A 12-year-old mixed-breed mare (horse 1) was examined for chronic lameness that failed to resolve following a year of rest involving paddock turnout with no riding. No specific injury was witnessed at the initial onset of lameness. Physical examination revealed moderate effusion of the right medial femorotibial joint and mild effusion of the right femoropatellar joint. Lameness examination revealed grade 3/5 lameness of the right hind limb,1 which did not change or become exacerbated when the horse was circling on soft ground in either direction. Digital flexion of both hind limbs elicited no response. Results of flexion testing of the full left hind limb and stifle joint were similarly unremarkable, but results for the right hind limb were moderately to severely positive. Ten minutes following intra-articular injection of 2% mepivacaine hydrochloride into the medial femorotibial and femoropatellar joints, the right hind limb lameness appeared to have improved slightly, and by 15 minutes after injection, the lameness was judged to have resolved by approximately 50%.
Radiographs of the right stifle joint were obtained, including lateromedial (flexed and weight-bearing), caudocranial, and multiple oblique views. Standard 45° caudolateral-craniomedial oblique views revealed an ill-defined lateral margin of the intercondylar fossa of the femur in the region of the origin of the CCL. This prompted the decision to obtain views with the opposite obliquity, Ca45M–CrLO, to highlight the origin of this ligament, which revealed a radiolucent area in the caudoaxial aspect of the lateral femoral condyle with an irregular rounded radiopacity superimposed over that area (Figure 1). These findings were consistent with enthesopathy and chronic avulsion fracture of the origin of the CCL.
Radiographic views (45° caudolateral-craniomedial oblique [A], Ca45M–CrLO [B], and caudocranial [C]) of the right stifle joint of a 12-year-old mixed-breed mare (horse 1) examined for chronic grade 3/5 lameness of the right hind limb. Notice the well-defined radiopacity (arrow) in the intercondylar fossa at the origin of the CCL in panel B. In contrast, in panel A this region (arrow) is obscured by the lateral femoral condyle, which is superimposed over the fragment. An area of irregularity (arrow) is visible in the origin of the ligament in panel C as well as an osteophyte of the medial proximal aspect of the tibia.
Citation: Journal of the American Veterinary Medical Association 254, 4; 10.2460/javma.254.4.508
Ultrasonographic examination was performed of the right stifle joint, including the menisci (transverse view), cranial meniscotibial ligaments (long-axis view), femoral condyles, and patellar ligaments. Caudal portions of the femorotibial joint were also evaluated.2,3 A portable ultrasound machinea and multifrequency linear transducer were used for all portions of this examination except for that of the caudal aspect of the stifle joint, which was examined with a convex probe. Severe effusion, capsulitis, and synovitis of the medial femorotibial and femoropatellar joints were identified. There was moderate osseous irregularity of the caudoaxial aspect of the lateral femoral condyle, which in conjunction with the marked effusion was suggestive of possible avulsion or severe enthesopathy of the origin of the CCL. The cranial portion of the CCL could not be adequately assessed. All other soft tissue structures were ultrasonographically unremarkable; therefore, CT arthrography was recommended for further evaluation.
For this examination, the horse was sedated with xylazine hydrochlorideb (0.5 mg/kg [0.23 mg/lb], IV). Anesthesia was induced by IV administration of ketamine hydrochloridec (3 mg/kg [1.4 mg/lb]) and diazepamd (0.1 mg/kg [0.05 mg/lb]) and maintained with isoflurane in oxygen. Once anesthetized, the horse was positioned in left lateral recumbency, and CT of the right stifle joint was performed with a 16 -slice CT scanner.e All 3 joints within the stifle joint were injected with iohexolf diluted 1:1 in 0.9% sterile saline (0.9% NaCl) solution as described elsewhere.4 Results of arthrography confirmed the presence of an osseous fragment at the origin of the CCL consistent with an avulsion fracture of the ligament (Figure 2). There was no evidence of diffusion of contrast medium into the CCL. The remaining soft tissue structures were unremarkable in appearance.
