Signs and Diagnosis

Osteochondrosis may be present asymptomatically. Lameness is often acute in onset and varies from a subtle gait deficit to marked lameness. Lameness is often more acute in onset and more severe in foals and young yearlings than in older horses. Distention of the femoropatellar joint capsule is often present and can be severe, especially in foals and yearlings. Gluteal muscle atrophy is seen in horses with severe lesions. Flexion tests are mostly positive. Synovial fluid may be hemorrhagic, but it is often normal. Intraarticular analgesia of the femoropatellar joint should improve lameness. However, in mature horses lameness may be mild, with no effusion and a poor response to intraarticular analgesia. In such horses arthroscopic evaluation often reveals an extensive area of cobblestone-like cartilage, with extensive fibrillation over a large portion of the lateral trochlea of the femur. This cartilage is often well adherent to the subchondral bone and little clinical benefit is derived from surgery.

Radiological changes include the following: no detectable signs, slight loss of contour or loss of outline of the lateral trochlear ridge, irregular defects in the trochlear ridge, radiodense fragments within the defect (Figure 46-2), round radiopaque bodies loose in the joint, and more rarely, irregularities on the patellar apex or the medial trochlear ridge.^1,32,33 Lateromedial and caudolateral-craniomedial oblique images are the most useful projections. Horses with radiological lesions do not always show lameness.^25,27 Some horses have no detectable radiological abnormalities, but osteochondrosis lesions are diagnosed on arthroscopic examination. Lesions without fragmentation in young foals may resolve with time,^32,33 but many progress.³⁴

Fig. 46-2 Lateromedial radiographic view of the femoropatellar joint of a yearling Thoroughbred colt. There is a large irregular defect in the subchondral bone of the lateral trochlear ridge containing several radiodense fragments.

Treatment

Conservative management, with confinement and correction of dietary imbalances, and arthroscopic debridement of the lesions are the main treatment options. Conservative management is appropriate for horses with mild lesions. Because of the insensitivity of radiological evaluation of osteochondrosis lesions, an argument can be made for arthroscopic examination of most horses with lesions seen radiologically or persistent femoropatellar effusion and lameness that fails to respond to conservative treatment.³⁵ Arthroscopic examination would ensure that horses with radiologically silent cartilage lesions are treated effectively. OA can also be evaluated. For horses with fragmentation and clinically significant radiolucent defects of subchondral bone, arthroscopic surgery is probably the treatment of choice.³¹ In my opinion, more caution is required when treating foals arthroscopically because some foals with large lesions seen radiologically are found to have intact cartilage at arthroscopy. Debridement of such lesions can leave unacceptably large deficits in the lateral trochlear ridge. Reattaching these cartilage flaps with polydioxanone pins may be a more appropriate treatment and has shown good results with seven of nine foals achieving athletic use.³⁶

A variety of lesions are seen arthroscopically. The articular cartilage may appear intact, but if probed, large flaps may lift from the subchondral bone. Large defects on the lateral trochlear ridge may contain nodules of mineralized cartilage, which are readily removed, and often large tufts of fibrillated cartilage are associated with the lesion. The exposed subchondral bone is frequently soft and crumbly. Extensive areas of fibrillated cartilage over the adjacent lateral trochlear ridge and the opposing patella are often present in older horses.⁵ Loose cartilage should be removed, and the lesion should be curetted to healthy subchondral bone, which is a source of pluripotential cells. The cartilage perimeter should be vertical to allow better attachment of tissue regrowth.³⁷ Thorough lavage to remove all debris, particularly of the suprapatellar pouch, at the completion of surgery is essential. Six weeks of stable rest with daily handwalking after 2 weeks is recommended postoperatively. The horse should then be left for another 4 to 5 months at pasture before returning to work.

Prognosis

Mild lesions in foals were shown to heal with conservative management.^32,33 For foals with more severe lesions, better results were reported with arthroscopic debridement.³¹ Sixty-four percent of 161 horses were able to perform athletically. In this series, treatment of older horses and those with mild to moderate lesions was most successful, which has also been the experience in my practice. The presence of extensive secondary articular cartilage fibrillation did not have a significant effect on the outcome in horses more than 2 years of age.⁵

Signs and Diagnosis

A horse with upward fixation of the patella stands with the hindlimb locked in extension with the fetlock flexed (Figure 46-3). The leg releases with a snap, usually unaided, but occasionally the horse needs assistance. Some horses merely show intermittent delayed release of the patella, especially when turned toward the affected limb. This can be mistaken for stringhalt. Delayed patellar release is manifested by a catching of the patella as the limb is protracted, usually as the horse moves off. Delayed release of the patella may be evident as a rather jerky movement of the patella when the horse moves over in the stable or as it decelerates from canter to trot or trot to walk. Horses in which the condition is chronic develop stifle soreness and may be resistant to work, especially in deep going. If the condition is more serious, horses try to avoid extending the hindlimbs while walking uphill or downhill. Femoropatellar effusion may be present. Diagnosis may depend on the history and the owner’s description if the horse does not lock the patella during the examination. Locking the patella manually may be possible by pushing it proximally, although this can be difficult and is resented by many horses. A careful search should be made for concurrent stifle disease such as osteochondrosis or soft tissue injury, and the site of any lameness should be confirmed by diagnostic analgesia. Radiographic examination of both stifles is prudent because any pathological condition caused by upward fixation or concurrent with it affects treatment and prognosis.

