History and presenting complaint

Horses with ‘bucked shins’ present with an acute onset of bilateral soft tissue swelling, heat and sensitivity over the dorsal aspect of the metacarpus, with an associated lameness or ‘stiffness’ immediately after a high-speed workout (‘breeze’) or race. Very often this is the first race or first speed work for the horse at near-racing distances. In some horses there may be a more gradual onset of these signs, with a marked exacerbation following the first race or a longer ‘breeze’, If training continues, the lameness typically worsens considerably, as opposed to the horse ‘warming out of it’. The signs of ‘bucked shins’ are generally so specific that most experienced trainers can make a reliable diagnosis.

Physical examination

Horses with ‘bucked shins’ exhibit variable degrees of soft tissue swelling, heat and sensitivity on palpation over the dorsal diaphyses of MC-III. When viewing the metacarpi from the lateral aspect, there is often a distinct dorsal convexity. Firm digital pressure in this location will elicit a painful response. These signs are particularly pronounced in the acute stages, but after a period of rest and anti-inflammatory treatment, there is generally considerable improvement. The exceptions are horses that have progressed to the chronic or ‘recurrent’ category and have developed a marked periosteal reaction along with chronic inflammation and associated soft tissue swelling. Less commonly, a more focal area of swelling may be present at some point along the dorsal diaphysis,¹ which must be differentiated from a true stress fracture (see section below).

Lameness examination

Horses with acute ‘bucked shins’ typically exhibit a bilateral stiff or choppy forelimb gait at a trot (sometimes mimicking a foot or carpal lameness), but in those in which one metacarpus is more severely affected than the other, a distinct head nod may be evident. Lameness in these horses ranges from grade 1 to 3.² The most severely affected horses may acutely exhibit mild lameness at the walk. The severity of the lameness will vary greatly with the stage of the disease and the timing of the examination in relation to the last speed work.

Diagnostic analgesia

Diagnostic analgesia is generally not necessary to localize the source of pain in a horse with acute ‘bucked shins’. High palmar analgesia (high palmar nerve block) with a dorsal ring block in the proximal metacarpus can be helpful in confirming the location of pain in those horses with subacute or chronic ‘bucked shins’.

Nuclear scintigraphy

Bone-phase (delayed-phase) nuclear scintigraphy classically reveals diffuse moderate-to-intense abnormal increased radiopharmaceutical uptake along the dorsal diaphyses of the affected MC-III³ (Fig. 16.1).

Radiography

Radiographic findings vary with each case and the stage of disease. Radiographs in mildly affected horses or in the very early stages of the disease (subclinical) are often negative or equivocal for osseous abnormalities. In more severely affected horses, diffuse subperiosteal osteolytic change in combination with smooth, low-density periosteal proliferative reaction is typically seen along the dorsal and dorsomedial diaphysis of MC-III (Fig. 16.2). High-detail digital radiographs are superior for detecting the subtle abnormalities. Soft tissue swelling, when present, will also be evident radiographically in this location.

Thermography

Thermography in the hands of an experienced operator has been shown to be a valuable diagnostic aid for the detection of abnormalities in the metacarpi of racing Thoroughbreds, with up to 60% of two year olds in training exhibiting abnormal findings.⁴

Therapeutic aims

The goals of treatment for acute ‘bucked shins’ are two-fold: decrease or eliminate further excessive cyclic strains on MC-III and shift the balance from net bone resorption to net bone apposition, and reduce acute inflammation.

Exercise restriction

The degree of exercise restriction depends on several factors, of which the severity of clinical signs, in conjunction with radiographic and/or scintigraphic findings, is the most important.

Initially, all horses diagnosed with acute ‘bucked shins’ should receive stall rest and hand grazing (no purposeful hand-walking exercise) until soft tissue swelling and pain on palpation of the dorsum of MC-III have subsided. A program of controlled exercise can begin. In horses without extensive periosteal new bone formation or other severe radiographic changes, 2 weeks of stall rest with daily hand-walking (10–15 minutes once or twice a day) are initially recommended. Once horses are sound at a trot in-hand then formal training can commence, ideally employing a modified exercise protocol (see below).