Transverse (A) and coronal (B) multiplanar reconstruction images from CT arthrography of the right stifle joint of the horse in Figure 1. In both images, the avulsion fragment of the CCL is evident at its origin in the caudolateral aspect of the intercondylar fossa of the femur (arrows). Osteophystosis of the distomedial aspect of the femur is also visible. Window width, 1,626 HU; window level, 339 HU.
Citation: Journal of the American Veterinary Medical Association 254, 4; 10.2460/javma.254.4.508
Arthroscopy of the cranial regions of the medial and lateral femorotibial joints was performed immediately following CT.5 The horse was positioned in dorsal recumbency. The medial femorotibial joint was initially approached via a portal lateral to the lateral patellar ligament, midway between the tibia and patella. The medial femorotibial joint was explored, and an instrument portal was created between the middle and medial patellar ligaments. The portals were reversed to facilitate examination of the lateral femorotibial joint. The septum between the medial and lateral femorotibial joints was resected by use of synovial biopsy rongeurs and a synovial resector. The ability to see the cruciate ligaments, particularly the CCL, was obscured by a large amount of fibrous scar tissue. The CCL was lax when probed with a right-angle probe, and its origin was not visible. Attempts to remove the osseous fragment associated with the CCL with a suction punch, motorized synovial resector, periosteal elevator, and right-angle probe were unsuccessful because of the largely inaccessible location and firm fibrous attachment of the fragment. Fibrillation of the cranial pole of the lateral meniscus was identified, with no evidence of meniscal prolapse or damage to the lateral cranial meniscotibial ligament. Mild fibrillation of the medial cranial meniscotibial ligament was also noted, but no damage to the medial meniscus was observed.
Recovery from anesthesia was unassisted, and the horse recovered without complication. A grade 4/5 lameness was observed immediately after anesthetic recovery. Broad-spectrum antimicrobials (cefazolin at 11 mg/kg [5 mg/lb], IV, q 8 h; and gentamicin at 5 mg/kg [2.3 mg/lb], IV, q 24 h for 24 hours) and phenylbutazone were administered in the perioperative period. The horse was discharged from the hospital with a prescription for phenylbutazone (2.2 mg/kg [1 mg/lb], PO, q 12 h for 10 days) and recommendations for 2 weeks of strict stall rest, followed by 2 weeks of stall rest with 5 minutes of handwalking/d.
A 6-year-old Friesian gelding (horse 2) was examined for severe left hind limb lameness of nearly 2 months’ duration. The lameness had been noticed suddenly, but no traumatic event was observed. The horse had been examined by another veterinarian, who began corticosteroid and hyaluronic acid treatment (dosage unknown) with no improvement. Initial physical examination at our institution revealed severe effusion of the left medial femorotibal and femoropatellar joints, which reportedly had lessened in severity since first noticed, and grade 4/5 lameness of the left hind limb. Mild effusion of the right tarsocrural joint was also evident. No further lameness examination, including joint flexion testing, was performed.
Radiography of the left stifle joint, including lateromedial, flexed lateromedial, standard 45° caudolateral-craniomedial oblique, Ca45M–CrLO, and caudocranial views, revealed large amounts of soft tissue thickening over the femoropatellar joint. A large, rectangular mineral opacity was visible within the intercondylar fossa on multiple views, consistent with mineralization in the origin and body of the CCL and possible avulsion fracture (Figure 3). Circular, well-defined radiolucencies were visible on the proximal aspect of the tibia, specifically at the attachment of the cranial medial meniscal tibial ligament, and ill-defined radiolucencies at the proximal aspect of the tibia at the attachment of the cranial cruciate on the axial aspect of the medial intercondylar eminence. Overall, the patella, femoral trochleae, and proximal aspect of the tibia had a coarse trabecular pattern indicative of osteopenia, with sclerosis.
Radiographic views (caudocranial [A], 45° caudolateral-craniomedial oblique [B], and Ca45M–CrLO [C]) of the left stifle joint of a 6-year-old Friesian gelding with chronic grade 4/5 lameness of the left hind limb. In panel A, mineral opacity (arrow) is visible extending proximal to the medial intercondylar eminence of the tibia to the lateral aspect of the intercondylar fossa of the femur. A radiolucent area (arrow) is evident in panel B at the level of the intercondylar fossa and is superimposed with the lateral femoral condyle. In the opposite oblique view in panel C, radiolucency (arrow) is visible at the origin of the CCL with mineralization of the ligament body as well as an osteophyte on the distomedial aspect of the femur.