Fig. 46-3 Three-year-old Welsh Cob gelding with the typical stance of upward fixation of the patella in the right hindlimb.

Treatment

For a horse that has the patella locked, pushing the patella medially and distally and backing the horse is recommended but difficult to do. Pulling the limb forward with a side line may provide relief. If the upward fixation of the patella is intermittent and not causing lameness, a conditioning program should be undertaken. This includes an exercise regimen, the administration of anthelmintics, an increased plane of nutrition, and dentistry as appropriate for each horse. The exercise regimen depends on the specific circumstances for each horse. Daily lunging should be instituted to a level that is appropriate for the age and type of horse. Stable rest is usually contraindicated, and turning the horse out to pasture as much as possible is preferable. Immature horses should be allowed time to outgrow the problem. Injection of counterirritants containing iodine into the medial and middle patellar ligaments has been used at this stage of the disease.⁴⁰ Horses with delayed patellar release require the same management.

Because of potential complications, which include fragmentation of the patella and lameness, surgery is only indicated when the following criteria have been fulfilled:

The surgery can be performed under local anesthesia in the standing horse.⁴¹ A small incision is made over the distal part of the medial patellar ligament. I find that minimizing the incision length seems to reduce the incidence of postoperative swelling. A curved Kelly forceps is then advanced caudally under the ligament, developing a path for a blunt-ended bistoury. The bistoury is passed until its end can be palpated caudal to the medial patellar ligament, before the ligament is severed close to its tibial insertion. Stringent asepsis should be observed. Once the ligament is severed, the border of the tendon of the sartorius muscle is palpable caudally. Some surgeons prefer to perform this surgery with the horse under general anesthesia, which allows for complete asepsis: the ligament can be exteriorized before severing, and the fascia overlying the ligament can be sutured before skin closure.

An alternative treatment involving numerous splitting incisions in the medial patellar ligament was described and was successful in four horses and three Shetland ponies, but only two horses were followed beyond 5 months.⁴²

Postoperatively I prefer to confine the horse for 2 months to allow the patella to settle in its new position in the intertrochlear groove. Handwalking can be introduced during the second month.

Prognosis

A substantial number of horses respond to conservative treatment. Occasional recurrences happen if the horse has enforced stable rest, but many grow out of the condition. After surgery and in the absence of degenerative changes in the joint, the horse should return to normal use, although some appear to have a slightly restricted gait. Recurrence of the condition is unusual. Some fibrous thickening is palpable at the surgical site for many years in most horses and indefinitely in some horses. Clinically significant complications including lameness, local swelling, fragmentation of the patella, and fracture of the patella were reported.^43-48 Fragmentation of the patella was produced after experimental medial patellar desmotomy.⁴⁶ If fragmentation causes lameness, horses can be managed arthroscopically with good results.³³ In my experience, up to 30% of horses have minor fragmentation of the patella, without clinical signs, after medial patellar desmotomy. Injury of the middle patellar ligament can also occur secondary to medial patellar desmotomy.^49,50

Signs and Diagnosis

Lameness varies from a stiff hindlimb action to an obvious lameness. Flexion is resented and worsens the lameness. Synovial effusion is common, and excessive fibrous tissue reaction may be present at the surgical site. Radiologically, small bone fragments are present close to the apex of the patella (Figure 46-4), often combined with radiolucent defects of subchondral bone and roughening or spurring of the distal cranial aspect of the patella.

Fig. 46-4 Lateromedial radiographic image of the stifle of a 7-year-old Thoroughbred cross gelding that had previously had a medial patellar desmotomy to treat intermittent upward fixation of the patella. The apex of the patella is fragmented (arrow).

Treatment

Arthroscopic debridement is indicated. The lesions are most commonly on the lateral surface of the apex of the patella and may be partly obscured by synovial villi; therefore a careful arthroscopic examination should be performed before deciding on the site of the instrument portal. Debridement of the lesion to healthy subchondral bone is required.

Prognosis

The prognosis for athletic function is reasonable, although some horses appear to have a slightly stiff hindlimb action because of the original medial patellar desmotomy. Ten of 15 horses returned to athletic use.⁴³ In my experience, the incidence of the condition has decreased in the past 8 years, which may be because fewer patellar desmotomies are performed or because more care is taken during convalescence.⁵ However, the condition still occurs despite appropriate rest after medial patellar desmotomy.⁵⁰

Signs and Diagnosis

The condition may be unilateral or bilateral and has been graded as follows:

Severely affected foals are unable to extend the stifle and stand in a characteristic crouching position. If less severe, the condition may not be obvious clinically, but horses are usually reluctant to flex the stifle and have a stiff gait in the affected limb. Some horses show little evidence of the disease until degenerative changes provoke lameness. I have seen a TB yearling with severe osteochondrosis of the lateral trochlear ridge, which led to a diminution of the ridge and allowed the patella to luxate laterally. One of the Editors (MWR) has seen numerous STB foals with severe osteochondrosis of the lateral trochlear ridge of the femur and patellar luxation. Lateromedial, cranioproximal-craniodistal oblique, and caudocranial radiographic images are the most useful to ascertain the position of the patella and to evaluate the trochlear ridges.

