David L. Dycus, Jeffery Biskup, Michael G. Conzemius and Ron Ben‐Amotz The cranial cruciate ligament (CCL) is a robust intraarticular, yet extrasynovial structure responsible for preventing stifle hyperextension, excessive internal rotation, and cranial subluxation of the tibia in relation to the femur. It originates from the caudomedial aspect of the lateral femoral condyle, and travels in a craniomedial direction to insert on the cranial intercondyloid region of the tibia [1]. It is composed of two distinct bands: the craniomedial and caudolateral portions. During stifle extension, both the craniomedial and caudolateral bands are taut, while during flexion the craniomedial band remains taut while the caudolateral band becomes lax [2]. Cranial cruciate ligament disease is considered to be the most common cause of pelvic limb lameness in the canine, affecting approximately 2.55% of the population [3, 4]. It is a broad term that encompasses a variety of different pathological disorders that may affect the ligament. For example, in skeletally immature canines, avulsion of the CCL may occur secondary to a traumatic event. In the skeletally mature canine, traumatic rupture occurs less commonly, although it may still be induced by forced hyperextension with internal tibial rotation [5]. The most likely etiology for rupture of the CCL in mature dogs is progressive degeneration of the ligament. This degenerative process likely explains the high incidence of bilateral and contralateral CCL pathology. Contralateral CCL pathology has been documented in over 50% of canines [6]. Complicating the matter is the fact that the exact cause of degeneration is poorly understood. Various factors have been investigated in the etiology and pathogenesis of CCL degeneration. Tibial plateau angle [7], genetics, age, bony confirmation, body weight, gait, and vascularity of the ligament [8–10] have all been identified as risk factors for CCL rupture. To date, none of these factors has proved definitive and as such, the degeneration of the CCL is considered multifactorial. Regardless of the cause of CCL damage, rupture results in a cascade of events that causes altered kinetics and kinematics of the stifle. It is these altered dynamics that likely lead to progressive osteoarthritis (OA) and increased likelihood of meniscal pathology. Kinematic analysis of the CCL‐deficient stifle has shown that the joint remains in a more flexed position throughout the gait cycle. As a result of the increased stifle flexion, the hip and tarsocrural joints compensate by maintaining a greater degree of extension during the stance phase [11]. Kinetic analysis has revealed decreases in peak vertical force (PVF), vertical impulse, braking, and propulsion impulses in dogs with CCL pathology [12]. For example, the PVF in the normal canine pelvic limb was 70% of static body weight; however, when the CCL was transected, the PVF decreased to 25% of static body weight. This was only improved to 32% and 37% at 6 and 12 weeks post transection respectively [13]. Therefore, this demonstrates continued loss of PVF even after periarticular fibrosis has developed. It could be argued that because of this lack of improvement in kinetic function, surgical stabilization of the cruciate‐deficient stifle should be considered. Along with altered weight bearing and joint flexion/extension, there is also evidence to suggest that the CCL‐deficient stifle exhibits increased cranial subluxation of the tibia in relation to the femur. Up to 8–12 mm of subluxation has been noted during the stance phase of the gait [14]. Long‐term changes have been evaluated in the canine following CCL transection. Following initial transection of the CCL, there was 10 mm more tibial subluxation compared to patients with an intact CCL. Two months following transection, tibial subluxation was noted only during the stance phase and not during the late swing/early stance phase (paw strike). Two years following transection, 5 mm of tibial thrust was noted at the end of the swing phase. It was suggested that the reason for these changes was the presence of an intact medial meniscus. It was theorized that in the CCL‐deficient stifle, the meniscus minimizes tibial subluxation by elastically deforming during tibial subluxation and aiding in reduction of the subluxation once the swing phase begins (alternatively, as the load from the stance phase is removed) [15]. Interestingly, tibial subluxation as the result of instability has been called into question as it demonstrated that instability following CCL rupture is actually a caudal slippage of the femur at the beginning of the stance phase. As such, documented continuation of instability in some stifles exists following common osteotomy procedures such as the tibial plateau leveling osteotomy (TPLO) and tibial tuberosity advancement (TTA) [16]. In addition to controlling sagittal joint motion of the stifle, the CCL also aids in limiting internal rotation. To date, no osteotomy modifying procedures effectively eliminate excessive internal rotation. Initially, this was thought to play a minimal role in the CCL‐deficient stifle. While significant changes in internal rotation were not noted immediately following transection of the CCL, 2 months