis given is for horses with no radiographic signs of osteoarthritis (i.e., the horse is given its best chance of recovery). † Articular fractures of long bones (except for the metacarpus and metatarsus) have not been included because of insufficient numbers from which to derive prognoses or other complicating factors, or both. ‡ All fractures repaired surgically with stab incisions or arthrotomies, or both, except C3 slabs, in which repair was guided by arthroscopic visualization. Two grades are given when percentages spanned two categories. C3, Third carpal bone; M, medical; MC, metacarpus; P, phalanx; S, surgical; SB, Standardbred; TB, Thoroughbred. Adapted from Caron JP: Principles of Treatment of Joint Disease. p. 678. In Auer JA, Stick J (eds): Equine Surgery. 2nd Ed. Saunders, Philadelphia, 1999.

Some septic equine joints appear to produce more fibrin than others (tarsocrural, distal interphalangeal, and elbow joints are among the most prolific), which requires visualization of the joint space and synovectomy rather than ingress–egress flushing using large-gauge needles. In some cases of chronic osteoarthritis, marked hypertrophy of the synovium can be encountered, and current practice is to perform a subtotal or complete synovectomy of the affected membrane to reduce cytokine production as well as physical impingement. The carpal joints and the metacarpophalangeal and metatarsophalangeal joints appear to benefit clinically from this type of treatment.8 The role that the synovial membrane plays in equine joint disease is not as well characterized as it is in humans. In human osteoarthritis, the synovial membrane is thought to play a secondary role to the cartilage lesion in the pathogenesis. Conversely, in rheumatoid arthritis, the synovial membrane is thought to be the primary instigator and to propagate the ongoing degeneration of the cartilage. Thus an effective method of controlling rheumatoid arthritis in people is through synovectomy, although it has a limited duration of clinical effectiveness.9-12 A rheumatoid condition has not been identified in the horse.

Different methodologies have been used to accomplish synovectomy, including use of surgery, chemicals, and radioisotopes. Typically, surgical methods in horses use motorized synovial resection. Experimentally, synovectomy has been performed in normal horses and has shown no ill effects, but the regeneration of the synovial membrane was slower than expected when compared to other species.8,13,14

Joint Resurfacing Partial-thickness lesions and full-thickness articular cartilage lesions greater than 5 mm in diameter do not heal spontaneously in the horse. In spite of the recent interest in assessing treatments for chondral defects, efforts have been under way for more than 250 years to heal articular cartilage with only moderate progress.15 The reason is related to the highly specialized nature of articular cartilage and the need for an intact structure to perform its biochemical and physiologic functions. Damage to articular cartilage is common in horses and typically is described in two forms: chronic degenerative lesions and acute damage. Chronic lesions are often considered OA, and whereas these lesions would benefit from joint resurfacing, this



CHAPTER 80  Surgical Treatment of Joint Disease

type of lesion is the most challenging in which to achieve longterm repair because of generalized joint pathology that is not addressed with most current joint-resurfacing techniques. Conversely, acute lesions typically comprise a discrete or focal area of cartilage loss without other chronic manifestations of joint degeneration. Such lesions are currently best treated with equine joint resurfacing techniques. The outcome of cartilage repair is typically assessed on biochemical content (including type II collagen and aggrecan), histologic appearance (resemblance to hyaline cartilage), biomechanical properties, and functional outcome of the joint and patient. As a general rule, it appears that cartilage in younger patients has a better capacity for repair compared to that of older patients. When intra-articular osteochondral fragmentation occurs in the horse, surgical treatment involves removal of the fragment and débridement of the damaged cartilage and subchondral bone. In general, because of a generalized poor regenerative response, articular cartilage is usually minimally débrided, doing no more than is necessary to remove damaged cartilage. Partial-thickness cartilage lesions are typically not converted into full-thickness lesions, but rather the fibrillated cartilage is removed, leaving the intact cartilage below the fibrillated cartilage in place. In the case of a full-thickness lesion, the edges of the damaged articular cartilage are débrided until cartilage that is firmly attached to the subchondral bone plate is reached. The edges of the cartilage are débrided so that they have a sharp vertical border. The bone is always débrided down to a level of the subchondral bone plate so as to fully remove the calcified cartilage, which has been shown to impede the repair process. When necrotic bone is encountered, it is débrided aggressively to ensure that healthy bleeding bone is being left in the lesion. Chapter 79 covered general concepts regarding treatment based on the lesion depth, size, and basic repair or treatment options. Two basic approaches are historically considered in joint resurfacing: stimulated endogenous repair and transplantation or grafting of tissues. Although these techniques are covered as separate entities, many cutting-edge approaches are combining the techniques as well as augmenting either or both techniques with growth factors.