Treatment

Lateral release and medial imbrication of the femoropatellar compartment are necessary to maintain the patella in the intertrochlear groove.^52-54 Both lateral release and medial imbrication appear to be important. Recession sulcoplasty is valuable in the presence of hypoplasia of the lateral trochlear ridge of the femur.⁵⁴

Prognosis

Poor success can be expected with surgery in the presence of OA, large osteochondrosis lesions, and in larger horses. In foals there is a moderate prospect of achieving athletic function. Aggregating the results from the three reported case series, the patella maintained its position postoperatively in eight of 11 foals.^52-54 Breeding from affected horses should be discouraged.

Signs and Diagnosis

The clinical signs depend on the cause and severity of the condition. Lameness is usually persistent, and chronic joint distention may be present. If osteochondrosis is responsible for OA, radiological changes typical of chronic osteochondrosis are likely to be present (see page 536). Cartilage fibrillation, ranging from focal tufting to widespread involvement of the femoral trochlear or patellar articular cartilage, may be seen arthroscopically, and full-thickness defects of the articular cartilage may be present in more severely affected horses.

Treatment

Initially treatment depends on the inciting condition and is described in the appropriate sections. However, once chronic osteoarthritic changes have developed, realistically therapy is likely only to be palliative. Intraarticular medication with small doses of corticosteroids, such as 10 mg of triamcinolone acetonide combined with hyaluronan, may give temporary relief. A controlled exercise regimen may help, and an arthroscopic debridement prolongs working life in some horses.

Prognosis

The femoropatellar joint is more forgiving than the femorotibial joints, and although OA will not resolve, if mild it may be tolerated enough for a horse to perform useful work. More severely affected horses are unlikely to return to athletic use.

Signs and Diagnosis

Lameness can be moderate to severe in the acute phase but varies. The severity of lameness is usually commensurate with the degree of ligamentous damage and is most severe in horses with partial ruptures. Sometimes no localizing signs are apparent, but femoropatellar effusion, periarticular thickening, or edema may be seen in some horses. Intraarticular analgesia of the femoropatellar joint may slightly improve lameness in some horses, but in others there is no effect on the lameness. The diagnosis is confirmed by ultrasonography. Proximal, midbody, and distal lesions have been identified. Differentiation should be made between core lesions and partial-thickness tears. Radiological changes are unusual, and one should bear in mind that entheseous change on the cranial distal aspect of the patella may be seen as an incidental radiological finding. However, extensive entheseous new bone may be of clinical significance. Scintigraphy may show focal IRU in the patella or more commonly the cranioproximal aspect of the tibia in association with proximal or distal lesions of the middle patellar ligament.

Treatment

Horses with severe injuries may require rest for up to 6 months. In one Editor’s experience (SJD) conservative management has yielded poor results in horses with extensive core lesions, and treatment by injection of porcine urinary bladder matrix or mesenchymal stem cells has improved the prognosis. The presence of periligamentous fibrosis is a poor prognostic finding. Horses with partial-thickness tears have also responded poorly to any form of management, including surgical debridement.

Prognosis

Lameness is often slow to resolve and is recurrent in some horses.

Signs and Diagnosis

The condition is reported to be more common in horses less than 4 years old,⁵⁶ but in my practice it is encountered in horses of all ages.⁵ Lameness is mild to moderate but can be severe at first and acute in onset. Lameness may be intermittent, especially in older horses. Affected horses seem to be lamer when turning. Occasionally mild medial femorotibial effusion occurs, but often no signs are obvious on physical examination. Intraarticular analgesia of the medial femorotibial joint may be required to diagnose the site of pain causing lameness. Because the subchondral bone is probably the site of pain, local anesthetic solution must diffuse into the lesion and may not be completely effective. A 50% improvement in lameness justifies radiographic examination.

The caudocranial, caudolateral-craniomedial oblique, and flexed lateromedial radiographic images are the most useful for demonstrating the lesion. Subchondral bone cysts in the medial femoral condyle are relatively round or oval, with a variably sized base and communication with the joint (Figure 46-5). Increased radiopacity of the rim is usually seen only in horses with older lesions. Radiological signs of OA may also be apparent in some horses. The osseous cystlike lesions in the tibia have a similar morphology. Subchondral bone cysts can also occur as incidental radiological findings in sound horses. Lesions in the caudal aspect of the femoral condyles in foals may appear radiologically as localized or extensive osseous defects. Scintigraphic findings in horses with subchondral bone cysts are inconsistent,²⁴ but most have IRU. Flattening or indentation of the distal medial femoral condyle is sometimes seen radiologically and may be a precursor of a subchondral bone cyst. These lesions are relatively common and frequently do not cause lameness. Occasionally IRU is seen associated with these defects.⁵ In my experience, positive scintigraphic findings, together with a positive response to diagnostic analgesia, are good indications that the defect is a cause of lameness, but some scintigraphically positive lesions do not result in clinical signs; the Editors consider this unusual. Arthroscopic evaluation of horses with subtle osteochondral defects of the medial femoral condyle detected radiologically revealed that flattening of the medial condyle or a subchondral lucent area was associated with a focal or more generalized cartilage defect in 18 of 20 and four of four limbs, respectively. Treatment by abrasion arthroplasty and microfracture resulted in seven of nine horses with focal cartilage lesions returning to full athletic function, and two of six with generalized cartilage pathology.⁶¹

Fig. 46-5 A caudocranial radiographic image of the right stifle of a yearling Thoroughbred colt. Medial is to the left. There is a subchondral bone cyst in the medial femoral condyle with increased radiopacity of the rim and a wide base that communicates with the medial femorotibial joint.

