Incomplete fracture of the talus secondary to maladaptive stress remodeling in a horse

Scott A. Katzman 1Department of Surgical and Radiological Sciences, William R. Pritchard Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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Mathieu P. Spriet 1Department of Surgical and Radiological Sciences, William R. Pritchard Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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Beau R. Beck 2South Valley Large Animal Clinic, 1791 W 11400 S, South Jordan, UT 84095.

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Myra F. Barrett 3Department of Environmental and Radiological Health Sciences, James L. Voss Veterinary Teaching Hospital, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523.

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Dean A. Hendrickson 4Department of Clinical Sciences, James L. Voss Veterinary Teaching Hospital, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523.

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Abstract

CASE DESCRIPTION

A 6-year-old Quarter Horse gelding used for barrel racing was evaluated for acute onset of non–weight-bearing lameness of the left hind limb following strenuous exercise.

CLINICAL FINDINGS

Nuclear scintigraphic imaging revealed focal increased radiopharmaceutical uptake centrally within the left talus. Subsequent standard radiographic and ultrasonographic examinations of the tarsus failed to identify the cause of the increased radiopharmaceutical uptake; however, the lameness was definitively localized to the tarsocrural joint by intra-articular anesthesia. Subsequent MRI sequences of the left tarsus revealed an incomplete fracture of the talus that extended distally from the trochlear groove and evidence of maladaptive stress remodeling of the trochlear groove of the talus and distal intermediate ridge of the tibia.

TREATMENT AND OUTCOME

The horse was treated conservatively, with management consisting of stall confinement, physical rehabilitation, therapeutic laser therapy, and intra-articular autologous conditioned serum administration. The lameness resolved, and the horse was competing at its previous level within 15 months after lameness onset.

CLINICAL RELEVANCE

Although rare, incomplete fracture of the talus should be considered as a differential diagnosis for horses that develop acute hind limb lameness following strenuous exercise, especially when that exercise involves abrupt changes in direction while the horse is traveling at maximal speed. Acquisition of additional oblique projections during radiographic evaluation of the tarsus might be useful for identification of such fractures, but definitive diagnosis may require advanced diagnostic imaging modalities such as CT and MRI. Horses with incomplete fractures of the talus can be successfully treated with conservative management.

Abstract

CASE DESCRIPTION

A 6-year-old Quarter Horse gelding used for barrel racing was evaluated for acute onset of non–weight-bearing lameness of the left hind limb following strenuous exercise.

CLINICAL FINDINGS

Nuclear scintigraphic imaging revealed focal increased radiopharmaceutical uptake centrally within the left talus. Subsequent standard radiographic and ultrasonographic examinations of the tarsus failed to identify the cause of the increased radiopharmaceutical uptake; however, the lameness was definitively localized to the tarsocrural joint by intra-articular anesthesia. Subsequent MRI sequences of the left tarsus revealed an incomplete fracture of the talus that extended distally from the trochlear groove and evidence of maladaptive stress remodeling of the trochlear groove of the talus and distal intermediate ridge of the tibia.

TREATMENT AND OUTCOME

The horse was treated conservatively, with management consisting of stall confinement, physical rehabilitation, therapeutic laser therapy, and intra-articular autologous conditioned serum administration. The lameness resolved, and the horse was competing at its previous level within 15 months after lameness onset.

CLINICAL RELEVANCE

Although rare, incomplete fracture of the talus should be considered as a differential diagnosis for horses that develop acute hind limb lameness following strenuous exercise, especially when that exercise involves abrupt changes in direction while the horse is traveling at maximal speed. Acquisition of additional oblique projections during radiographic evaluation of the tarsus might be useful for identification of such fractures, but definitive diagnosis may require advanced diagnostic imaging modalities such as CT and MRI. Horses with incomplete fractures of the talus can be successfully treated with conservative management.