Horses with moderate-to-marked periosteal reaction and/or subperiosteal osteolytic change, along with moderate-to-intense abnormal increased radiopharmaceutical uptake scintigraphically, require a more extended period of rest and controlled exercise. Generally, this encompasses four weeks of hand-walking, followed by 4–8 weeks of turnout exercise in a small paddock or ‘shed row’ exercise daily. The duration and extent of exercise restriction is modified based on the specifics of each case. Horses with chronic or recurrent ‘bucked shins’ (i.e. those that have had several acute episodes with or without an appropriate period of convalescence) should be allowed a total of 90–120 days’ rest and in many instances they are simply turned out for the remainder of the season and training is resumed the following year.

Follow-up radiographic and scintigraphic examinations can help guide the recommendations for resumption of training in those cases where this is economically feasible.

Anti-inflammatory therapy

Anti-inflammatory therapy should be initiated immediately in cases of acute ‘bucked shins’ and continue until signs of swelling and ‘shin sensitivity’ (pain) subside. Up to 30 minutes of cold hosing or icing, several times a day, along with bandaging, are generally effective. Anecdotally, application of a poultice or antiphlogistic dressing (e.g. Gel-o-cast®) for several days may also help decrease swelling.

The use of NSAIDs for their anti-inflammatory and analgesic effects in patients with inflammatory bone disorders is controversial in light of the gathering body of evidence that these drugs, when used chronically at high doses, may impair bone healing in horses.⁵ However, it is this author’s opinion that a brief period (i.e. a few days) of NSAID treatment during the acute stage of ‘bucked shins’ is warranted in horses with moderate-to-severe signs. Phenylbutazone or flunixin meglumine at standard doses is generally effective. Long-term NSAID treatment is contraindicated, in this author’s opinion, for the reasons noted above.

Modified training protocol

The key to preventing ‘bucked shins’ is to stress the dorsal cortices of the developing metacarpi in such a way as to stimulate adaptation to the cyclic compressive loads under conditions that are similar to those experienced during a race, i.e. to train at racing speeds.⁶ Traditional training strategies for flat-racing Thoroughbreds have employed a basic scheme of daily galloping exercise for extended distances (e.g. 1–2 miles) with speed work or ‘breezes’ at shorter distances (e.g. 2–6 furlongs) weekly to every third week. In immature (untrained) horses the timing (too infrequent) and distance (too long) of the high-speed work sets up a state of maladaptive remodeling in which bone resorption outpaces apposition and fibrous periosteal new bone predominates.⁶ Eventually, this inferior bone develops microfractures and resulting inflammation, which manifests clinically as periostitis or ‘bucked shins’.

To prevent or mitigate the potential for this vicious cycle, horses should be trained in such a way as to increase the frequency of high-strain cyclic compressive loading (high-speed exercise or ‘breezes’) and decrease the total distance at which they are galloped.⁶ It is recommended that horses be worked at or near racing speed at least twice a week, initially at very short distances, for example one furlong. The distance of the speed work is increased gradually (e.g. adding one furlong every 1–2 weeks) and then as the horse is asked to go faster, the distance is reduced and the process repeated until the horse is conditioned to race. Throughout this process, daily galloping is limited,⁶ for example to no more than one mile/day. Upon resumption of training, horses are continually monitored for signs of ‘shin soreness’, lameness or dorsal metacarpal swelling and exercise intensity should be modified accordingly.

