Meniscal and Cruciate Injuries

Meniscal and Cruciate Injuries

C H A P T E R 193 Meniscal and Cruciate Injuries   JENNIFER FOWLIE   JOHN STICK MENISCAL INJURY The menisci are paired, semilunar, fibrocartilag...

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C H A P T E R

193

Meniscal and Cruciate Injuries



JENNIFER FOWLIE   JOHN STICK

MENISCAL INJURY

The menisci are paired, semilunar, fibrocartilaginous, wedgeshaped disks interposed between the convex femoral and flat tibial condyles of the femorotibial joints. The menisci are held in place by cranial and caudal meniscotibial ligaments and an additional caudal meniscofemoral ligament on the lateral meniscus (Figure 193-1). The menisci and the associated ligaments are primarily composed of circumferential type I collagen fibers. These fibers undergo circumferential tensile strains during joint loading, a concept known as hoop stress. The menisci function in equitable load transmission, shock absorption, joint stability, joint lubrication, and proprioception. Meniscal injury may develop secondary to a fall or other type of traumatic injury, although owners often report an insidious onset. Meniscal tears are the most common soft tissue injury identified in the stifle. An isolated injury of the cranial horn of the medial meniscus and its associated meniscotibial ligament is the most common arthroscopically identified site of meniscal lesions in the horse, being affected in 79% of reported cases. The cranial horn of the medial meniscus is the least mobile of the four horns during passive flexion–extension range of motion, and it becomes compressed at full extension. The relative immobility of the cranial horn of the medial meniscus may predispose it to injury on hyperextension. Meniscal injury may also occur concurrently with other soft tissue injuries in the stifle, such as cruciate and collateral ligament injury. However, in contrast to meniscal tears in dogs and humans, only 14% of meniscal tears in horses are associated with cranial cruciate ligament injury. Medial meniscal injury has also been reported concurrently and sequentially with medial femoral condyle subchondral cystic lesions (Figure 193-2). The pathogenesis of these lesions is not established at present, but theories include the following: a single traumatic incident resulting in both lesions, alterations in femoral condyle geometry at the debrided defect resulting in meniscal trauma, or altered femoral condyle loading secondary to meniscal injury. Degenerative-appearing menisci are seen in association with chronic arthritis, although the pathophysiology of these changes has not been established.

Clinical Signs Meniscal injury leads to lameness that is often moderate to severe initially and lingers as mild to moderate lameness. A history of acute-onset unilateral hind limb lameness may be reported. A severe traumatic event may lead to injury of multiple soft tissue structures in the stifle and more severe lameness. It has been reported that only 39% of affected horses have joint effusion at presentation, so the absence of

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palpable effusion does not rule out a lameness of stifle origin. Hock and stifle flexion tests are commonly positive, but intraarticular anesthesia is required to definitively localize the lameness to the femorotibial joints.

Diagnosis

Clinical Examination Localization of lameness to the stifle area with a lameness examination, flexion tests, and intraarticular anesthesia is the first step in diagnosis of meniscal injury. There are no pathognomonic clinical signs for meniscal injury.

Radiography Radiographs may be unremarkable with soft tissue injuries of the stifle; however, 48% to 83% of cases of meniscal injury have been reported to have associated radiographic changes. Changes may include new bone formation at the cranial aspect of the medial intercondylar eminence of the tibia, mineralization of the meniscus, and generalized osteoarthritic changes (Figure 193-3). If the meniscus is protruding from the joint space or is severely torn, narrowing of the femorotibial joint space may be evident.