A 6-year-old Quarter Horse gelding was brought to the UCD William R. Pritchard VMTH for nuclear scintigraphic evaluation of the hind limbs following acute onset of left hind limb lameness. The horse was used for barrel racing. The injury was characterized as acute development of non–weight-bearing lameness (lameness score,1 5/5) of the left hind limb 30 minutes after its fifth and final run during a competition. The lameness rapidly improved and appeared to be completely resolved within 1 hour after onset. The horse was returned to the stable where it was housed. Approximately 72 hours following the initial episode, the horse was again non–weight bearing on the left hind limb. The veterinarian who evaluated the horse at that time was unable to localize the source of lameness during physical examination. The horse was briefly examined at a walk, but a full lameness evaluation was not performed owing to the severity of lameness. Results of manipulation and palpation of the limb were considered unremarkable, which raised concern that the lameness originated from the pelvic or proximal femoral region. Because of the lack of evidence to the contrary and the severity of lameness, the horse was referred to the UCD VMTH for further evaluation and diagnostic imaging. Radiographs of the left hind limb were not obtained prior to referral. The horse received phenylbutazone (2 g, IV) prior to transport to the teaching hospital.

During the initial physical examination at the teaching hospital, the horse was bright, alert, and responsive, and all vital parameters were within reference limits. The horse was placed in a square box stall (3.7 × 3.7 m [12 × 12 feet]) that was equipped to support it in a sling if necessary. The horse was non–weight bearing on the left hind limb when ambulating but would touch the toe of the left hind limb to the ground for balance and eventually bear full weight on the limb when standing. While standing, the horse extended both hind limbs caudally (ie, adopted a parked-out stance). The application of a hoof tester to the left hind hoof elicited no response. Symmetric effusion of the tarsocrural region was noted bilaterally and was subjectively assessed as mild. The horse was willing to flex, extend, and abduct the left hind limb but mildly resented adduction of the limb. When the right hind limb was lifted, the horse was able to place the left hind limb squarely underneath itself and bear full weight on it. Digital pulses of the right hind limb were mildly increased from normal at the time of the initial physical examination, and a support boota was applied to that limb to aid in the prevention of laminitis.

A 14-gauge, 5.25-inch catheterb was aseptically placed in the left jugular vein, and administration of alternating doses of phenylbutazone (2.2 mg/kg [1 mg/lb], IV, q 12 h [ie, at 8 am and 8 pm]) and morphine sulfate (0.1 mg/kg [0.05 mg/lb], IV, q 12 h [ie, at 2 am and 2 pm]) was initiated. Forty-eight hours later, the horse appeared substantially more comfortable, as evidenced by the fact that it spent most of the time standing squarely and bearing weight equally on all 4 limbs. Morphine administration was discontinued, and phenylbutazone (2.2 mg/kg, q 12 h) administration was continued by the oral route for the remaining duration of hospitalization.

Nuclear scintigraphy was performed the day after initial examination at the teaching hospital. The horse was administered technetium Tc 99m methylene diphosphonate (0.3 mCi/kg [0.14 mCi/lb], IV) 4 hours before bone-phase scintigraphy. Just prior to imaging, the horse was sedated with detomidine hydrochloride (0.01 to 0.03 mg/kg [0.005 to 0.014 mg/lb], IV) and butorphanol tartrate (0.01 to 0.02 mg/kg [0.005 to 0.009 mg/lb], IV). The horse was positioned squarely on all 4 limbs; however, full weight bearing on the affected limb could not be achieved during image acquisition. Lateral and plantar images of the appendicular skeleton of both hind limbs and dorsal and oblique images of the lumbar vertebrae and pelvis were obtained. One-minute static frames were acquired with a gamma camera.c A dedicated computer systemd was used for postprocessing and interpretation of the images, which revealed marked focal IRU in the proximal region of the left talus (Figure 1). Mild diffuse IRU at the distal aspect of the right tarsus was also identified but was considered an incidental finding and suspected to be associated with osteoarthritis.

Figure 1—
Figure 1—

Lateral nuclear scintigraphic image of the left tarsus (A) and plantar nuclear scintigraphic image of the left and right tarsi (B) of a 6-year-old Quarter Horse gelding used for barrel racing that was evaluated for acute onset of non–weight-bearing lameness of the left hind limb following strenuous exercise. Notice the marked IRU within the tarsocrural region at the level of the talus.