Traditional or alternative therapies

Over the course of time, seemingly endless ‘traditional’ therapies or essentially ‘home remedies’ have been promoted for treating ‘bucked shins’, as well as the many other inflammatory lesions and injuries of racehorses. Many have gone by the wayside but a handful have persisted and remain in use today and other ‘alternative’ therapies continue to arise on almost a daily basis. The list includes: ‘paints’ (topical rubefacients), ‘blisters’ (chemical vesicants), ‘pin firing’ (thermocautery), ‘freeze firing’ (focal cryotherapy), electrostimulation, periosteal ‘picking’ (or ‘needling’) and extracorporeal shockwave therapy, Unfortunately, many of these modalities have not undergone the necessary scientific scrutiny to enable rational conclusions regarding their efficacy, and some may be contraindicated. Some of these adjunct therapies will be covered in detail in other chapters, and the interested reader is referred there.

Prognosis

The prognosis for the vast majority of horses with ‘bucked shins’ is generally very good if appropriate intervention is undertaken and adhered to. Recurrence is rare; however, a variable proportion of horses will experience repeated episodes or ‘chronic’ DMD. Horses not given adequate convalescence and those that have not had their training protocol modified (see above) are at high risk for recurrence. ‘Bucked shins’ is quite rare in older horses (>4 years of age)⁷ once the immature bone has remodeled and changed its inertial properties in response to the demands of high-speed exercise. However, horses that have experienced clinical ‘bucked shins’ as two or three year olds are in the high-risk group for dorsal cortical stress fractures (see section below).⁸

History and presenting complaint

Horses with an acute dorsal cortical stress fracture of MC-III typically exhibit a moderate-to-severe lameness immediately following high-speed work (‘breeze’) or a race. Less commonly, the lameness will not be evident until several hours after the horse has ‘cooled out’. Acutely, these horses are too lame to continue training. There is almost invariably a focal area of soft tissue swelling, focal periosteal irregularity and sensitivity at the fracture site along the dorsal aspect of MC-III.

Some horses have a history of low-grade, chronic or intermittent lameness on the affected limb for several weeks prior to the acute onset of a more severe lameness once overt fracture has occurred. Another subset develops signs of acute fracture upon resumption of training after a brief period of lay-up (a few to several weeks) for an unrelated illness or injury.

Some horses may become sound enough to train or even race after extended rest, but continue to be plagued by recurrent lameness and poor performance. This is a common scenario for those with chronic stress fractures that have gone undiagnosed. Almost all horses with dorsal cortical stress fractures of MC-III will have a history of clinical ‘bucked shins’ in the 6–12 months preceding the fracture.²⁰

Physical examination

For horses with acute fracture, physical examination will classically reveal a focal area of soft tissue swelling along the dorsum of the metacarpus at the site of the fracture, with a corresponding bony ‘knot’ or periosteal irregularity (hard swelling or exostosis) along the dorsal or dorsolateral diaphysis of MC-III. Firm digital pressure at the fracture site will consistently elicit a painful response. These signs are less dramatic in horses with chronic or subacute fractures. Horses with multiple fractures may have signs more suggestive of ‘bucked shins’ (i.e. diffuse pain and swelling along the diaphysis). Fractures are almost always unilateral in Thoroughbreds (in contrast to ‘bucked shins’) and involve predominantly the left forelimb in the US.22–25 Bilateral fractures occur, but are rare.

Lameness examination

Acutely, horses exhibit a moderate-to-severe lameness on the affected limb, which is typically grade 3–4.² Many are lame at a walk and all are profoundly lame at a trot. With a brief period of rest (a few days to a few weeks), horses generally walk comfortably but exhibit a mild-to-moderate lameness at a trot in-hand (grade 2–3). Horses with chronic fractures may exhibit only mild lameness at a trot in-hand. Firm pressure applied over the fracture site will exacerbate the lameness in most acute and subacute cases.

Diagnostic analgesia

Diagnostic analgesia is rarely necessary to localize the source of lameness in horses with acute and subacute dorsal cortical stress fracture of MC-III (owing to the specificity of clinical signs) and in fact, it is arguably contraindicated in these horses. Diagnostic analgesia can be useful for this purpose in horses with chronic fractures when clinical signs are less specific. High palmar analgesia (a ‘high palmar block’) will be positive.