Citation: Journal of the American Veterinary Medical Association 254, 4; 10.2460/javma.254.4.508
The horse was anesthetized, and CT arthrography was performed in a similar manner as for horse 1, revealing a large area of mineralization of the CCL (Figure 4) in addition to a lytic lesion in the cranial aspect of the tibia at the site of ligament insertion. The pattern of absorption of contrast medium evident at the origin of the caudal cruciate ligament indicated tearing of the ligament. There was also evidence of osseous resorption and bone irregularity consistent with chronic enthesopathy, but no evidence of avulsion. The horse was euthanized while anesthetized because of the poor prognosis associated with severe mineralization of the CCL, bone irregularity, and simultaneous injury of the caudal cruciate ligament. No necropsy was performed.
Coronal images from CT arthrography of the left stifle joint of the horse in Figure 3. Dystrophic mineralization (arrows) of the origin (A) and body (B) of the CCL is evident. Osteophytes are also visible on the medial and lateral distal margins of the femur. Window width, 1,124 HU; window level, 186 HU.
Citation: Journal of the American Veterinary Medical Association 254, 4; 10.2460/javma.254.4.508
Discussion
Although radiography cannot reveal lesions within the body of the CCL unless dystrophic mineralization is present, cruciate ligament injuries in horses commonly involve entheses and may be accompanied by radiographic changes at affected sites.6 A study7 of orthopedically normal limbs from equine cadavers revealed specific radiographic views that best detail each enthesis. Findings for the 2 horses of the present report suggested the clinical value of the Ca45M–CrLO view. With knowledge of the radiographic anatomic findings, specifically the location of the entheses of the cruciate ligaments of the stifle joint, CCL injury that involves the origin of the ligament may be diagnosed with this useful radiographic view.
Injury to the CCL can occur from direct trauma, secondary to degenerative changes in the joint, and likely from hyperextension or sudden rotation as described for humans, dogs, and horses.8–11 Onset of lameness is typically sudden, can be quite severe, is accompanied by femorotibial or femoropatellar joint effusion, and is usually exacerbated by flexion of the stifle joint.12 Unlike for dogs, the cranial drawer test has little diagnostic value for nonanesthestized adult horses, and diagnosis relies on localization of the lameness to the stifle joint via intra-articular analgesic administration, followed by appropriate diagnostic imaging, arthroscopy, or both.12
The clinical workup described for the horses of the present report highlighted the importance of careful evaluation of the origins and insertions of soft tissue structures when evaluating standard radiographs of the stifle joint and the availability of alternative views, such as the caudomedial-craniolateral oblique. In horse 1, a focal radiolucency with irregular sclerotic margins was noted on the caudoaxial aspect of the lateral femoral condyle at the level of the origin of CCL and an ill-defined lateral margin of the intercondylar fossa on standard 45° caudolateral-craniomedial oblique and caudocranial views. These findings caused us to suspect an injury to the origin of the CCL and prompted acquisition of the Ca45M–CrLO view. The enthesopathy and avulsion were best defined on this view. Whereas the mineralization within the CCL was visible on standard views, including the caudocranial view of the stifle joint in horse 2, the Ca45M–CrLO view was key in supporting the diagnosis of a lesion localized to the proximal segment of the CCL, but not a discrete avulsion fragment.
In both horses of the present report, CT was pursued to further characterize the lesions, particularly the extent of ligamentous injury that was suggested on radiography. Although not essential for diagnosis, CT provided additional valuable information about the integrity of the CCL and, in horse 2, revealed concurrent injury to the caudal cruciate ligament. The decision to pursue CT arthrography for both horses was prompted by the radiographic findings. Ultrasonography is often the diagnostic modality best suited for the diagnosis of soft tissue lesions of the stifle joint in horses; however, only the distal third of the cranial cruciate ligament is visible ultrasonographically with a cranial approach.13 With experience and good equipment, the origin of the CCL can be evaluated via a caudal ultrasonographic approach to the stifle joint; however, the tissue depth may limit the examination. Furthermore, whereas MRI would be the ideal modality to assess pathological changes in both bone and soft tissue, few institutions have the capability to perform MRI of the stifle joint in horses.