following transection the range of abduction and adduction in the stifle was increased. These rotary changes remained increased 2 years following tran section [15]. Recognition of the importance of preventing excessive internal rotation has led to the idea and development of augmentation to prevent excessive internal rotation following certain osteotomy procedures such as the TPLO (Figure 1.1). Interestingly, a population of CCL‐deficient canines will exhibit persistent internal rotation following surgical stabilization. This persistent internal rotation likely falls under the umbrella term of “pivot shift.” Unfortunately, to date, it is not possible to predict which population of patients will exhibit persistent internal rotation following surgical stabilization. In the authors’ opinion, patients with acute CCL rupture, large medial meniscal bucket handle tears, and lack of periarticular fibrosis tend to have persistent internal rotation following certain surgical procedures such as the TPLO. Recently, it was shown that the use of a lateral fabellotibial suture in combination with a TPLO was effective for managing CCL instability in patients with excessive internal rotation identified either preoperatively or intraoperatively [17]. Therefore, the authors recommend the use of adjunct lateral fabellotibial suture in identified patients with excessive internal rotation or “pivot shift” (Figure 1.1). Figure 1.1 An immediate postoperative radiograph of stifle stabilization via a TPLO. Intraoperatively persistent excessive internal rotation was noted so a lateral fabellotibial suture was placed. Note the metallic crimp (red arrow) that has been added. The diagnosis of CCL pathology is made based on signalment, history and clinical signs, orthopedic examination findings, and diagnostic imaging. While the old saying “a hindlimb lameness in a mature dog is cruciate disease until proven otherwise” holds true, it is important to ensure that the lameness is due to CCL pathology and not another underlying pathological condition of the stifle or another anatomical structure of the pelvic limb. Signalment information in canines with CCL pathology varies, with most affected dogs presenting for evaluation between 2 and 10 years of age. However, the authors have seen dogs as young as 12 weeks (Figure 1.2) and as old as 16 years present for CCL pathology. The authors (DD and RBA) have also observed a high incidence of 9–13‐month‐old American Pit Bull Terriers and American Staffordshire Terriers presenting with bilateral CCL pathology. The reason for this is unknown but could be due to demographics and possible breeding practices. Virtually any breed can be affected with CCL pathology; one study revealed the highest prevalence in the Rottweiler, Newfoundland, and Staffordshire Terrier [18]. Another study revealed that breeds at risk for suffering CCL rupture before 2 years of age included the Neapolitan Mastiff, Mastiff, St Bernard, Rottweiler, Akita, Newfoundland, Chesapeake Bay Retriever, Labrador Retriever, and American Staffordshire Terrier [19]. Female dogs have an increased prevalence of CCL pathology (similar to human female athletes), as do neutered canines compared to sexually intact canines [19]. Figure 1.2 Radiograph of a 12‐week‐old dog that suffered a traumatic CCL injury. Historical findings of patients with CCL pathology may include an acute or chronic onset of hindlimb lameness that may range in severity from mild to nonweight bearing. Some patients may only exhibit stiffness when rising or after heavy activity or may offload the affected limb at a stance (Figure 1.3). When questioning owners, it is important to obtain a timeline of abnormalities they have noticed even when the lameness appears acute. The authors have found that when questioning owners, many patients have a longer standing history of subtle clinical signs before an acute lameness develops. This further emphasizes the degeneration of the CCL. The common scenario following complete rupture of the CCL is a nonweight‐bearing status for several days. As the inflammatory phase starts to subside, patients will begin to toe touch and use the limb with a noticeable weight‐bearing lameness. Many owners perceive this as their dog improving, when in reality this is consistent with the normal progression of CCL pathology. Figure 1.3 Representation of offloading the left pelvic limb at a stance. This patient was diagnosed with a left CCL rupture. Notice when the dog is standing full weight is not applied to the left pelvic limb. The orthopedic examination is aimed at demonstrating stifle instability; however, other aspects of the stifle and pelvic limb should be evaluated. Pending the severity of the condition as well as the timeframe, there may be pain upon flexion and extension of the stifle, in particular with hyperflexion and hyperextension. In chronic cases of CCL pathology, there may be thickening of the proximal medial tibial or the so‐called “medial buttress” which is development of periarticular fibrosis. The periarticular fibrosis can limit range of motion in the stifle, which may ultimately result in loss of active range of motion. A loss of active range of motion can translate into loss of limb function [20]. In cases with