Ultrasound Ultrasound is invaluable for diagnosis and prognostication of soft tissue injuries, and its value in evaluating meniscal tears is ever increasing. A 7- to 14-MHz linear transducer should be used to evaluate meniscal injuries in two perpendicular planes. Some meniscal lesions may be more apparent when the limb is non–weight bearing, or when a flexed cranial view is used. Ultrasound of the meniscus is challenging because the tissue fibers cannot be kept perpendicular to the probe at all sites, and a hypoechoic appearance is created in certain regions (i.e., the cranial medial meniscus). Additionally, because of the large soft tissue mass caudal to the stifle, the caudal aspect of the meniscus is very difficult to diagnostically image, even when a 4- to 6-MHz curvilinear probe is used. Abnormal ultrasonographic findings with meniscal injury may include hypoechoic regions of fiber disruption, core lesions, protrusion of the meniscus from the joint space, and generalized synovitis or arthritis changes (Figure 193-4). The sensitivity and specificity of ultrasound for identifying meniscal injuries are 79% and 56%, respectively, compared with arthroscopic findings. The apparent high rate of false-positive diagnoses may occur in part because a large portion of the meniscus is not visible on arthroscopic exam (specifically, the medial and lateral aspects of the joint) and because horizontal tears within the meniscus may not be visible on arthroscopic exam of the menisci. Thus combining findings from ultrasonographic and arthroscopic evaluation of the meniscus will yield the greatest diagnostic information.



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Medial

Lateral b

a

e f g

d c

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e Lateral

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Caudal

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Figure 193-1  Anatomy of the equine menisci. A, Proximal-distal view of the menisci from the left stifle joint of a cadaver. B, Caudal view of the left stifle of a cadaver. Cranial meniscotibial ligaments of the lateral (a) and medial (b) meniscus, and caudal meniscotibial ligaments of the lateral (c) and medial (d) meniscus. The meniscofemoral ligament of the lateral meniscus (e) is transected in image A and intact in image B. The cranial cruciate ligament is transected (f), and the caudal cruciate ligament is intact (g).

standing of meniscal injuries and concurrent pathologic processes in the stifle joint. Nuclear scintigraphy identifies lesions based on their physiologic characteristics (blood flow and osteoblastic activity). Scintigraphy has been inconsistent in revealing stifle lesions, including subchondral bone cysts, and although it has the potential to identify meniscal lesions and associated lesions (osteoarthritis or cysts), it appears to have a relatively poor sensitivity and specificity for soft tissue lesions of the stifle.

Arthroscopy

Figure 193-2  Arthroscopic view of a grade III tear in the cranial horn of the medial meniscus. The tear developed in the postoperative period following debridement of a subchondral bone cyst of the medial femoral condyle (arrow).

Advanced Imaging Advanced imaging modalities for the equine patient are available at select referral hospitals. Magnetic resonance imaging (MRI), considered a gold standard for soft tissue evaluation, is used extensively in humans to evaluate meniscal injury. Magnetic resonance imaging allows for excellent evaluation of bone and soft tissue components of the entire stifle joint. Given the large size of the equine stifle joint and its proximity to the abdomen, MRI of the equine stifle is limited to the large or open-bore magnets. The wide (70 cm) and ultrashort (125 cm) bore of the Siemens Magnetom Espree 1.5 T magnet1 is still only able to accommodate adult horses with relatively long limbs and narrow hips. General anesthesia is required for MRI and computed tomography (CT) evaluation of the equine stifle joint. Computed tomography is helpful in identifying soft tissue injuries, particularly when contrast arthrography is used to enhance CT imaging. The most significant advantage of MRI and CT imaging is that they enable evaluation of the entire equine stifle, which is not possible with ultrasound or arthroscopic examination. This will lead to a greater under1

Siemens Medical Solutions USA, Inc., Malvern, PA.

Arthroscopy allows for direct observation and assessment of the lesion (Figure 193-5) and thus is valuable for its role in diagnosis, treatment, and prognostication of meniscal injury. It also allows for observation and treatment of concurrent cartilage injury on the femoral condyles, which is commonly associated with meniscal tears (in approximately 71% of cases). The limitation of arthroscopic meniscus evaluation is that horizontal tears and tears in a large portion of the abaxial part of the menisci cannot be seen. Arthroscopic diagnosis of meniscal tears has led to the establishment of a grading system for cranial meniscal tears: Grade I: Tears extending longitudinally down the cranial meniscotibial ligament into the cranial horn of the meniscus with minimal separation of tissues Grade II: Tears of similar orientation to grade I tears but with further separation of tissue, although the entire tear is still visible on arthroscopic exam Grade III: Severe tears that extend beneath the femoral condyle and cannot be fully visualized arthroscopically (Figure 193-6)