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Based on the human and equine literature, the current recommendations for stimulated endogenous repair of an articular lesion are débridement of lesions to the level of the subchondral bone plate (abrasion arthroplasty) alone or in conjunction with subchondral bone microfracture.17 If the lesion crosses the subchondral bone plate into the cancellous bone, the addition of subchondral bone microfracture is probably not necessary. In the presence of sclerotic bone, the lesion is débrided to a depth that produces petechial bleeding (in the absence of fluid pressure) but does not enter the cancellous bone. In this case, subchondral bone microfracture is also used. Currently, subchondral bone plate drilling is not widely used based on subsequent formation of subchondral bone cysts and poor histologic appearance of repair tissue, especially when compared to other, more recently developed techniques such as subchondral bone microfracture.18,19 The greater depth of penetration, smooth penetration through the bone, and heat generated with the drilling process probably contribute to the less-than-optimal tissue repair. Bone cyst formation associated with the drilling technique is probably a result of synovial fluid movement into the bone through the drill holes (see Chapter 89). Subchondral bone microfracture allows access to the cells and growth factors beneath the subchondral plate, without disrupting the subchondral plate’s biomechanical stability (Figure 80-3). In addition, the penetration of the stainless steel bone awl causes cracks in the bone as well as spicules of bone that protrude from the penetration site, both of which are believed to aid in the attachment of the repair tissue. Experimental studies have demonstrated that large articular cartilage defects (1 to 2 cm in diameter) débrided to the level of the subchondral bone have significantly greater volume of healing tissue following subchondral bone microfracture compared to defects that were débrided to the level of the subchondral bone plate but did not undergo microfracture. Biochemical analysis of the repair tissues also has shown a greater type II collagen content in repair tissue of microfractured defects in two experimental

Stimulated Endogenous Cartilage Repair Because bone marrow has a good supply of both stem cells and growth factors thought to be integral to cartilage health and repair, direct communication of articular lesions to these elements beneath the subchondral bone plate has been a cornerstone of stimulated cartilage repair. Growth factors believed to be important in cartilage repair include insulin-like growth factor-1 (IGF-1), transforming growth factor-β (TGF-β), and bone morphogenetic proteins (BMPs) 2 and 7. Access to these marrow elements has been facilitated by various surgical techniques, including abrasion arthroplasty, which involves débridement to the level of the subchondral bone plate; spongialization, which is débridement past the subchondral plate into cancellous bone; focal drilling to the depth of cancellous bone in discrete locations throughout the cartilage lesion (osteostixis); and subchondral bone microfracture, which also penetrates to the level of the subchondral bone in discrete locations. Current literature and clinical practice do not favor spongialization, in part because it is thought to destabilize the subchondral bone plate.16,17

Figure 80-3.  Arthroscopic image of microfracture spacing on the medial femoral condyle.