Citation: Journal of the American Veterinary Medical Association 255, 1; 10.2460/javma.255.1.102

Twenty-four hours after completion of the nuclear scintigraphic evaluation, a standard radiographic study of the left tarsus was performed. The radiographic study consisted of the minimum number of projections necessary to provide a basic evaluation of the tarsus and included dorsoplantar, lateromedial, and dorsal 45° lateral-plantaromedial and dorsal 45° medial-plantarolateral oblique projections. Flexed lateromedial and fexed dorsoplantar projections were also obtained. Notable radiographic findings included 2 approximately 1.5-cm-long, smoothly marginated, ovoid osseous fragments; 1 was located adjacent to the dorsal aspect of the medial malleolus, and 1 was located just distal to the dorsomedial aspect of the medial malleolus. Additional findings included a small focal concavity in the proximal aspect of the medial trochlear ridge of the talus and mild intracapsular swelling of the tarsocrural joint; those findings were static in appearance when compared with tarsal radiographs that had been obtained during a prepurchase examination 8 months prior to the injury. No abnormalities were detected in the region of IRU. Review of radiographs of the right tarsus confirmed the presence of osteoarthritis in the distal intertarsal and tarsometatarsal joints. The radiologist who reviewed the radiographic images was satisfed with the comprehensiveness of the study, and acquisition of additional nonstandard oblique projections was not pursued at that time.

Ultrasonographic examination of the left tarsus was performed. Notable findings included moderate desmitis of the short component of the medial collateral ligament origin and moderate tarsocrural joint effusion and synovitis. The 2 osseous bodies identified on radiographs were associated with medial malleolar avulsion fractures.

Because the abnormalities identified during the radiographic and ultrasonographic examinations were not correlated with the nuclear scintigraphic findings and did not appear to be sufficient to explain the severity of lameness, intra-articular anesthesia of the left tarsocrural joint was performed. Immediately prior to intra-articular anesthesia, the horse was obviously lame on the left hind limb when observed at a walk. Following aseptic preparation of the left tarsal region, a 21-gauge, 1.5-inch hypodermic needle was inserted into the dorsomedial pouch of the tarsocrural joint, and 20 mL of 2% mepivacaine hydrochloride was injected into the joint. Five minutes later, the horse was observed at a walk, and the left hind limb lameness had improved by > 90%, which confirmed that the source of pain originated from the tarsocrural joint.

It was suspected that the primary lesion responsible for the IRU identified during scintigraphy was a bone contusion because a fracture was not identified radiographically. Thus, standing MRI of the left tarsus with a low-feld 0.27-T magnete was attempted on 2 different occasions, but the resulting images were nondiagnostic owing to motion artifact. In sedated horses undergoing standing MRI, the degree of motion artifact in images of proximal structures (eg, tarsus) is typically greater than that in images of more distal structures (eg, phalanges) because truncal sway is more evident in proximal structures, which makes acquisition of diagnostic images difficult. Computed tomographic imaging of the left tarsus was discussed at that time but was discouraged because of the perceived risk for further orthopedic injury associated with recovery from anesthesia.

Although a definitive diagnosis was not achieved, the lameness was definitively localized to the tarsocrural joint. The decision was made to medicate the joint in an effort to decrease inflammation, support the articular cartilage, and facilitate restoration of joint homeostasis. Various intra-articular joint therapies were discussed with the owner, and ACSf was selected primarily on the basis of the owner's positive experience with that modality for the treatment of joint disease in other performance horses. A series of 3 intra-articular injections of ACS into the left tarsocrural joint with a 2-week interval between injections was prescribed. The dosing interval for the ACS was based the clinical experience of the attending clinician (SAK).

It was recommended that the horse be strictly confined to a stall for 30 days with reevaluation at 2-week intervals and a follow-up radiographic study of the left tarsus obtained at the end of 30 days. It was further recommended to house the horse at the UCD Center for Equine Health during this period to allow for continued monitoring of its condition and decrease the distance the horse would have to travel given the severity of lameness. The owner, however, elected to transport the horse 1,086 km (675 miles) to an equine rehabilitation facility. The horse received the first intra-articular injection of ACS into the left tarsocrural joint prior to discharge from the UCD VMTH.