Treatment

Conservative treatment involves stable or pasture rest, with or without nonsteroidal antiinflammatory medication or intraarticular corticosteroids.^62,63 Horses with nonarticular osseous cystlike lesions or small articular defects are probably best managed conservatively. For articular lesions and horses that do not respond to conservative management, arthroscopic debridement has been advocated.^56,59,64 Debridement of the cyst lining and removal of all debris from the joint are the goals. Experimentally the use of cancellous bone grafts did not improve the outcome.⁶⁵ Postoperative intralesional corticosteroid has been advocated to suppress the inflammatory mediators.⁶⁰ Subchondral bone forage is contraindicated because reports indicate that it may worsen the lesion.⁵⁶ Debridement of small medial condylar defects should be approached with caution because this may provoke a worsening of the lesion. Tibial osseous cystlike lesions can be debrided arthroscopically, but many of them lie beneath the cranial meniscal ligament, which must be divided to gain access. It was reported that the success rate for horses more than 3 years of age was poor (35% of 46 horses sound at follow-up evaluation),⁶⁶ and many surgeons now lean toward intralesional corticosteroid treatment. There is evidence that numerous injections of corticosteroids into the fibrous lining of the cyst under arthroscopic guidance is the most effective method of management in older horses, and early reported success appears to be superior to that achieved using debridement in older horses (13/18 horses sound at follow-up evaluation).⁶⁷

Prognosis

A 50% success rate was reported with conservative treatment of horses with medial femoral condylar subchondral cysts, but remodeling of bone may be more prolonged than with surgical treatment.⁶² Arthroscopic debridement carries a 70% to 75% success rate in horses less than 3 years old.^56,64 Preexisting OA results in a more guarded prognosis. Improvement of clinical signs after surgery frequently occurs without radiological resolution. Limited reports of surgical treatment of tibial osseous cystlike lesions⁵⁸ suggest that horses with lateral proximal tibial osteochondrosis-associated lesions may respond best, and this is also my experience.

Signs and Diagnosis

Lameness is often acute and severe in onset after trauma but mostly becomes low grade and persistent. Distention of the femoropatellar or medial femorotibial joints can be expected in horses with more severe injury.⁷¹ Lameness is exacerbated by flexion of the limb in about 90% of horses.⁵⁵ Diagnostic analgesia is usually necessary to confirm the site of pain causing lameness but may not render the horse completely sound. Radiological signs occured in 52% of horses that I have diagnosed with meniscal injury. New bone formation on the cranial aspect of the medial intercondylar eminence of the tibia was the most frequent finding (25%)⁷² and appears to be more common with meniscal than cruciate ligament disease, in which it occurred in five of 71 (7%) cases treated at my hospital⁷² (Figure 46-6). Dystrophic mineralization and osteoarthritic radiological changes may be seen in horses with severe lesions. Ultrasonography can be a valuable aid in diagnosis, although some lesions will not be visible ultrasonographically, and artifactual changes can be difficult to differentiate.^73,74

Fig. 46-6 Lateromedial radiographic image of the left stifle of a 7-year-old Thoroughbred cross gelding. There is new bone on the cranial aspect of the intercondylar eminences of the tibia (arrow). Note also the large radiolucent zone in the proximal aspect of the tibia. There is an old osteochondrosis lesion involving the lateral trochlear ridge of the femur. Arthroscopic examination revealed a tear of the medial meniscus.

Arthroscopy offers the best chance of a definitive diagnosis and an assessment of concurrent damage. Because only the cranial and caudal poles of the menisci can be seen, assessment of meniscal injury is limited. Owing to these limitations, I graded changes visible from cranially as follows:

Fig. 46-7 Arthroscopic photograph of the left lateral femorotibial joint of a 6-year-old eventer gelding. The lateral meniscus has a grade 2 tear (arrow).

Treatment

Horses with acute stifle injuries that have no definitive diagnosis should be managed with rest and antiinflammatory medication, followed by controlled exercise. Arthroscopy is indicated if conservative therapy is unsuccessful or for severely lame horses. Grade 1 meniscal tears can only be superficially debrided. Intraarticular suturing for some horses may be a way forward. Grade 2 and 3 tears are debrided as effectively as possible by removing all loose tissue. A careful assessment of visible concurrent damage should be made. Postoperatively controlled exercise begins at 2 to 3 weeks and can gradually be increased over 3 months, depending on progress and the extent of the injury. Free exercise at pasture should be avoided for 6 months.

Prognosis

Return to full athletic use can be expected in about 50% of horses overall, although improvement may be seen in another 10%.^71,72 Full function was regained in 60% of 67 horses with grade 1 tears, 65% of 35 horses with grade 2 tears, 10% of 24 horses with grade 3 tears, and neither of 2 horses with two menisci affected. In the Editors’ experience the prognosis for return to full athletic function in upper level sports horses is guarded. Concurrent articular cartilage damage significantly worsened the prognosis,⁷¹ and nine of 18 horses with concurrent cruciate ligament injury became sound. Horses treated arthroscopically within 2 months of injury fared 25% better than those treated later than 2 months.⁷² If radiological signs of OA were present, the prognosis was also significantly worsened.⁷¹

Signs and Diagnosis

Lameness is often associated with a history of trauma and is usually acute in onset and severe at first. Distention of the femoropatellar or the femorotibial joints is sometimes present. In horses with severe injuries, crepitus may be detectable. The cruciate draw test appears to be valueless in the conscious horse, but a proximal limb flexion test is usually positive, especially with severe injury. In horses with mild injuries, diagnostic analgesia is required to confirm the site of pain causing lameness. In my series of 75 horses with cranial and caudal cruciate ligament injuries diagnosed at arthroscopy, radiological signs included the following⁵:

Ultrasonographic evaluation of the cruciate ligaments is difficult. Arthroscopy offers the best evaluation of the cruciate ligaments. The cranial cruciate ligament is covered by the median septum, which may make the ligament difficult to assess, but the septum is often disrupted in cranial cruciate ligament injury. Motorized debridement of the septum may be required to see the ligament. The caudal cruciate ligament is viewed from the cranial and caudal aspects of the medial femorotibial joint. The caudal medial aspect of the femorotibial joint can be approached cranially⁸⁰ or caudally.⁸¹ Mild cranial cruciate ligament changes are difficult to quantify because of inflammatory changes in the median septum, but fiber disruption is seen in moderate injuries (Figure 46-8). With acute, severe injuries of the cranial cruciate ligament, inflammatory debris must be removed before the torn ends of the ligament can be seen. Concurrent articular cartilage or meniscal damage within the joint is common.

Fig. 46-8 An arthroscopic view of the right femorotibial joint of an 8-year-old Warmblood gelding. The median septum has been removed with the motorized synovial resector to reveal a chronic, low-grade fiber disruption of the cranial cruciate ligament.

Treatment

With acute injuries the same treatment criteria apply as for meniscal injuries. The indications for arthroscopy and postoperative management are also similar. Arthroscopic debridement is best performed with a motorized synovial resector. Repair in horses with complete cruciate ligament rupture has not been reported, and the best treatment that can be offered is good debridement of loose tissue to allow less severe injuries the best chance to heal.

Prognosis

Prognosis is poor in horses with moderate to severe injuries. In one report, two of 10 horses were pasture sound and one raced,⁷⁵ and in another report two of six were pasture sound.⁷⁹ In my series, lameness persisted in four of six horses with severe injuries; 10 of 17 horses with moderate injuries became sound; and 18 of 29 horses with minor superficial changes became sound.⁵

Signs and Diagnosis

The most easily diagnosed collateral ligament injuries are complete ruptures of the medial collateral ligament, which manifest as acute, severe lameness after trauma. Instability of the stifle occurs with swelling and pain over the ligament. Sprains of the collateral ligaments are less obvious. Heat and pain may be palpable, and chronic thickening develops in some horses. The collateral ligament test can be useful but is not specific. Flexion of the limb is usually painful, but intraarticular analgesia of the medial femorotibial joint may be negative. If complete rupture of the ligament has occurred, stressed caudocranial radiographs are diagnostic. Widening of the joint space occurs on the affected side (Figure 46-9). Enthesophyte formation at the origin and insertion may be seen in horses with chronic injuries. Ultrasonography can be helpful in diagnosing and assessing the injury.¹⁸

Fig. 46-9 Stressed caudocranial radiographic image of the left stifle of a 10-year-old riding horse with rupture of the medial collateral ligament of the femorotibial joint. Medial is to the right. There is widening of the medial joint space. Note also the osseous opacity proximal to the intercondylar eminences (arrows).

Treatment

Horses with mild sprains, in which no instability occurs, are treated with stall rest for 6 weeks and antiinflammatory medication until the inflammation subsides, followed by controlled exercise for another 6 weeks. One report describes the repair of a complete rupture of the medial collateral ligament using braided polyester material attached to two 6.5-mm cancellous screws in the femur and tibia to stabilize the joint.⁸³ Orthopedic wire was originally used, but it dislodged postoperatively. The surgery is a salvage procedure and is not well documented, and concurrent injury and horse compliance should be carefully assessed before undertaking surgery.

Prognosis

Horses with mild sprains have a moderate chance of returning to athletic use, depending on the extent of any concurrent injury. Results are not well documented, and in my view the prognosis is probably poor if entheseous change develops at the medial collateral ligament attachments. The prognosis for horses with complete ruptures is grave. The horse described above that was treated surgically was comfortable at pasture until it became lame after falling 9 months postoperatively. Because associated meniscal or cruciate injury is common, a high chance exists of OA in the long term, even if the medial collateral ligament heals.

Signs and Diagnosis

Horses in which articular cartilage lesions are a primary cause of lameness usually have mild to moderate lameness. Diagnostic analgesia is required to define the site of pain causing lameness. Abnormalities are rarely seen radiologically. At arthroscopy, a variety of lesions may be present. These include thickening, softening, and creasing of the cartilage, widespread fibrillation, focal tufts of fibrillated cartilage, circumscribed nodules of cartilage, apparent tears of the articular surface, and areas of exposed subchondral bone.^72,84,85

Treatment

Doubt about the long-term effect of debridement of cartilage lesions still exists.⁸⁶ Small, full-thickness lesions are probably best debrided to subchondral bone; micropicking the bone appears to improve healing to a degree.⁸⁷ The effect of smoothing partial-thickness defects is still controversial and may provoke the development of an osseous cystlike lesion.^56,86 Debris should be thoroughly lavaged from the joint. Postoperative intraarticular medication with disease-modifying OA drugs could be helpful.