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studies, although histologic appearance of the repair tissues was similar.20,21 Further improvement in the repair tissue obtained following subchondral bone microfracture has been achieved by supplementing IGF-1 and interleukin-1 (IL-1) receptor antagonist using gene transfer.22 Experimental work assessing subchondral bone microfracture has also confirmed the poor attachment of repair tissue in areas where the calcified cartilage layer had been incompletely removed. Confirmation of the level of débridement can be achieved using a microarthroscope or focusing close to the defect margins with a standard arthroscope. A granular appearance of the defect should be evident, differentiating the subchondral bone plate from the glasslike appearance of the calcified cartilage layer. Following débridement of the lesion, microfracture holes are spaced 2 to 3 mm apart, avoiding communication between sites and penetrating approximately 2 mm into the bone (see Figure 80-3). To date, no long-term follow-up on clinical results after resurfacing therapy have been published relating specifically to horses, although anecdotal reports have been promising. However, human data compared long-term follow-up of the most commonly used cartilage resurfacing techniques: autologous cartilage implantation (ACI) as described by Brittberg,23 and subchondral bone microfracture first described by Steadman.24,25 The short-term and long-term results of this study show minor significant improvement with subchondral bone microfracture over ACI but no significant differences in histologic appearance of repair tissue or patient outcome between the two techniques. Both of these techniques are considered better than débridement alone for most human and equine patients. Because subchondral bone microfracture does not require a second surgery and is less technically challenging compared to ACI, it is favored by most equine surgeons. Articular Cartilage Grafting Many different tissues have been transplanted or grafted into cartilage defects; they include periosteal and perichondrial autografts, osteochondral, chondral, or isolated chondrocyte autografts or allografts, and stem cell transplants from bone marrow or fat. Periosteal and perichondrial grafts have been performed in laboratory animals with some success, but results in the horse have been very disappointing and are no longer a focus of ongoing research.26,27 Osteochondral grafting procedures have been well developed for use in people, but they have had limited success in the horse. Early work in the horse demonstrated short-term success but resulted in long-term failures.28-30 Many of the failures with osteochondral grafting have been attributed to lack of congruity of the recipient and donor tissues as well as difficulties with surgical technique. Some concern also revolves around morbidity in the donor graft site. Typically, in people, a non–weight-bearing region is used for donor harvest, reducing morbidity, but lack of suitable non–weight-bearing donor tissue has been a limitation in horses. More recently, with the advent of specialized surgical tools designed for human osteochondral grafting, studies are under way using this technique in the horse. Surgical technique and donor site selection are the main hurdles yet to be overcome before this technique reaches mainstream practice.31-34 Chondrocyte transplantation has been a very active area of equine research since the 1990s. Techniques using both allografts and autografts have been reported, but most work, especially in

humans, has focused on autografts. The technique described by Brittberg and marketed by Genzyme is the most well studied grafting technique.23 This technique uses autologous chondrocytes harvested from a non–weight-bearing region, usually the trochlea of the distal femur, followed by a 4-week in vitro expansion of chondrocytes. The expanded cell population is then implanted during a second surgical procedure and held in the defect beneath autologous periosteum, which is sutured to the cartilage bordering the defect to create a watertight seal. Although this technique has been performed in horses with outcomes similar to those seen in people, the cost, laboratory facilities, need for multiple surgeries, and technical challenges of the procedure have limited its usefulness in clinical cases. Techniques using frozen chondrocytes harvested from neonatal foals, which are implanted in a fibrin glue to help retain the cells in the chondral defect, have had some success in a limited number of chondral defects. The technique is being used more commonly in cystic defects to date.35 Other materials used to fill cystic lesions are discussed in Chapter 89. Techniques using autologous chondrocytes harvested from the non–weight-bearing region of the lateral trochlea of the distal femur, implanted into 15-mm-diameter defects, have been successful in experimental equine trials. One of the tested procedures uses fibrin glue holding minced cartilage to a bioresorbable scaffold, which is subsequently stapled to the subchondral bone of the defect in a one-step surgical procedure.36,37 In comparable equine experimental trials this technique has been superior to the ACI technique. This technique is now undergoing human clinical trials, and because of the ease, cost, and promising results in equine experimental trials, it is likely to be used in equine clinical cases in the near future. Considerable research is being directed toward the use of mesenchymal stem cells for implantation in cartilage defects. This cell population has been shown to improve healing in experimental animals, but gaining access to a sufficient number of stem cells without in vitro expansion is a hurdle yet to be resolved in horses.35