We believe that the Ca45M–CrLO view of the stifle joint can be used to diagnose injury to the CCL in horses when avulsion or enthesopathy is present. This view may also be useful in further evaluating mineralization of the ligament in some horses, even if no avulsion has occurred. When CT is unavailable or not financially feasible, the Ca45M–CrLO view may be particularly important to glean as much information as possible if injury to the CCL is suspected in a horse.
Acknowledgments
Presented in part at the American College of Veterinary Surgeons Surgery Summit, San Diego, October 2014.
ABBREVIATIONS
| Ca45M–CrLO | Caudomedial-craniolateral oblique view obtained 45° medial to the caudocranial line |
| CCL | Cranial cruciate ligament |
Footnotes
GE Logiq E portable ultrasound machine, GE Healthcare, Chicago, Ill.
AnaSed, Lloyd Inc, Shenandoah, Iowa.
Zetamine VetOne, MWI, Boise, Idaho.
Hospira Inc, Lake Forest, Ill.
Gemini TF big bore PET/CT scanner, helical CT x-ray tube with 85-cm bore, Philips Healthcare, Andover, Mass.
Omnipaque, GE Healthcare, Little Chalfont, England.
References
1. Swanson T. Guide for veterinary service and judging of equestrian events: endurance rides, competitive trail rides. 3rd ed. Golden, Colo: American Association of Equine Practitioners, 1984.
2. Adrian AM, Barrett M, Werpy N, et al. A comparison of arthroscopy to ultrasonography for identification of pathology of the equine stifle. Equine Vet J 2017;49:314–321.
3. Frisbie DD, Barrett MF, McIlwraith CW, et al. Diagnostic stifle joint arthroscopy using a needle arthroscope in standing horses. Vet Surg 2014;43:12–18.
4. Nelson BB, Kawcak CE, Goodrich LR, et al. Comparison between computed tomographic arthrography, radiography, ultrasonography, and arthroscopy for the diagnosis of femorotibial joint disease in Western performance horses. Vet Radiol Ultrasound 2016;57:387–402.
5. McIlwraith CW, Nixon AJ, Wright IM. Diagnostic and surgical arthroscopy of the femoropatellar and femorotibial joints. In: Diagnostic and surgical arthroscopy in the horse. 4th ed. St Louis: Mosby, 2015;175–242.
6. Walmsley JP. Diagnosis and treatment of ligamentous and meniscal injuries in the equine stifle. Vet Clin North Am Equine Pract 2005;21:651–672.
7. Aldrich ED, Goodrich LR, Monahan MK, et al. Radiographic localization of the entheses of the equine stifle. Equine Vet J 2017;49:493–500.
8. Arnoczky SP, Marshall JL. Pathomechanics of cruciate and meniscal injuries. In: Bojrab MJ, ed. Pathophysiology of small animal surgery. Philadelphia: Lea & Febiger, 1981;590–603.
9. Prades M, Grant BD, Turner TA, et al. Injuries to the cranial cruciate ligament and associated structures: summary of clinical, radiographic, arthroscopic and pathological findings from 10 horses. Equine Vet J 1989;21:354–357.
10. Sanders-Shamis M, Bukowiecki CF, Biller DS. Cruciate and collateral ligament failure in the equine stifle: seven cases (1975–1985). J Am Vet Med Assoc 1988;193:573–576.
11. Shimokochi Y, Shultz SJ. Mechanisms of noncontact anterior cruciate ligament injury. J Athl Train 2008;43:396–408.
12. Walmsley JP. The stifle. In: Ross MW, Dyson SJ, eds. Diagnosis and management of lameness in the horse. 2nd ed. St Louis: WB Saunders, 2011;532–549.
13. Barrett MF, Frisbie DD, McIlwraith CW, et al. The arthroscopic and ultrasonographic boundaries of the equine femorotibial joints. Equine Vet J 2012;44:57–63.