One week after discharge from the UCD VMTH (17 days after initial onset of lameness), the horse was transported to the CSU James L. Voss Veterinary Teaching Hospital for MRI of the left tarsus at the recommendation of the veterinarian who had been overseeing the care of the horse at the equine rehabilitation facility. During the initial examination at CSU, all vital parameters were within reference limits, and the left hind limb lameness was improved (lameness score,1 2/5). The horse was not appreciably lame during baseline movement and observation, and fexion of the left tarsus was necessary to elicit consistently evident lameness. On the basis of the physical and lameness examination results, the risks associated with anesthetic recovery were considered acceptable, and the horse was scheduled to be anesthetized for MRI.

Food but not water was withheld from the horse for 12 hours prior to anesthesia induction. A catheter was aseptically placed in a jugular vein. Thirty minutes before anesthesia induction, the horse received potassium penicillin (22,000 U/kg [10,000 U/lb], IV) and funixin meglumine (1.1 mg/kg [0.50 mg/lb], IV). The horse was sedated with xylazine hydrochloride (0.75 mg/kg [0.34 mg/lb], IV) and butorphanol (0.02 mg/kg, IV), and anesthesia was induced with a combination of ketamine hydrochloride (2.2 mg/kg, IV) and diazepam (0.09 mg/kg [0.04 mg/lb], IV). Following orotracheal intubation, anesthesia was maintained with isoflurane in oxygen, and the horse was mechanically ventilated.

The horse was positioned in left lateral recumbency, and MRI of the left tarsus was performed with an intermediate-feld 1.0-T magnet.g T1 fast-spin echo, proton-density fast-spin echo, T1 gradient echo, and short tau inversion recovery sequences were obtained in the sagittal, dorsal, and transverse planes.

The MRI images revealed an undulating fracture with irregular margins that extended across the talus. The fracture originated at the trochlear groove and extended in a dorsomedial direction into the medial trochlear ridge of the talus (Figure 2). Subchondral defects of both the trochlear groove of the talus and adjacent distal intermediate ridge of the tibia were identified at the origin of the fracture. Marked osseous sclerosis coupled with an increase in the osseous fluid signal was present along the length of the fracture. A mild step defect associated with the fracture was detected at the dorsoproximal aspect of the medial trochlear ridge. A small round osseous fragment was identified embedded in the origin of the short component of the medial collateral ligament and was associated with thickening of the ligament at its origin.

Figure 2—
Figure 2—

Dorsal plane T1 gradient echo (A) and short tau inversion recovery (B) MRI images of the left tarsus of the horse of Figure 1 that depict an incomplete fracture in the talus (long arrows; A). Notice the marked abnormal fluid signal (short arrows; B) that is characteristic of osseous contusion. These images were obtained approximately 2.5 weeks after the onset of lameness and the nuclear scintigraphic evaluation.

Citation: Journal of the American Veterinary Medical Association 255, 1; 10.2460/javma.255.1.102

Following completion of MRI image acquisition, the horse was allowed to recover from anesthesia with assistance from the use of head and tail ropes. No complications were encountered during anesthesia recovery.

Additional radiographs of the left tarsus were obtained to further characterize the fracture. The fracture was best visualized on a dorsal 20° lateral-plantaromedial oblique image (Figure 3).

Figure 3—
Figure 3—

Dorsal 20° lateral-plantaromedial oblique radiographic image of the left tarsus of the horse of Figure 1 obtained following completion of the MRI examination. Notice that the talus fracture (arrow) is evident. The 2 approximately 1.5-cm-long, smoothly marginated, ovoid osseous fragments adjacent to the medial malleolus that were observed in the initial radiographic study performed 24 hours after the nuclear scintigraphic evaluation are also present. Medial is to the left.

Citation: Journal of the American Veterinary Medical Association 255, 1; 10.2460/javma.255.1.102

With a definitive diagnosis achieved, the horse was discharged from the CSU Veterinary Teaching Hospital with recommendations for stall confinement and daily hand-walking for 3 months. Ninety days after discharge, a follow-up examination was performed by one of the authors (BRB). At the time of that examination, the owner reported that the horse was not visibly lame at a walk or trot. The horse was housed in a box stall (3.7 × 3.7 m) most of the time. It was allowed access to an outdoor paddock (6.1 × 6.1 m [20 × 20 feet]) for exercise daily, and the duration it was allowed to remain in the paddock was being gradually increased. Following discharge from the hospital, the owner had initiated administration of a dietary zeolite supplementh (amount unknown) to promote bone and joint health and local treatment of the left tarsus with a therapeutic laser,i which was performed on a daily basis for the first 4 weeks and then every other day for the next 4 weeks. After the 90-day follow-up examination, a physical rehabilitation program was initiated, which consisted of gradually increasing exercise and access to a larger paddock. Fifteen months after the injury, the horse was competing at its previous level with no residual lameness.