Treatment Treatment of equine meniscal tears ideally consists of arthroscopic evaluation and debridement of the torn meniscal tissue, along with debridement of any associated cartilage injuries. Arthroscopy-assisted suturing of meniscal tears has been documented with successful outcomes in particular cases; however, it may be challenging or impossible, depending on the orientation and degree of tissue injury. Typical postoperative recovery consists of 6 to 8 weeks of stall rest

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B

A

Figure 193-3  Radiographic signs of meniscal injury. A, Dystrophic mineralization (black arrow) of the meniscus is evident in the caudal aspect of the joint in this lateral-medial radiograph of the stifle. B, Dystrophic mineralization of the meniscus (white arrow), severe narrowing of the medial femorotibial joint space, and advanced arthritic changes are seen in this caudal-cranial radiograph of the stifle.

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Figure 193-4  Sonogram of the meniscus obtained with a linear 7- to 14-MHz probe. A, Normal medial meniscus imaged at the level of the medial collateral ligament. B, Abnormal protrusion of the meniscus from the joint space and hypoechoic fiber disruption in the midsubstance of the lateral meniscus, imaged at the level of the lateral collateral ligament.

CrMT ligament CrMT ligament

LFC MFC

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Figure 193-5  Arthroscopic evaluation of the meniscus. A, Normal cranial meniscotibial ligament (CrMT lig) and cranial horn of the lateral meniscus. Lateral femoral condyle (LFC). B, Abnormal fibrillation and tearing of the CrMT and adjacent cranial horn of the medial meniscus extending under the medial femoral condyle (MFC).



Figure 193-6  Grade III tear (black arrow) of the cranial horn of the lateral meniscus and the adjacent cranial meniscotibial ligament evident on postmortem evaluation.

with hand walking and at least 4 months of small-paddock rest, depending on the severity of injury. In cases in which surgery is not an option, systemic antiinflammatories given in the acute stage after injury and a period of prolonged rest (6 to 12 months) are indicated. Intraarticular injection of autologous bone marrow–derived mesenchymal stem cells improves regeneration of meniscal tissue in other species and anecdotally has been beneficial in treatment of equine meniscal tears. Injection of platelet-rich plasma-fibrin clots has been investigated as a method of improving healing of meniscal tissue, although further research is required in equine meniscal tears. Successful treatment of meniscal injury should include prompt recognition, appropriate treatment, and provision of an adequate rest and rehabilitation program to decrease pathologic loading of the articular cartilage and limit secondary osteoarthritis.

Prognosis The prognosis for recovery from meniscal injury is dependent on the degree of meniscal damage and the presence of other lesions in the joint. In one study, return to previous athletic function was seen in 63% of horses with grade I tears, 56% with grade II tears, and 6% with grade III cranial horn meniscal tears. The presence of concurrent articular cartilage injury or radiographic changes (e.g., dystrophic mineralization of the meniscus or significant narrowing of the femorotibial joint space) is associated with a poorer prognosis. Severe stifle injuries involving multiple soft tissue structures may leave persistent joint instability and severe lameness, and euthanasia may be indicated in some cases. The prognosis for horses with meniscal tears and subchondral bone cysts (diagnosed concurrently or sequentially) is poor, with only about 20% of cases attaining a successful outcome.

CRUCIATE LIGAMENT INJURY

The cruciate ligaments are located in the extrasynovial space between the medial and lateral femorotibial joints. The cranial cruciate ligament (CrCL) arises from the lateral wall of the intercondyloid fossa of the femur and runs cranially and distally, ending on the central fossa of the tibial spine (the cranial aspect of the medial intercondylar eminence of the tibia [MICET]). The CrCL prevents cranial displacement of the tibia relative to the femur, limits excessive internal rotation of the tibia on the femur, and prevents