Prognosis

The prognosis for return to soundness for horses with cartilage defects is generally considered guarded. Six of seven horses with focal defects returned to racing, but five horses with larger lesions remained lame.⁸⁴ In my practice, a full-thickness articular cartilage defect was diagnosed arthroscopically in 38 horses as being the primary cause of lameness. Sixteen of 24 horses (67%) for which follow-up information was available became sound.⁵ Of the horses with less severe lesions, 30 of 38 (79%) of those with mild changes (mild fibrillation, mild soft creased cartilage, mild focal fibrillation, n = 77) and 17 of 22 (77%) of those with moderate changes (generalized fibrillation, shear lesions, severe thickening and creasing, partial-thickness linear defect, n = 37) returned to full use. In the Editors’ experience prognosis for upper level sports horses to return to full athletic function is guarded.

Signs and Diagnosis

Many horses have a history of lameness that has already been treated or chronic lameness of varying intensity. Diagnostic analgesia may be required to identify the site of pain causing lameness, but joint effusion and thickening are palpable on the medial aspect of the joint in many horses. Flexion of the limb is painful, and some horses resent holding up the limb for shoeing. Radiological examination reveals typical changes associated with OA, including osteophytosis, flattening of the articular surfaces of the femoral condyles, increased radiopacity and radiolucent zones in the subchondral bone, narrowing of the joint space, and dystrophic mineralization of soft tissues.

Treatment

Management of OA is at best palliative. If possible, the inciting lesion should be treated appropriately in an attempt to prevent worsening of the changes. Intraarticular corticosteroids, glycosaminoglycans, or any medication designed to slow the progress of the disease, as well as arthroscopy in some horses, may give temporary relief.

Prognosis

Once radiological changes of OA are manifest, in particular, joint space narrowing, the prognosis for athletic soundness is poor. With careful management, less severely affected horses may be able to perform light work or be kept at pasture.

Signs and Diagnosis

The history and clinical signs often strongly suggest the possibility of patellar fracture. Initially lameness may be severe and remains so in horses with midsagittal and horizontal fractures. In horses with many of the smaller avulsion fractures or fractures of the medial aspect, lameness becomes moderate to mild after a few days. Often evidence of trauma and local swelling are apparent in the stifle region. Crepitus is occasionally present, and pain may be elicited on palpation of the patella. The femoropatellar joint is usually distended. Horses with chronic, less severe fractures often have surprisingly little direct evidence of the injury. Flexion of the limb is usually painful.

Radiography is essential to confirm the diagnosis and to evaluate the fracture. Lateromedial images may give no indication of the fracture, so a cranioproximal-craniodistal image is essential (Figure 46-10). Severely injured horses greatly resent positioning for this radiographic image and may require analgesia. Occasionally general anesthesia is required, but it should not be attempted without treatment options being in place.

Fig. 46-10 Cranioproximal-craniodistal radiographic image of the right patella of a 10-year-old eventer gelding that hit a cross-country fence with the right stifle. Medial is to the right, and cranial is to the top. There is a displaced fracture of the medial pole of the patella.

Treatment

Horses with open wounds must be treated with debridement and antibiotics, and it is vital to establish if joint infection exists and treat it appropriately. Horses with small nondisplaced, nonarticular fractures may be managed conservatively with stable rest. Most heal by fibrous union only. Horses may return to work in 8 weeks. Horses with fragments originating from the base of the patella need arthroscopic debridement if debris is loose in the joint. Small fragments at the base of the patella, which are embedded in the soft tissue attachments, may not require removal.⁹¹ Articular fractures of the medial aspect are best removed.⁸⁸ This can be done by arthrotomy or arthroscopy (Figure 46-11) and requires careful dissection of the fragment from the medial patellar ligament. The distal end of the fracture is clearly seen arthroscopically. Concurrent joint damage should be evaluated and can have an important bearing on the outcome. Horses with complete horizontal fractures must be treated by internal fixation.^89,92,93 Lag screw fixation with 5.5-mm cortex screws or partially threaded 6-mm cancellous screws, possibly with reinforcement with tension band wiring, is necessary to combat the huge distraction forces of the extensor muscles. Recovery from general anesthesia has to be carefully controlled by delaying attempts of the horse to stand by use of sedation to avoid breakdown of the repair. Sagittal fractures can also be repaired using the lag screw principle.⁹⁴

Fig. 46-11 Arthroscopic photograph of the left patella of the horse in Figure 46-10 showing the fracture line (with probe inserted) in the medial aspect of the patella.

Prognosis

Horses with small, nonarticular fractures usually have a good prognosis with conservative management.⁹¹ Ten of 12 horses with medial fractures without concurrent joint disease treated by partial patellectomy returned to athletic use.⁸⁸ My experience has been similar. Internal fixation of horizontal and midbody vertical fractures can be rewarding, but the risk of breakdown during recovery from general anesthesia is substantial, especially in horses with horizontal fractures. Horses with severely comminuted fractures have a poor prognosis.

Signs and Diagnosis

The history and clinical signs are similar to those seen with other acute, severe stifle injuries, and confirmation of the fracture is made radiologically. The caudocranial and flexed lateromedial images are the most useful. Once the acute inflammation has subsided, lameness can be mild to moderate in horses that do not have clinically significant injuries to vital soft tissue structures.