Discussion

Fractures of the talus have been well described in horses, with most being the result of direct trauma from a kick or other blunt force.2,3 Most fractures of the talus involve the trochlear ridges, with the distal aspect of the lateral trochlear ridge most frequently affected, followed by the proximal aspect of the medial trochlear ridge.3 Incomplete sagittal fractures of the talus have been described but are rare and are most commonly diagnosed in Standardbred and, less commonly, Thoroughbred racehorses.4 Moderate to marked effusion of the tarsocrural joint and diffuse periarticular swelling are common features associated with fractures of the talus owing to the articular nature of the fractures and the energy released from the bone at the time of fracture, which is subsequently absorbed by the adjacent soft tissues.3,4

Tarsal lesions are the second most common overall cause of lameness and most common cause of hind limb lameness in horses used for barrel racing.5 The talus fracture described in the horse of the present report was unusual. From a mechanical aspect, such a fracture would seem to be more likely to occur in horses used for barrel racing because of the substantial loads placed on the medial aspect of the hind limbs as those horses turn around the barrels. However, this type of talus fracture should be considered in any equine athlete that makes abrupt changes in direction during competition and develops acute hind limb lameness.

The physical examination findings were generally unremarkable for the horse of the present report. During the initial examination at the UCD VMTH, the horse would preferentially stand with its hind limbs extended caudally, but it was able to place the affected hind limb squarely under itself and bear full weight on it when the contralateral hind limb was lifted. Additionally, adduction of the left hind limb was the only manipulation that elicited a mild pain response. Those findings are not specific for a tarsal injury, and given that talus fractures are fairly rare, a fracture of the talus was not considered a likely differential diagnosis at that time. However, given the definitive diagnosis for the horse of this report, it would seem prudent to perform a thorough radiographic study of the tarsus for any horse with similar clinical findings. That radiographic study should include several oblique projections to maximize the likelihood of identifying a fracture.

A talus fracture with the configuration described for the horse of the present report was most likely caused by a combination of compression, shear, and torsional forces in conjunction with the unique articulation between the talus and distal aspect of the tibia. We believe that the pathogenic mechanism of the talus fracture in the horse of this report was similar to that of first phalanx fractures, which result primarily from the transmission of compressive and torsional forces from the sagittal ridge of the distal aspect of the third metacarpal bone through the sagittal grove of the first phalanx, leading to a fracture that originates at the sagittal groove and propagates distally.6

Talus fractures are commonly associated with torsional and shear forces that disrupt the surrounding periarticular soft tissue structures.3 However, the affected tarsus of the horse of the present report did not have any evidence of periarticular soft tissue injury identified during ultrasonographic and MRI examinations. The lack of periarticular soft tissue injury in the horse of this report was most likely a reflection of the incomplete nature of the talus fracture and the limited amount of energy released during fracture development. If the energy released during fracture development is less than that required for fracture propagation, fracture formation and the subsequent release of energy will cease.7

Overload arthrosis, or maladaptive remodeling, is well described in racehorses8 and was identified on MRI images of the affected tarsus for the horse of the present report. In this horse, maladaptive remodeling of the trochlear groove of the talus and distal intermediate ridge of the tibia, which appeared as sclerosis on the MRI sequences, may have acted as a stressor and contributed to the fracture of the talus. However, it is also possible that the maladaptive remodeling observed on the MRI sequences developed subsequent to the fracture. Recognition of maladaptive remodeling prior to fracture development would be optimal because it would allow affected horses to be rested until the bone recovers. Identification of maladaptive remodeling changes radiographically would be ideal but is difficult because radiographic delineation of signs associated with the early stages of the condition, such as sclerosis, resorption, periostitis, subchondral bone injury, and microfractures, is unreliable.9 Thus, advanced diagnostic imaging is often necessary to detect maladaptive modeling, as it was for the horse of this report. Moreover, horses with maladaptive remodeling may not be visibly lame, or if they are lame, the lameness can range from mild to severe and intermittent to persistent, which complicates diagnosis.9 Physical examination findings, such as swelling or effusion or signs of pain during palpation of the affected region, are often mild or absent.9 For the horse of the present report, sclerosis was the only imaging feature indicative of maladaptive remodeling, and it was only apparent on MRI sequences. Evidence of sclerosis was not identified on radiographic images at any point during the diagnostic workup. In fact, the only clinical deficits identified for the horse of the present report were severe acute non–weight-bearing lameness of the left hind limb, which rapidly resolved only to recur, and mild to moderate tarsocrural effusion bilaterally.