Scintigraphy

Bone-phase (delayed-phase) nuclear scintigraphy will reveal a focal (or multifocal in horses with multiple fractures) area of moderate-to-intense abnormal increased radiopharmaceutical uptake in the dorsal diaphysis of the affected MC-III in acute and subacute cases (Fig. 16.3). The intensity of radiopharmaceutical uptake will be less intense in chronic cases and will vary with the time course of the injury.³

Radiography

The classic radiographic abnormality is a short, oblique intracortical (unicortical) fracture line in the dorsal or dorsolateral cortex of MC-III (Fig. 16.4). Most commonly the fractures are diaphyseal and are oriented dorsodistal to palmaroproximal at a 30–45° angle with the dorsal cortex. Most extend to the junction of the middle and palmar third of the dorsal cortical width and do not enter the medullary cavity. Occasionally, a complete fracture will extend proximodorsally out through the dorsal cortex (a true saucer fracture’). Metaphyseal fractures, those that begin and propagate in a dorsoproximal-to-palmarodistal direction, and those that enter the medullary cavity are less common.

A full series of radiographs (four views: lateral, dorsopalmar, DMPLO and DLPMO) of the entire MC-III should be taken. Multiple fractures are sometimes present. In rare cases fracture lines may propagate or radiate away from the primary fracture site.²⁶ The majority of fractures are oriented in a frontal or near-frontal plane, but occasionally sagittally oriented fractures are seen.²⁷ Variable degrees of periosteal and endosteal callus may be present, as will soft tissue swelling and more diffuse osteolytic and proliferative periosteal reaction associated with previous ‘bucked shins’ in many horses.

Radiographs may be negative in acute cases. As with other stress fractures, high-detail radiographic films or digital radiographs are advantageous for detecting subtle cortical abnormalities. When initial radiographs are negative or have equivocal findings, and clinical signs and/or scintigraphic findings are highly suggestive of stress fracture, follow-up radiographs should be taken in 7–10 days.

Therapeutic aims

The primary goal of treatment for dorsal cortical stress fractures of MC-III is to promote fracture healing and, although uncommon, minimize the potential for catastrophic fracture.

Therapy

Complete cessation of exercise (stall confinement) and anti-inflammatory treatment are the initial steps in the immediate postfracture period. A light padded bandage and local cold therapy (hosing/icing as previously described), along with NSAID treatment for a few days, are helpful to reduce soft tissue swelling and improve comfort in the acute phase.

Non-surgical management

There is debate among clinicians regarding the merits of surgical and non-surgical management of dorsal cortical stress fractures of MC-III. These fractures are notorious for being slow to heal or for following an unpredictable course between horses.12,19 Fractures in younger horses (two and three year olds), those that enter the medullary cavity or that involve the metaphyseal regions are the most likely to heal expediently without surgical intervention. In general, this involves a period of 3–4 months of controlled exercise; however, it is not unusual for some fractures to require 4–6 months or longer for satisfactory healing.²⁸

When non-surgical management is chosen, 4–6 weeks of stall confinement with daily hand-walking is recommended. This is followed by 6–8 weeks of controlled exercise in the form of small paddock turnout or very light jogging. Some form of controlled exercise is important to stimulate remodeling and fracture healing.22,23 Complete cessation of exercise for a prolonged period (e.g. long-term stall confinement) favors the development of a chronic fracture (i.e. a delayed or non-union).

Follow-up radiographs should be taken every 4–6 weeks to assess healing before increasing the intensity of exercise or for determining whether surgical intervention is warranted (to overcome delayed healing). Follow-up scintigraphic scans can also help in making these decisions.³ A radiographically visible fracture exhibiting low or diminishing scintigraphic activity would warrant strong consideration as a candidate for surgery.

Surgical management

With the above exceptions, the majority of horses with acute dorsal cortical stress fractures of MC-III, and all horses with chronic fractures, are candidates for surgical intervention. Surgical treatment stimulates healing, thereby assuring a more rapid and predictable convalescence, and in the hands of an experienced surgeon carries a low rate of complications.