more advanced OA, crepitus may be noted as range of motion is evaluated, and in cases in which meniscal pathology is present, there may be either a consistent or intermittent clicking (“meniscal click”) during range of motion of the stifle. A recent study concluded that a meniscal click in CCL‐deficient stifles carries a high specificity for a bucket handle tear of the meniscus. In addition, the presence of a meniscal click during examination is strongly indicative of a meniscal tear being diagnosed at surgery. However, a lack of meniscal click carries a low sensitivity in diagnosing the absence of meniscal tear [21, 22]. This emphasizes the need for meniscal evaluation in every joint undergoing CCL stabilization. Figure 1.4 A patient with instability of the left pelvic limb secondary to a CCL rupture. Notice the degree of muscle loss on the left hindlimb compared to the right. Loss of function of a limb will ultimately lead to loss of muscle strength. Unfortunately, in the canine, loss of muscle strength has never been reported but loss of muscle mass has [23] (Figure 1.4). Therefore, it is important to measure mass at the time of the initial consultation as well as at each follow‐up visit. Additional information on measurement of hindlimb muscle mass can be found in Chapter 15. In addition, measurement of joint motion of the stifle should be performed [24] to determine the flexion and extension of both the affected and unaffected limbs not only at the initial consultation but at all follow‐up visits. Additional information on measurement of joint motion can be found in Chapter 15. Figure 1.5 An example of a positive sit test in a patient with a right CCL tear. Notice how the right hindlimb is projected outward and the patient is not sitting squarely. One question that every clinician should ask themselves is: how do you know your patients are truly improving and how can you detect subtle complications? Gathering as much objective information as possible is vital; muscle mass measurements as well as measurement of joint motion of both the affected and unaffected limbs should be part of the objective information gathered (more information on this can be found in Chapter 15). With CCL pathology, there may be an abnormal sit, sometimes referred to as a “positive sit test.” This is characterized by patients sitting with the affected limb projecting out to the side or tucked under them (Figure 1.5) rather than sitting square (Figure 1.6). Alternatively, patients may sit with weight shifted off the affected limb (Figure 1.5). The abnormal sitting posture is thought to be due to discomfort associated with hyperflexion of the stifle when forced to sit squarely. Unfortunately, some dogs may still exhibit an abnormal sit test following CCL stabilization. The reason for this is unknown but it could be due to continued stifle discomfort upon full flexion. Figure 1.6 An example of a square sit in a patient with no CCL pathology. Notice how both stifles are fully flexed and the patient is sitting square. Instability of the stifle is commonly demonstrated through the cranial drawer test and tibial compression test. The cranial drawer test (Figure 1.7) is performed most commonly and tends to be the mainstay of testing for stifle instability by general veterinarians. It is performed by applying a force to the tibia while holding the femur stable, thereby creating craniocaudal translation of the tibia. The operator may stand either behind (caudal) the patient or behind and slightly to the side (caudal and lateral). One hand is placed on the distal femur with the thumb on the lateral fabella and the index finger on the patella. The other hand is placed on the proximal tibia with the thumb on the fibular head and the index finger on the tibial tuberosity. The goal is to move the hand on the proximal tibia cranially while holding the hand on the distal femur stable. Commonly, mistakes made by the inexperienced operator stem from trying to move both hands simultaneously or trying to grab the tissues (both soft and bony) too firmly. Forcing cranial drawer or grasping the tissues too firmly will cause the patient’s muscles to tense, making interpretation difficult. Cranial drawer should first be checked in extension, and if positive is likely indicative of a complete tear (typically greater than 75% tearing of the CCL as subjectively noted by one author, DD). If negative, it should then be checked in flexion. A positive cranial drawer in flexion but negative in extension typically indicates an incompetent (unstable) partial CCL tear (usually 50–75% tearing of the CCL as subjectively noted by one author, DD). If cranial drawer is negative in both extension and flexion, then the stifle should be placed in hyperextension to evaluate for discomfort. Discomfort with joint effusion and negative cranial drawer may indicate a competent (stable) partial CCL tear (usually less than 50% tearing of the CCL as subjectively noted by one author, DD). Figure 1.7 Demonstration of the cranial drawer test. One hand is placed on the distal femur with the thumb on the lateral fabella and the index finger on the patella. The other hand is placed on the proximal tibia with the thumb on the fibular head and the index finger on the