In horses, nuclear scintigraphy has long been used to localize areas of abnormal bone turnover and identify incomplete or stress fractures in the appendicular skeleton. At the UCD VMTH, nuclear scintigraphy is occasionally used as the initial diagnostic imaging modality for horses with severe acute lameness, particularly when the cause of lameness cannot be identified during physical and standard lameness examinations. This is because maladaptive remodeling, bone contusion, and incomplete fractures are considered the primary differential diagnoses for such animals, and those conditions are best detected by scintigraphy.

For the horse of the present report, the talus fracture was not detected on preliminary radiographic images that were obtained 24 hours after scintigraphic evaluation. This may have been the result of the incomplete nondisplaced nature of the fracture or failure to obtain multiple additional (nonstandard) oblique projections that would have allowed for a more thorough examination of the talus. The location and configuration of the fracture were identified on MRI sequences, which facilitated determination of the best projections for radiographic visualization of the fracture. Additionally, the 14 days that elapsed between the initial radiographic study at the UCD VMTH and the radiographic study performed following MRI at the CSU Veterinary Teaching Hospital may have allowed for sufficient resorption of damaged bone along the fracture line (which is a normal process during the inflammatory phase [ie, first 2 to 3 weeks after fracture] of fracture healing7) to make the fracture more radiographically evident.

Ultrasonographic examination of the left tarsus revealed moderate desmitis of the short component of the medial collateral ligament origin, which was associated with chronic medial malleolar avulsion fractures, and moderate tarsocrural joint effusion and synovitis. Those findings were considered incidental because the appearance of the medial collateral ligament and the associated malleolar fragmentation were consistent with a chronic orthopedic disorder, and the observed effusion and moderate synovitis were, by definition, signs of joint lesions and not primary causes of lameness. Furthermore, the abnormalities identified during ultrasonographic evaluation were not commensurate with the severity of lameness. It is possible that injury to the medial collateral ligament could have resulted in some degree of tarsocrural joint instability and maladaptive remodeling, which contributed to the subsequent fracture of the talus. The malleolar fragmentation was initially identified on radiographs obtained during a prepurchase examination performed 8 months before the onset of lameness. At that time, the horse was not visibly lame, and the sellers stated that they had no previous knowledge of the fragmentation. The horse also had no history of hind limb lameness, medial collateral ligament desmitis, or rehabilitation for any orthopedic injury. It is unfortunate that the onset of the medial collateral ligament injury was unknown because that information may have provided additional support for the theory that the ligament injury and subsequent maladaptive modeling led to fracture of the talus.

In horses that become acutely and severely lame, a lameness examination and regional anesthesia should be performed with extreme caution because those procedures could lead to propagation of an incomplete fracture and catastrophic limb failure, necessitating euthanasia. For the horse of the present report, a tarsal fracture was at the top of the differential diagnosis list, and intra-articular anesthesia of the tarsocrural joint was performed after scintigraphic, radiographic, and ultrasonographic examinations. Because the horse of this report was so severely lame (lameness score, 5/5) at the time of intra-articular anesthesia, it only had to be walked to determine whether the lameness improved following the intra-articular injection of mepivacaine. For that reason, intra-articular anesthesia for this horse was considered to be associated with less risk than it might for a similar, but less severely lame, horse that would require observation at a trot to determine the response to intra-articular anesthesia.