Surgery involves either osteostixis (fenestration), screw fixation (either positional or compression) or a combination of the two. One clear disadvantage of screw fixation over osteostixis alone is the need for a second surgical procedure to remove the screw. For any technique, the procedure can be performed with the horse under general anesthesia or standing under sedation and using local anesthesia (high palmar analgesia with a dorsal ring block). With the standing approach there is a slight increase in risk for non-catastrophic complications (e.g. contamination/infection or drill bit or tap breakage if the horse moves unpredictably), but the risk of catastrophic fracture during recovery, although rare, and other potential anesthetic-related problems is eliminated and the overall length of the procedure is minimized.

The basic surgical approach is similar with any method. After routine aseptic preparation and draping, the fracture should be localized using radiopaque markers. (In many cases it is not possible to accurately identify the fracture simply through surgical exposure and periosteal elevation.) A row of stainless steel skin staples or hypodermic needles inserted perpendicular to the skin is placed along the dorsal metacarpus in the region of the fracture and a lateral (or slightly oblique if appropriate) radiograph is taken.

Osteostixis

A 4–6 cm longitudinal incision is created between the digital extensor tendons, centered over the fracture, and extended through all tissues, including the periosteum, in a single cut. Self-retaining retractors (Gelpi, sharp Weitlaner) are used to maintain exposure and the periosteum is elevated. Alternatively, individual stab incisions can be used for each hole. In either approach, four to seven holes in a diamond pattern are then drilled across the fracture line perpendicular to the long axis of MC-III and entering the medullary cavity, using the pre-placed markers as a guide. It is appropriate to monitor hole placement radiographically and therefore a radiograph should be taken after the first hole is drilled to ensure proper location. Successive holes are then drilled using the first hole as a reference point.

Drill bit preference varies with surgeon but 2.5–3.5 mm diameter bits are appropriate. Smaller bits (e.g. 2.0 mm) are more easily broken in the standing patient and larger holes may unnecessarily weaken the bone, as does an excessive number of holes.²⁷ Distance between holes should be kept at approximately 1.0 cm. A large number of holes placed close together can result in sequestrum formation or resorption of a core of bone or significantly weaken MC-III.²⁹ Copious lavage during drilling, and frequent cleaning of the bit, are important to minimize the potential for the bit to break. After final radiographic confirmation of adequate hole placement the incisions are closed routinely and a padded bandage is applied.

Horses are confined to a box stall for a total of 4–6 weeks following surgery. Skin sutures are removed 12–14 days postoperatively, at which time daily hand-walking exercise should commence. A bandage is maintained for 2–3 weeks after surgery. After this period of stall confinement and hand-walking, horses are allowed daily turnout exercise in a small paddock for four weeks. If at that point follow-up radiographs reveal good progression of healing, daily light jogging exercise can begin. Harder training should not commence until fractures have sufficiently healed radiographically. Drill holes may persist radiographically for many months (beyond the point of fracture healing), even while horses are training at speed. Based on studies in other species³⁰ and on clinical observation in horses,²³ it is assumed that these holes should no longer act as stress risers by that stage.

Osteostixis is believed to accelerate or promote healing by facilitating access of mesenchymal cells and other osteogenic medullary elements to the fracture line.7,31 The ‘cores’ of new bone that form across the fracture line may act to stabilize the fracture and further promote healing.³² Osteostixis may also stimulate fracture healing through activation of the ‘regional acceleratory phenomenon’.³³

Screw fixation

If osteostixis is to be employed along with screw placement, the surgical approach is identical to that described above. If a single screw is being used without osteostixis, a smaller (~1.0 cm) ‘stab’ incision can be used. A 3.5 or 4.5 mm ASIF cortex screw is appropriate. Although screw insertion using the lag technique has been described, the majority of surgeons place these screws in a positional (‘neutral’) fashion. The latter approach is technically easier and the results are comparable. Regardless of the technique, either compression (‘lag screw’) or positional (‘neutral’), screws are placed in a unicortical manner. Transcortical screws that engage the palmar cortex are contraindicated and no longer recommended, as they are associated with a higher incidence of osteolysis around the implant and implant-associated pain,¹² as well as fracture and the risk of suspensory ligament damage during placement.³⁴

Standard ASIF techniques are employed for drilling, tapping and countersinking. Screws should be placed as close to perpendicular to the fracture line as possible (Fig. 16.5). Osteostixis, if employed, is then performed as previously described and the incisions are closed routinely.