Treatment

An arthroscopic assessment is essential for evaluating the fracture and concurrent soft tissue damage in the joint, which is extensive in some horses. If accompanying soft tissue injuries are not severe, treatment can be rewarding. Small fragments should be removed. Horses with large fragments can be treated by internal fixation.⁹⁷ Alternatively, large fragments can be removed, but this depends on fragment configuration and the involvement of soft tissue structures, such as the cranial cruciate ligament or the cranial ligament of the medial meniscus that wraps around the cranial surface of the eminence.^95,96

Prognosis

If soft tissue damage is reparable, the prognosis for fracture treatment can be good. The possibility always exists of articular cartilage or soft tissue damage that is not detected at arthroscopic examination⁷⁸ but that may ultimately cause chronic lameness.

Signs and Diagnosis

Characteristically there is a sudden-onset, moderate to severe lameness, with a history of acute trauma. Effusion of the femoropatellar joint is usually present. With condylar fractures there is also effusion of the medial femorotibial joint. Crepitus may be present, and flexion of the joint causes pain. In the femoropatellar joint, fragments arise most commonly from the distal aspect of the lateral trochlear ridge and are best seen on flexed and standing lateromedial radiographic images. Caudocranial images are also important for identifying the position of fragments in the cranial or caudal femorotibial joints, and cranioproximal-craniodistal oblique images are necessary to rule out concurrent patellar fractures. The fracture site may not be obvious. Because these fractures are commonly caused by direct trauma, often the stifle region has a wound, and in these circumstances a strong chance of infection in the joint exists. Infection should be ruled out by arthrocentesis. Infection can also occur by extension into the joint, hours or even days after the injury. If a sudden increase in lameness occurs, arthrocentesis must be repeated.

Treatment

Fragments should be removed to prevent the development of OA. Most can be removed arthroscopically,^91,98 but arthrotomy may be necessary for excision of large fragments.⁹⁹ In many horses I prefer to wait a few days before examining the joints arthroscopically because the initial intraarticular hemorrhage hinders surgery. Many horses have a severely inflamed synovium in which fragments may be embedded and difficult to find. Fragments in the femoropatellar joints are often loose, whereas in the femorotibial joints they more often have soft tissue attachments, but conditions vary greatly, and intraoperative radiography to ensure removal of all fragments can be useful. Evaluation of the remainder of the stifle joint for concurrent injuries is important.

Prognosis

Horses with trochlear ridge fractures have a good prognosis after fragment removal.^91,98 If no clinically significant soft tissue damage occurred, the prognosis is also favorable after removal of fracture fragments in the femorotibial joint. One should bear in mind on the initial assessment that some of these injuries are not as catastrophic as the radiological changes suggest.

Signs and Diagnosis

Foals with minimally displaced fractures may be weight bearing, but the others usually have acute, severe lameness, swelling, pain, and often crepitus in the affected joint. Radiology confirms the fracture and should include enough views to establish its configuration.

Treatment

Conservative treatment may be appropriate for horses with stable, minimally displaced fractures.¹⁰⁰ Internal fixation is indicated for horses with displaced or unstable fractures. Repairs using lag screw fixation, cobra head bone plates, and angle blade plates have been reported.^100-103 Implanting screws through the articular cartilage of the femoral trochlea is sometimes necessary, and crossing the physis with an implant does not seem to have affected growth in the distal femoral physis in older foals.¹⁰⁰ The dynamic condylar screw plate may be of value.

Prognosis

The few published reports¹⁰⁰ indicate that foals with minimally displaced fractures have a good chance of achieving athletic use with conservative treatment. If surgery is required, the outcome is more equivocal, but good success has been achieved in some horses.

Signs and Diagnosis

Most horses are acutely, severely lame immediately after sustaining the fracture, but in some this may settle into a milder lameness if left untreated. Swelling and crepitus are common. Occasionally with minimally displaced fractures there is only mild lameness and no history suggestive of a fracture. A wound on the lateral aspect of the tibia may be present, and intraarticular fractures may be associated with joint effusion. Care should be taken to rule out other injuries in the stifle, such as fracture of the patella, or joint infection if an open wound exists. Infection can even develop by extension into the joint through a skin graze. Because of the lateral curvature of the tibial tuberosity, several radiographic images are often required to identify the contour of the fracture, the caudolateral-craniomedial oblique image being the most useful. The tibial tuberosity does not fuse until at least 3 years of age,¹⁰⁶ and its physis should not be confused with a fracture.

Treatment

Nonarticular fractures may heal with conservative treatment. Horses with large intraarticular fractures can also be treated by internal fixation. Lag screw fixation does not provide a secure enough repair, so tension band wiring,¹⁰⁷ a lateral narrow dynamic compression plate,¹⁰⁸ and a cranial narrow dynamic compression plate⁸⁵ have been used. I believe that the most secure repair is achieved with the latter (Figure 46-12). The plate should extend well distal to the distal extremity of the fracture to withstand the distraction forces of the quadriceps muscles. Because of the shape of the cranial proximal aspect of the tibia, contouring of the plate demands considerable twisting and bending, but this does not seem to affect its efficacy. A technique for preoperative plate bending was reported as a way of saving surgery time,¹⁰⁹ but in my experience plate contouring is not especially time consuming. Most horses are substantially more comfortable postoperatively, but they should be prevented from lying down for 2 weeks.

Fig. 46-12 Postoperative lateromedial radiographic image of the right tibia of a 13-year-old pony gelding that had sustained a fracture of the tibial tuberosity. The horse has been managed using internal fixation with a narrow dynamic compression plate.