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hyperextension of the femorotibial joint. The caudal cruciate ligament (CaCL) runs medial to the cranial cruciate ligament, and it arises in the cranial aspect of the femoral intercondyloid fossa, inserting on an eminence at the popliteal notch of the tibia. The CaCL functions to prevent caudal displacement of the tibia relative to the femur and, in conjunction with the CrCL, limits excessive internal rotation of the tibia on the femur. Generally, a traumatic incident is reported or suspected to have occurred to cause injury to the cruciate ligaments (e.g., the horse taking a fall or being struck by a vehicle). Cruciate injury may also occur concurrently with other soft tissue injuries in the stifle, such as collateral ligament and meniscal injury. The CrCL is under tension when the stifle joint is in extension, and hyperextension or rotation of the stifle joint are suspected to be involved in its injury. Cranial cruciate ligament injuries are appoximately 18 times as common as those of the CaCL, and both ligaments may undergo either partial or complete tearing. Partial tearing of the CrCL occurs most commonly at the midbody segment, but partial detachment of its insertions can occur. Avulsion fracture of the insertion of the ligaments on the tibia may occur, involving the MICET for the CrCl or the eminence at the popliteal notch for the CaCL (Figure 193-7).

Clinical Signs The severity of lameness generally corresponds with the degree of cruciate ligament injury and the presence of coinciding bone or soft tissue injury. Horses may be severely lame at a walk or non–weight bearing with complete cruciate ligament tears. Joint effusion and periarticular swelling may be observed. Testing for joint instability in the standing horse may be attempted in cooperative horses, but this is rarely diagnostic because of the horse’s guarding of the painful limb. To evaluate for complete CrCL rupture, one may stand behind the affected limb and grasp the proximal aspect of the tibia with both hands; the tibia is pulled caudally, and on release, abnormal cranial displacement or crepitus may be recognizable. Additionally, a second test for CrCL injury has been described, in which the cranial proximal tibia is rapidly pushed caudally and released 20 to 25 times, and then the horse is trotted away to evaluate for an increase in lameness.

Diagnosis

Clinical Examination Localization of lameness to the stifle joint, by use of clinical and lameness examination, and potentially flexion tests and intraarticular anesthesia, is the first step in diagnosis of cruciate ligament injury. In horses with severe lameness, trotting and intraarticular anesthesia should be avoided.

Radiography Radiographs may reveal an avulsion fracture of the MICET or, more rarely, the femoral attachment in horses with CrCL injury. Fractures of the MICET may avulse all or part of the insertion of the CrCL with relatively little or no disruption of the cruciate ligament fibers. These fractures may be caused by a traumatic lateral force from the medial femoral condyle on the MICET compared with the more typical pathogenesis of avulsion fractures. Enthesiophyte formation at the MICET (best seen on a flexed lateromedial radiograph) may be present in chronic cases of CrCL injury and was seen in 7% of cruciate injuries in one study. Additionally, radiographs may reveal osteoarthritic changes that occur secondary to cruciate ligament injury–associated joint instability.

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Figure 193-7  Radiographic signs of cruciate ligament injury. A, Avulsion fracture of the medial intercondylar eminence of the tibia at the insertion of the cranial cruciate ligament (circle). B, Avulsion fracture of the eminence at the popliteal notch at the insertion of the caudal cruciate ligament (circle).

A

B

Figure 193-8  Arthroscopic evaluation of the cranial cruciate ligament. A, A right-angled probe is used to palpate for abnormal laxity of the cranial cruciate ligament. The synovial membrane is torn over the ligament, enabling viewing of its fibers. B, The probe is used to retract the synovial membrane, allowing viewing of mild hemorrhage and fibrillation of the cranial cruciate ligament fibers.

Ultrasound Diagnostic ultrasound of the cruciate ligaments is challenging because of their deep position and oblique orientation. The ligaments thus tend to have a hypoechoic appearance, which makes evaluation of changes in fiber pattern chal­ lenging. To evaluate the cruciate ligaments, a 4- to 6-MHz curvilinear transducer is used to evaluate the cranial aspect of the stifle with the limb held in 90-degree flexion and the caudal stifle region (during weight bearing). Ligament disruption and avulsion fragments may be evident ultrasonographically.

Advanced Imaging As discussed earlier (see Meniscal Injury), MRI and CT provide an excellent ability to visualize the the soft tissue and bone structures of the entire joint in great detail and thus may be invaluable for cruciate ligament injury diagnosis. General anesthesia is required for these imaging techniques, and with it comes the risk that a partial cruciate tear may progress to a complete tear on anesthetic recovery. The risks of

imaging must be weighed, and a smooth, assisted recovery is essential.