Bandaging and initial aftercare are similar to that described for osteostixis. Screw removal is usually performed between two and three months after surgery. Proponents of the combination of a positional screw and osteostixis feel that two months is generally adequate.²² The decision for screw removal is based on adequate progression of healing on follow-up radiographs. Screws are removed with the horse standing and using sedation and local anesthesia. An additional period of controlled exercise is recommended before resuming training following screw removal. This period varies from 2–8 weeks.^22,35 Unicortical screws in the dorsal cortex of MC-III do not cause pain in all horses upon resumption of training and return to racing.³⁴ However, screw removal in the early postoperative phase (i.e. at the 2–3 month point) obviates the need to take the horse out of training if pain develops and it eliminates the screw being implicated as the cause for any number of unrelated problems in the future.

The benefits of interfragmentary screw compression (‘lag screw’ technique) in fracture healing are quite clear and well understood. The mechanisms by which a neutral or positional screw acts specifically to promote or accelerate healing of stress fractures of the dorsal cortex of MC-III remain incompletely understood. In one uncontrolled study,²² dorsal cortical stress fractures of MC-III treated surgically by a combination of screw fixation using a positional (non-compression) screw and osteostixis were reported to heal faster (95% of fractures healed in two months) than fractures treated with osteostixis alone (3–4 months for radiographic healing).^23,25 Differences in postoperative exercise regimens between studies may have influenced the results, but interfragmentary stabilization and the ‘regional acceleratory phenomenon’ have been proposed as mechanisms by which screws facilitate fracture healing over osteostixis alone.²²

History and presenting complaint

The classic presentation of a horse with a condylar fracture is an acute onset of moderate-to-severe lameness during or immediately after a race or high-speed work. In most cases the rider or driver is immediately aware that the horse has sustained an injury. In others, the horse successfully finishes the race or workout with lameness immediately obvious after pulling up (slowing down). Less commonly, the injury will not become apparent until several hours after the horse has ‘cooled out’ or even until the following day. Acutely, most horses exhibit lameness of varying degrees at a walk. Joint effusion and periarticular soft tissue swelling may also be noted.

The vast majority of horses are not able to continue training. On rare occasions a horse with a chronic fracture (generally short and incomplete) will be presented with a history of recurrent lameness and/or poor performance that is exacerbated with exercise. Some horses have a history of seemingly minor or low-grade ‘soreness’ on the affected limb or other concerns of an ‘ankle problem’, for several days or weeks prior to overt acute fracture (see discussion of pathophysiology below).

Physical examination

In the majority of horses with acute condylar fractures, there is little difficulty identifying the location of the injury. Most horses have obvious heat and effusion of the involved fetlock joint and flexion will elicit a marked painful response. In horses with displaced lateral condylar fractures, there is typically soft tissue swelling over the affected condyle and a noticeable deviation in the contour of the metaphysis. The same is true for horses with medial condylar fractures that have become displaced or have failed catastrophically in the diaphysis. (Open and/or unstable fractures in this category are common and are not a diagnostic challenge.)

Horses with chronic fractures (typically a non-displaced, short, lateral condylar fracture) tend to have less soft tissue swelling, but joint effusion and pain on lower limb (‘fetlock’) flexion persist, although the degree will vary from horse to horse.

Lameness examination

Radiographs should be taken first in all cases of suspected condylar fracture before proceeding with a formal lameness examination. Owing to the severity and relative specificity of the clinical signs, a full diagnostic lameness evaluation is generally unnecessary in these horses.