Prognosis

Conservative treatment of horses with nondisplaced, small fragments results in a good prognosis. Horses with larger fractures may also respond to conservative treatment with complete return to soundness. Fifteen horses with nonarticular fractures were treated conservatively, and 12 returned to full use. Neither size nor displacement of the fragment affected outcome, and the horses returned to work in a mean of 6.3 months.¹¹⁰ Those that remained lame had concurrent soft tissue injury in the stifle.¹¹⁰ Good results for return to full athletic function have been reported after repair with a cranially applied plate,¹⁰⁴ and in my view this is the treatment of choice for articular fractures. A potential risk exists for failure of the repair during recovery from general anesthesia or the early postoperative period¹⁰⁸ or for catastrophic tibial fracture. This emphasizes the importance of adequate fixation and restriction of the horse during early convalescence.

Signs and Diagnosis

The classical sign of rupture of fibularis tertius and avulsion of its origin is the ability to extend the hock while the stifle is flexed, resulting in a dimpling of the common calcaneal (“Achilles”) tendon. Synchronous flexion of the hock and stifle was reported with avulsions of the origin, presumably because the avulsed bone is held by the joint capsule.¹¹² Horses may bear weight normally, but during the protraction phase of a stride, the distal limb appears flaccid. Lameness can be severe at first, and distention of the femorotibial and femoropatellar joints may be present. Radiological examination is necessary for diagnosing avulsion fractures. Minor disruptions of the tendon of origin manifest as nonspecific lameness associated with pain in the stifle and can be diagnosed by arthroscopic examination; they may accompany other stifle injuries.⁵

Treatment

Horses with injuries to the tendon of origin are usually best evaluated arthroscopically, which also offers the opportunity to check for concurrent injury. Small bone fragments can be removed, but large fragments embedded in the joint capsule may be better left.¹¹² Six weeks of stable rest followed by controlled exercise for 3 months is recommended after surgery.

Prognosis

Horses with avulsion injuries have a guarded prognosis for full soundness, but successful outcome has been reported.¹¹² Minor disruptions of the origin may heal but much depends on concurrent injuries.

Signs and Diagnosis

The usual reason for examination is an unsightly lesion that has been slowly increasing in size. Occasionally the lesion appears to affect the horse’s gait. Lesions are usually hard, well circumscribed, and firmly attached to underlying tissue. The overlying skin is not involved. Caudocranial radiographs show a circumscribed, roughly oval lesion of mineralized tissue (Figure 46-13) lying close to the lateral aspect of the femorotibial joint, with the bulk of the lesion distal to this. These lesions may be seen incidentally on scintigraphic examination as focal areas of intense IRU on the lateral proximal aspect of the crus. The lesion is clearly visible in a caudal image in a subcutaneous location, superficial to the tibial cortex, but in a lateral image IRU could be confused with a proximal tibial stress fracture.

Fig. 46-13 Caudocranial radiographic image (lateral is to the left) of the left stifle of an 8-year-old riding horse with an oval mass of mineralized tissue lateral to the head of the left tibia. The lesion is typical of calcinosis circumscripta.

Treatment

Treatment is only indicated if the lesion causes clinical complications or for cosmetic reasons. Surgical excision is necessary to remove the mass. Care should be taken when embarking on excision because some lesions are attached to the femorotibial joint capsule, which may be entered inadvertently. Steps should be taken to prevent postoperative seroma formation by closing dead space, suturing a stent bandage over the wound, and preventing the horse from lying down for several days postoperatively. The mass usually has a thick fibrous capsule and contains deposits of gritty material.

Prognosis

In horses that are not treated, the mass remains but may not cause complications. A good result can be expected after surgical excision. Regrowth has not been reported, but postoperative problems with wound healing could be serious if the femorotibial joint is involved.

Signs and Diagnosis

A hematoma is manifested as a variably sized swelling, usually on the cranial aspect of the stifle, and may take several hours to reach maximum size. Smaller swellings may be difficult to differentiate from femoropatellar joint effusion. A hematoma is only painful on palpation until the initial bruising and swelling have settled. An uncomplicated hematoma does not usually cause lameness once the discomfort associated with the initial bleeding has passed. Other concurrent injury should be suspected if the horse is substantially lame, especially if lameness persists for several days. A hematoma may occasionally involve only the stifle initially but appears to spread to the inguinal and ventral abdominal areas. Huge swellings can cause oozing from the skin and skin loss. A careful search should be made for open wounds, which could lead to infection in the hematoma or cellulitis. Cellulitis usually takes at least 24 hours to form, and the swelling is firmer than a hematoma, hot, and painful. Lameness worsens as infection progresses.

Ultrasonography is a helpful tool for diagnosing hematoma, which can be confirmed by centesis of the swelling using aseptic technique. In the early stages, frank blood is retrieved, but as the blood clots, the fluid collected will be serum. Radiographic examination is indicated if lameness is severe or persists.

Treatment

In the initial phase, when hemorrhage is likely, the horse should be confined and cold applied to help to slow hemorrhage. Phenylbutazone can be given for its antiinflammatory effect. Antibiotics should be administered if the horse has an open wound. Although some clinicians believe that draining these hematomas is contraindicated, in my experience hematomas resolve better after effective drainage. Drainage should not be attempted until the hemorrhage has stopped and the free blood has clotted, usually 3 to 4 days after the injury. A 2- to 4-cm scalpel incision at the most dependent point of the hematoma ensures that drainage continues until the cavity has filled in.

Prognosis

In the absence of concurrent injury or infection and once the hematoma has resolved and is free of fluid, the prognosis for athletic use is good.