Many smaller breed dogs present with varying symptoms of neurologic compromise after having herniated a disc. They may appear to walk somewhat wobbly or off-balance or be totally paralyzed and dragging their rear end on the ground. Varying degrees of pain and discomfort are present or they may be so severely paralyzed that they appear non-painful because the spinal cord is “numbed out” from being squished. These three dogs illustrate the differing degrees of a presentation I commonly see at our hospital. The first dog was painful and reluctant to move and would stumble on its front limbs because of a herniating disc in the neck area. It responded well to a combination of special intravenous steroids as well as some other medications and can be seen walking normally within one day of aggressive medical management. While some veterinarians debate the usefulness of this regime to treat herniating disc injuries, the reality is that used intelligently it works very well with no adverse side effects as seen in this case. In spite of the debate, if you or I were to present similarly, we would unequivocably receive the same medical treatment administered to this dog. The second and third dogs presented acutely and totally paralyzed. A myelogram revealed extensive spinal cord compression (as seen on the x-ray) and so a combination of medical and surgical intervention was warranted. As seen in the video, the brown dog was back up and walking normally within 10 days of surgery. “Booger”, the black dog took a little longer but as can be seen in the video, is back up and walking well by 8 weeks after surgery; he should continue to make progress over the next few months and even the first full year after surgery. Prompt and aggressive medical and surgical intervention is warranted to achieve the best results in cases of paralysis, and success rates of approximately 90% (even in cases like Booger) can be expected.
Fractures involving the distal femoral physis are relatively common in immature dogs and cats with the greatest incidence occurring between the ages of 5 and 8 months.
Physel fractures have been classified by Salter and Harris into 5 categories: Type 1 traverse the physeal plate through the zone of hypertrophying cartilage; Type 2 involves the physis and continues through the mtaphysis; Type 3 involves the physis and continues through the epiphysis to involve the articular surface; Type 4 involves the articular surface, crosses the physis and continues into the metaphysis; and Type 5 a compression injury to the zone of resting cartilage of the physis.
Distal femoral physeal fractures are commonly Types 1 and 2; most physeal fractures in the dog are Type 2 while those in the cat are Type 1. This is due in part to the fact that the distal femoral metaphysis has four projections that correspond to four similar deep depressions in the epiphysis in the dog while in the cat, the projections are flatter and do not interdigitate as deeply with the corresponding epiphyseal depressions. Physeal fractures usually occur through the zone of hypertrophying cartilage, because this zone is characterized by large, vacuolated cells with minimal intercellular matrix. Therefore, this zone is the weakest.
A variety of treatment methods have been described for repair of distal femoral physeal fractures including closed reduction and external fixation, normograde or retrograde placement of a single intramedullary pin with or without an anti-rotational Kirshner wire, multiple intramedullary pins, paired Rush pins, Steinman pins, or Kirshner wires employed in Rush pin technique, cross pins, bone plates, and lag screws. The ultimate goal of treatment should be accurate reduction and rigid stabilization of these fractures with as little iatrogenic damage to the germinal cells of the physis and their blood supply as possible.
While closed reduction and external fixation may be successful in selected cases, every attempt should be made to satisfactorily stabilize the fracture internally so that early return to function is achieved and restricted joint movement is avoided. When closed reduction and external fixation is used, a good result is the most that one can expect.
Surgical exposure for open reduction and internal fixation is achieved via a lateral parapatella approach with reflection of the patella medially. Interference with growth is a consideration in the selection of the method of repair; however, recent studies have suggested that premature closure of the physis occurs more commonly as a result of the initial trauma than the method of treatment employed. Distal femoral physeal closure normally occurs between six and eight months of age; as the majority of physeal fractures occur in dogs and cats greater than five months of age, over 90 percent of their skeletal growth has already been achieved by the time of injury. Therefore, in animals over five months of age, while some degree of femoral shortening may occur, the overwhelming majority of animals clinically accommodate shortening by a change in stifle or hock angulation. In dogs and cats under five months of age with substantial growth potential, the method of fixation chosen should provide adequate stabilization but should not mechanically bridge the physis. Early implant removal may minimize premature physeal closure. Any implant, which traverses the growth plate, will result in some degree of permanent damage to the growth plate. The least damage occurs when round, smooth, non-threaded implants are placed perpendicularly to the long axis of the growth plate.
Single intramedullary pin fixation, Rush pinning and modified Rush pin technique, and cross pinning are the most commonly employed techniques used to treat Salter Type 1 and 2 fractures. A single intramedullary pin should provide excellent alignment and stability if the opposing surfaces of the fracture interlock following anatomic reduction. However, in large dogs, single pin fixation may be inadequate to allow early use of the limb. In addition, femoral intramedullary pins existing the trochanteric fossa have been associated with sciatic nerve injury. Normograde pinning of distal femoral physeal fractures is less likely to induce sciatic nerve injury then retrograde pinning. Implant migration may also result in damage to the intra-articular surface of the stifle joint.