Acutely, the majority of horses with a condylar fracture exhibit mild-to-moderate lameness at a walk. Some exhibit limited weight bearing, but generally after a few days of rest, bandaging and anti-inflammatory treatment, most will bear full weight and walk readily. In the early postfracture period, these horses generally remain moderately to severely lame at a trot in-hand (grade 2–4 of 5). Horses with chronic, incomplete fractures typically exhibit mild-to-moderate lameness at a trot (grade 1–3 of 5). Lameness in horses with chronic displaced fractures is often quite severe as degenerative joint disease progresses.

Diagnostic analgesia

Diagnostic analgesia is rarely needed to localize the site of pain in horses with condylar fractures and is contraindicated in all horses with clinical signs typical of acute fracture given the risks for exacerbation of the injury (i.e. development of a complete or even catastrophic fracture). In the exceptional case of a horse with a chronic, incomplete or unicortical lateral condylar fracture⁴⁶ (a horse that has been able to continue some level of exercise or does not have a history of acute onset of marked lameness and joint effusion), a full lameness examination with diagnostic analgesia would be acceptable. In these horses a low palmar/plantar nerve block or intra-articular local anesthetic block of the fetlock joint will result in improvement of the lameness.

Therapeutic aims

The goals in treating condylar fractures are to reduce healing time and minimize the potential for further degenerative changes in the affected joint. Optimal anatomic reconstruction of the articular surface and stabilization of the fracture are the keys. When dealing with medial condylar fractures (and the rare lateral fracture that extends into the mid-diaphysis), prevention of a catastrophic fracture is also paramount.

Emergency treatment

Horses with acute condylar fractures should be confined strictly to a stall. The majority of non-displaced or incomplete lateral condylar fractures can be managed by coaptation with a firm, padded bandage pending definitive treatment (see below). Horses with displaced lateral condylar fractures are initially best managed by more rigid coaptation with the distal limb in a neutral or ‘equinus’ position (oriented such that the metacarpus/metatarsus and digit are in line). This can be accomplished with a dorsally applied splint and bandage that extends from the toe to just distal to the carpus or tarsus (such as a Kimzey splint®). This type of coaptation is important until the full extent of the injury can be assessed to rule out concurrent suspensory apparatus pathology and to prevent further fracture displacement and damage to the fetlock joint.

Horses with short medial condylar fractures should at least be managed with a rigid heavily padded bandage (such as a Robert-Jones bandage), with the addition of splints a prudent option. In horses with radiographically identifiable fracture lines in the mid-diaphysis, dorsally and laterally applied splints in the forelimb (extending to the elbow) or plantar and lateral splints in the hind limb extending to the point of the hock are recommended. Rigid coaptation with a bandage and splints or application of a well-constructed full-limb cast should also be considered prior to transportation given the propensity for catastrophic failure.44,47

NSAIDs are administered as needed for analgesia.

Non-surgical management

In certain cases of short, incomplete condylar fractures, particularly those in which economic considerations preclude surgery, non-surgical treatment can result in a good outcome.41,44,52 The distal limb is kept in a bandage for 2–3 weeks to help minimize any soft tissue swelling and to provide some support. NSAIDs are administered only as needed to provide analgesia. Generally, the majority of horses in this category are quite comfortable within a few days to a week or so following the injury. Horses initially should have 1–2 months of strict stall rest, followed by another 1–2 months of stall confinement with daily hand-walking exercise. Follow-up radiographs are repeated three months from the time of fracture and if healing is progressing well, exercise in the form of small paddock turnout can begin. Under ideal circumstances, fractures heal in approximately four months.

The major disadvantage of non-surgical treatment is the tendency for fractures to exhibit delayed healing at the articular surface.41,52,53 Resumption of training should not commence until fractures have completely healed and this may take up to six months or longer in some horses treated non-surgically. However, in a small percentage of horses a gap or defect in the subchondral bone may persist indefinitely well beyond the point at which the fracture has healed, which can complicate the decision on when to resume training.