tibial tuberosity. The goal is to move the hand on the proximal tibia cranially while holding the hand on the distal femur stable. The make‐up of the craniomedial and caudolateral bands of the CCL can explain why it is possible for the cranial drawer test to be positive in flexion even if it is negative in extension. The craniomedial band is the primary supporter of tibial translation and tends to degenerate first. During range of motion, it is taut in both flexion and extension. The caudolateral band is a secondary supporter of tibial translation and is taut in extension but lax in flexion. Therefore, if the craniomedial band is torn, cranial drawer will be absent in extension but present in flexion. Lack of cranial drawer may indicate tearing of the caudolateral band with an intact craniomedial band or subtle tearing of the craniomedial band or both the craniomedial and caudolateral band. In anxious or nervous patients or those with negative cranial drawer, the authors recommend performing a sedated examination to ensure there is no instability. Unfortunately, when chronic periarticular fibrosis or advanced OA is present, cranial drawer may be negative due to the presence of significant fibrous tissue or permeant translation of the tibia in relation to the femur. Skeletally immature patients often exhibit some physiological cranial drawer (“puppy drawer”) of up to about 3–5 mm. However, there should be an abrupt stop point at the end of cranial drawer to differentiate this from pathological cranial drawer. The tibial compression test (Figure 1.8), while still a passive test, aims to mimic load bearing of the stifle. The operator may stand either behind (caudal) the patient or behind and slightly to the side (caudal and lateral). One hand is placed on the distal femur with the thumb on the lateral fabella and the index finger on the patella. The other hand is used to hold the metatarsals and tarsocrural joint. With the stifle held stable, the tarsocrural joint is flexed and extended. The clinician observes for a cranial‐to‐caudal motion of the tibial tuberosity indicating pathology of the CCL. Mistakes made by the inexperienced operator stem from trying to flex and extend both the stifle and tarsocrural joint simultaneously. In addition, the stifle should be held in a sagittal plane with no excessive internal or external rotation. Holding the stifle internally rotated can lead to a false positive of tibial thrust. Diagnostic imaging of the stifle in patients with CCL pathology is usually centered around radiographic evaluation. Radiographic examination is warranted in every case of hindlimb lameness even if surgical intervention is not an option. It should be suggested that good‐quality orthogonal views of both the affected and unaffected stifles should be performed (Figures 1.9 and 1.10). While the CCL itself is not visible on radiographs (unless associated with an avulsion of the CCL), there are two key findings that can be appreciated: osteoarthritic changes and intraarticular changes (meniscal edema, synovial hyperplasia, and joint effusion). Figure 1.8 Demonstration of the tibial compression test. One hand is placed on the distal femur with the thumb on the lateral fabella and the index finger on the patella. The other hand is used to hold the metatarsals and tarsocrural joint. With the stifle held stable, the tarsocrural joint is flexed and extended. The clinician observes for a cranial‐to‐caudal motion of the tibial tuberosity indicating pathology of the CCL. The earliest finding of CCL pathology is the presence of joint effusion (Figure 1.11). This is noted by cranial displacement of the infrapatellar fat pad on the lateral view. The normal fat pad should be triangular in shape and located adjacent to the cranial margin of the femoral condyles and the cranial aspect of the tibial condyles. In most cases, any displacement from these normal margins is consistent with the presence of joint effusion. In addition, there may be displacement of the caudal joint capsule (Figure 1.11). The degree of joint effusion in some cases can be roughly correlated with the degree of CCL pathology. Generally, patients with competent partial CCL pathology will have less joint effusion than patients with incompetent or complete CCL pathology. Evidence of likely synovitis can be noted as subtle regions of sclerosis noted on the caudal aspect of the trochlear groove as seen on the lateral view. Degenerative changes can readily be seen in patients with CCL pathology (Figure 1.12). In particular, changes will be noted at the proximal trochlear groove, lateral and medial femoral trochlea, distal pole of the patella (patella apex), caudal tibial plateau, medial and lateral aspects of the tibial condyle margins, and both fabellae. In some cases, the sesamoid bone of the popliteal muscle can be displaced proximally and/or caudally. The importance of taking contralateral radiographs at the time of initial diagnosis is for the evaluation of OA and joint effusion as well as detection of other pathologies that might exist. If noted on the contralateral stifle (even in the face of joint stability), one should assume there is already CCL pathology present and the likelihood of joint instability developing is high. If