Arthroscopy Arthroscopic evaluation of the medial and lateral femorotibial joints allows for a definitive diagnosis and debridement of CL injuries. Owners should be warned of the risks of general anesthesia with partial cruciate tears. A lateral or cranial arthroscopic approach to the medial femorotibial joint and lateral femorotibial joint is used. The synovial membrane between the two joints will typically be ruptured with the traumatic injury, enabling evaluation of the extrasynovial cruciate ligaments. In horses with mild CL injury and no significant synovial membrane disruption, the condition may be difficult to diagnose. In general, the CrCL may be seen more easily from the lateral femorotibial joint, and the CaCL can be seen more easily from the medial femorotibial joint. The cruciate ligament may appear fibrillated or torn and can be palpated for abnormal laxity with an arthroscopic

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probe (Figure 193-8). Arthroscopic evaluation has led to the establishment of a grading system for cruciate ligament tears:

Suggested Readings

Grade I: Mild—hemorrhage on the surface of the ligament and mild superficial disruption of the fiber pattern Grade II: Moderate—obvious superficial separation of the fibers of the ligament Grade III: Severe—rupture of the fibers of the cruciate ligament

Treatment Treatment for partial cruciate ligament tears consists of arthroscopic evaluation and debridement of the torn cruciate ligament tissue and debridement of any associated soft tissue injuries. In cases of avulsion fractures, the bone fragments should be removed arthroscopically, although there has been one report of successful internal fixation of a large MICET fragment. Successful repair or replacement of complete cruciate ligament tears has not been reported in horses. A prolonged rest period (6 to 12 months) is important to allow as much healing as possible to occur as well as to decrease secondary arthritic changes from the resultant joint instability.

Prognosis Partial cruciate ligament tears carry a better prognosis than complete tears, and recovery rates for grade I, II, and III lesions have been reported as 46%, 59%, and 33%, respectively. Associated cartilage injury was seen in 61% of cases and is associated with a decreased prognosis. Treatment of MICET fractures by fragment removal or internal fixation has resulted in successful outcomes. Complete rupture of the cruciate ligaments or the presence of multiple lesions (i.e., a meniscal or collateral ligament tear) carries a poor prognosis for the horse’s return to athletic function, and extensive arthritis may develop over time that may lead to severe lameness and the necessity for euthanasia.

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Cohen JM, Richardson DW, McKnight AL, et al. Long-term outcome in 44 horses with stifle lameness after arthroscopic exploration and débridement. Vet Surg 2009;38: 543-551. Fowlie JG, Arnoczky SP, Lavagnino M, et al. Resection of grade III cranial horn tears of the equine medial meniscus alter the contact forces on medial tibial condyle at full extension: an in-vitro cadaveric study. Vet Surg 2011;40: 957-965. Fowlie JG, Arnoczky SP, Lavagnino M, et al. Stifle extension results in differential tensile forces developing between abaxial and axial components of the cranial meniscotibial ligament of the equine medial meniscus: a mechanistic explanation for meniscal tear patterns. Equine Vet J 2012;44: 554-558. Fowlie JG, Arnoczky SP, Stick JA, et al. Meniscal translocation and deformation throughout the range of motion of the equine stifle joint: an in vitro cadaveric study. Equine Vet J 2011;43:259-264. Hendrix SM, Baxter GM, McIlwraith CW, et al. Concurrent or sequential development of medial meniscal and subchondral cystic lesions within the medial femorotibial joint in horses (1996-2006). Equine Vet J 2010;42:5-9. Hoegaerts M, Nicaise M, Van Bree H, et al. Cross-sectional anatomy and comparative ultrasonography of the equine medial femorotibial joint and its related structures. Equine Vet J 2005;37:520-529. Murphy JM, Fink DJ, Hunziker EB, et al. Stem cell therapy in a caprine model of osteoarthritis. Stem Cell Arthritis Rheum 2003;48:3464-3474. Walmsley JP. Diagnosis and treatment of ligamentous and meniscal injuries in the equine stifle. Vet Clin North Am Equine Pract 2005;21:651-672. Walmsley JP, Phillips TJ, Townsend HG. Meniscal tears in horses: an evaluation of clinical signs and arthroscopic treatment of 80 cases. Equine Vet J 2003;35:402-406.