In conclusion, incomplete fracture of the talus should be considered a differential diagnosis for horses that develop severe acute hind limb lameness following strenuous exercise when that lameness cannot be localized to the tarsus during a physical or lameness examination or is localized to the tarsus on the basis of results of intra-articular anesthesia or nuclear scintigraphy. As evidenced by the horse of this report, a basic radiographic evaluation of the tarsus, which consists of a minimum number of projections, may be insufficient for thorough assessment of that region, and several additional oblique projections, including dorsoplantar and dorsal 45° lateral-plantaromedial and dorsal 45° medial-plantarolateral oblique projections, may be necessary for identification of fracture lines. The importance of obtaining additional oblique projections during radiographic evaluation of the tarsus of horses cannot be overstated. In retrospect, had those additional projections been obtained during the initial radiographic study for this horse, the talus fracture may have been identified, which would have negated the need for the additional advanced diagnostic imaging that was performed. For patients with equivocal findings following conventional radiography, advanced diagnostic imaging modalities, such as CT and MRI, possibly in conjunction with surgical intervention, are often necessary for definitive diagnosis of fractures in the anatomically complex tarsal region. The talus fracture in the horse of this study was successfully managed with conservative treatment, and the horse was no longer lame and was competing at its previous level within 15 months after the initial onset of lameness. Thus, conservative management may be a viable treatment option for horses with talus fractures.

ABBREVIATIONS

ACS

Autologous conditioned serum

CSU

Colorado State University

IRU

Increased radiopharmaceutical uptake

UCD

University of California-Davis

VMTH

Veterinary Medical Teaching Hospital

Footnotes

a.

Soft-Ride Inc, Vermilion, Ohio.

b.

Angiocath Vascular Access, Becton, Dickinson and Co, Sandy, Utah.

c.

Segami Corp, Columbia, Md.

d.

IS2 Medical Systems, Ottawa, ON, Canada.

e.

Halmarq Veterinary Imaging Ltd, Surrey, England.

f.

Arthrex IRAP II, Naples, Fla.

g.

ONI OrthOne extremity scanner, GE Medical Systems, Waukesha, Wis.

h.

Osteon, Platinum Performance CJ, Buellton, Calif.

i.

Pegasus Therapy Lasers, Newark, Del.

References

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  • Figure 1—

    Lateral nuclear scintigraphic image of the left tarsus (A) and plantar nuclear scintigraphic image of the left and right tarsi (B) of a 6-year-old Quarter Horse gelding used for barrel racing that was evaluated for acute onset of non–weight-bearing lameness of the left hind limb following strenuous exercise. Notice the marked IRU within the tarsocrural region at the level of the talus.

  • Figure 2—

    Dorsal plane T1 gradient echo (A) and short tau inversion recovery (B) MRI images of the left tarsus of the horse of Figure 1 that depict an incomplete fracture in the talus (long arrows; A). Notice the marked abnormal fluid signal (short arrows; B) that is characteristic of osseous contusion. These images were obtained approximately 2.5 weeks after the onset of lameness and the nuclear scintigraphic evaluation.

  • Figure 3—

    Dorsal 20° lateral-plantaromedial oblique radiographic image of the left tarsus of the horse of Figure 1 obtained following completion of the MRI examination. Notice that the talus fracture (arrow) is evident. The 2 approximately 1.5-cm-long, smoothly marginated, ovoid osseous fragments adjacent to the medial malleolus that were observed in the initial radiographic study performed 24 hours after the nuclear scintigraphic evaluation are also present. Medial is to the left.

  • 1. American Association of Equine Practitioners. Lameness exams: evaluating the lame horse. Available at: aaep.org/horsehealth/lameness-exams-evaluating-lame-horse. Accessed Jan 3, 2019.

    • Search Google Scholar
    • Export Citation
  • 2. Jakovljevic S, Gibbs C, Yeats JJ. Traumatic fractures of the equine hock: a report of 13 cases. Equine Vet J 1982;14:6268.

  • 3. Auer J. Tarsus. In: Auer JA, Stick JA, eds. Equine surgery. 4th ed. St Louis: Saunders-Elsevier, 2012;13881409.

  • 4. Davidson EJ, Ross MW, Parente EJ. Incomplete sagittal fracture of the talus in 11 racehorses: outcome. Equine Vet J 2005;37:457461.

  • 5. Dabareiner R. Lameness in the sport horse; barrel-racing horses. In: Ross MW, Dyson SJ, eds. Diagnosis and management of lameness in the horse. 2nd ed. St Louis: Elsevier-Saunders, 2011;11801183.

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