this is present, it is important to educate the owner regarding this finding. Figure 1.9 A lateral radiograph documenting appropriate positioning of the stifle. Notice there is superimposition of the femoral condyles and the tibial plateau demonstrating a straight view in the sagittal plane. Figure 1.10 A cranial‐caudal radiograph documenting appropriate position of the stifle. Notice how the calcaneus intersects the center of the trochlear ridge of the talus demonstrating a straight view in the frontal plane. A number of methods for stifle stabilization exist. They are commonly characterized as extraarticular stabilization, intraarticular stabilization, and osteotomy modifying procedures. One of the complicating factors of stifle stabilization (and indeed, one of the reasons for the existence of so many surgical procedures) is the lack of definitive guidelines for what constitutes a successful postoperative outcome. Figure 1.11 Evidence of joint effusion in the stifle of a patient with CCL pathology. In the caudal compartment, there is displacement of the joint capsule as can be noted by the red arrows. The opacity in the cranial compartment (blue arrows) is joint effusion that is displacing the fat pad cranially. Figure 1.12 Evidence of degenerative changes in the stifle of a patient with CCL pathology. Commonly noted areas are the distal pole of the patella (blue arrow), cranial tibial plateau (orange arrow), caudal tibial plateau (yellow arrow), and fabella (red arrow). In addition, a small area of sclerosis can be seen around the trochlear groove (green arrow) indicative of synovitis or osteophytosis of the medial or lateral femoral trochlea. While all correctly executed surgical procedures can stabilize the stifle, not one of these procedures ultimately restores completely normal stifle kinematics or kinetics. In defining a good outcome, should we consider a stable stifle to be the predominant deciding factor? Interestingly, work has been completed that demonstrates ongoing instability following surgical stabilization [16, 25], yet retrospective and client assessment studies have shown high success rates with certain procedures. What about return to function? Success rates among all surgical procedures are in the high 80% to low 90% range when evaluating most retrospective studies. While this suggests that most surgical procedures do a good job of returning canines to “normal” function, probably the best way to tell would be return to sport or work for our canine athletes. Recent data have suggested that following TPLO, agility dogs have a good prognosis for return to sport [26]. Elimination of progression of OA has been stated as a possible determination of outcome and goal of treatment. This is likely not an achievable feat. Once the CCL has become damaged and instability in the stifle is present, there is abnormal joint loading. Thus, damage to the chondrocytes has occurred. Therefore, it is probably better to evaluate surgical stabilization procedures in terms of which are the most capable of slowing down and minimizing progression of OA, rather than which can eliminate it entirely. The ability to recognize and manage complications should be considered when choosing a surgical procedure. Generally, the complication rate of currently practiced surgical stabilization procedures is low, but individual techniques are associated with their own unique set of potential complications and it is of the utmost importance that the clinician is familiar with the management of these complications prior to undertaking the initial procedure. In the past, much focus has been on the actual surgical procedure and training of how to perform it. Unfortunately, what is missed is how to identify patients that might be at an increased risk of complications, how to identify intraoperative complications, decision making to avoid intraoperative complications, recognition of postoperative complications, and how to revise complications in the postoperative period should they occur. Although a high success rate (intended outcome) is important when deciding to perform a surgery, the risk of an unintended outcome, severity of potential adverse events, and owner financial burden need to be considered and communicated to the owner. Avoiding iatrogenic harm should be an emphasis of all practicing veterinarians. In veterinary orthopedics, standardized definitions of complications have been suggested in an attempt to improve consistency and comparability in veterinary orthopedic research [27]. For example, a method to classify catastrophic, major and minor complications has been published so results between studies can be accurately translated and to allow the clinician to decide if an intervention causes unacceptable morbidity. One method to quantify success and harm factors is a ratio between the number of patients needed to treat (NNT) and number needed to harm (NNH). NNT is defined as:
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Pathology, Diagnosis, and Treatment Goals of Cranial Cruciate Ligament Rupture and Defining Complications
1.1 Introduction
1.2 Diagnosis
1.3 Treatment
1.4 Defining a Complication
1.4.1 Assessment of Success and Complications
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