Arthrodesis Assisted fusion of a joint is sometimes indicated when destruction to the joint is beyond any other treatment. Although most commonly achieved through surgical methods typically involving internal fixation, arthrodesis can be carried out using chemical or laser-based methods as well.2,38-40 In high-motion joints, such as the antebrachiocarpal, midcarpal, metacarpophalangeal, and distal interphalangeal joints, surgical fusion using internal fixation is required (see Chapter 81). The expectation of this procedure is to alleviate the pain associated with movement of the joint and to salvage the animal for nonathletic function. Conversely, arthrodesis of low-motion joints often carries a reasonable prognosis for athletic soundness and can be accomplished using surgical, chemical, or laserbased techniques. This is especially true for the proximal interphalangeal, tarsometatarsal, carpometacarpal, and distal intertarsal joints. Some risks have been identified with chemical fusion of joints because unexpected anatomic communications with other synovial and nonsynovial structures can be encountered. Thus contrast studies outlining the structure and extent of the communication should be performed before chemical fusion, and caution should be used not to create further injury by overdistending the joint capsule.



CHAPTER 80  Surgical Treatment of Joint Disease

In the distal tarsal joints, some initial studies have been performed comparing surgical drilling to ablation of the joint space using a laser in both clinical and experimental cases.41 Early results indicate that some decrease in time to resolution of clinical lameness may be seen for the laser-based procedure, but actual bony union of the joint space appears to occur more quickly with drilling. Further research comparing these techniques is needed, but the morbidity associated with the early reports using the laser favors the continued use of surgical arthrodesis in the distal tarsal joints, using the modified drilling technique. Further discussion of the principles of arthrodesis can be found in more detail in Chapter 81.

Joint Replacement When reparative surgical procedures have failed, and the patient is unresponsive to medical management, many end-stage cases of osteoarthritis in people are treated using joint replacements, especially in the knee and hip. Joint replacement procedures are typically postponed until the patient is old enough that the implant will not fail during the expected remaining lifetime. Implant wear is improving, but it is still in the 10- to 20-year range, depending on the location and type of implant. Even in humans, where a large number of joint replacements are carried out annually, and to a lesser extent in dogs, relatively high morbidity is associated with such procedures, especially related to implant loosening. With respect to equine joint replacement, cost of implant design and manufacturing, difficulties with prolonged non–weight-bearing, and surgical morbidity continue to keep equine joint replacement out of mainstream clinical practice.

Aftercare The aftercare for surgical joint treatment is often as important as the central treatment itself. Treatment goals and pathophysiology of healing tissue should be kept in mind when the aftercare protocol is being designed. Each aftercare protocol varies depending on the procedure, but a common focus is to minimize the duration to full return to function without compromising the athletic soundness of the patient. Following surgery, the goals are to provide support to the weakened areas, often through bandaging, casts, and controlled exercise, which can range from strict stall rest to specific graded exercise programs. It is also well accepted that decreasing postoperative inflammation is beneficial in the healing process, as is controlling postoperative pain. Given that maximal inflammation in a surgical wound typically occurs 3 to 5 days postoperatively, nonsteroidal anti-inflammatory medication is administered systemically for at least this time period. The postoperative use of corticosteroids, although providing potent anti-inflammatory activities, is often contraindicated in the first 4 weeks because of their role in decreased cell metabolism, which affects healing time, as well as the decreased ability of the immune system to combat infection. Other medications believed to have chondro-enhancing or chondroprotective qualities, such as hyaluronan or polysulfated glycosaminoglycans (Adequan), have also been studied in an attempt to demonstrate enhanced postoperative healing. However, they have not shown significant benefit in most studies, with the exception of decreasing adhesions in tendon sheaths.42-44

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