Although cross pin fixation works well, it is associated with more complications than other techniques including caudal malalignment and/or displacement of the distal fragment and quadriceps tie-down. In very immature animals, cross pin fixation may interfere with physeal growth because of the excessive pin angulation necessary for adequate stabilization.
Rush pins provide excellent fixation for distal femoral physeal fractures. Their disadvantage is the need for special instrumentation and the cost of the implants. Rush pins provide three point fixation, thereby increasing stabilization and making their application especially indicated in large dogs. If Rush pins are used in very immature animals, great care must be taken when driving the pins to prevent excessive compression of the germinal cell layer, which may result in growth arrest.
Steinman pins or Kirshner wires may be used in exactly the same way as Rush pins. Once the fracture is reduced, the pins are inserted laterally just cranial to the tendon of origin of the long digital extensor muscle, and medially on the distal medial bondyle symmetric to the later pin placement. The pins are alternately advanced in the medullary cavity. I prefer that the pins do not exit the trochanteric fossa so as to minimize the potential complication of sciatic nerve injury. Pre-bending the pins accentuates a three point fixation and results in rigid internal fixation and rotational stability. This technique can be used in very immature animals when fear of Rush pin compression of the germinal layer may be a factor. Such pins may be placed with relative minor trauma to the physis, and most animals continue to lengthen their femurs despite the pins through the growth plate. With proper alignment and internal fixation, an excellent result should be expected.
Cranial cruciate ligament (CrCL) injury is the most common cause of stifle lameness in the dog.
CrCL deficiency results in both translational and rotational instability of the stifle joint that leads to the development of the degenerative joint disease. The joint pathology, including the complex of biologic and biochemical events that lead to ligament degeneration and the concurrent development of osteoarthritis (OA), has been coined cruciate disease. CrCL deficiency in dogs is a multifactorial disease involving genetics, conformation factors, and an inflammatory component that together create an imbalance between the biomechanical forces placed on the ligament and its ability to sustain these loads, eventually leading to rupture and joint instability. Biology and biomechanics are inextricably linked in health and disease of the CrCL, and it is vital to consider both aspects concurrently to develop a comprehensive understanding as well as medical and surgical therapeutic approaches to successfully manage this common cause of lameness in the dog. Simply put, this means that all of the tissues comprising the joint must function together, biologically and biomechanically, in order to maintain joint health and to allow full, pain-free function and range of motion. The CrCL cannot be isolated from the synovium, caudal cruciate ligament, articular cartilage, menisci, or subchondral bone, and all of these components must be considered critical interrelated elements, which are essential for long-term stifle function.
A definitive cause for CRCL disease remains unknown, but many presumed factors result in a final common pathway of abnormal biomechanics and abnormal biology causing OA and the clinical signs of lameness, pain, and limb dysfunction. The biologic components include inflammation, degradation and degeneration, impaired synthesis, and turnover of extracellular matrix and necrosis. The biomechanical components include instability of various types and degrees, muscle weakness and dysfunction, misalignment, conformational changes, altered kinematics, and distorted joint contact areas and pressures. While many of these components have been incriminated as causes of cruciate ligament disease, evidence is lacking with regard to any one factor being a sole causal agent. For this reason, all of these factors should be considered as potential components of a multifactorial disease process. The precise role each plays in the process and the nature and timing of each event is critical to improve our understanding of cruciate disease so that we can improve preventative, diagnostic, and therapeutic strategies, and treatment options for dogs afflicted with cruciate ligament injuries.
An excellent question with regard to the cause of CrCl injury is does cruciate disease result from abnormal biomechanics on a normal ligament, normal biomechanics on an abnormal ligament, or a combination of both? Currently, there is no definitive answer to this question. While acute, traumatic CrCl rupture occurs and is characterized by the absence of pre-existing degenerative signs (osteophytes, synovial hypertrophy, cartilage degeneration), other joint tissues are concomitantly affected (meniscal tears, multiple ligament injuries, bone bruising) such that the total clinical outcome is one of whole joint injury and damage. This type of injury is not representative of the majority of CrCl injuries in the dog. More commonly, cruciate injury includes a degenerative component (osteophytes, synovial hypertrophy, cartilage degeneration, periarticular fibrosis, subchondral bone sclerosis). This more common scenario implicates abnormal ligament biology as a driving force behind the eventual development of ligament failure; it does not exclude abnormal biomechanics as a primary force behind this abnormal biology. It is certainly possible that abnormal biomechanics initiates and perpetuates abnormal ligament biology sustaining a vicious cycle of stifle joint failure that is recognized as cruciate ligament disease.
Current thinking has focused on conformation of the proximal aspect of the tibia as the major contributor to abnormal stifle biomechanics leading to CrCL failure. While one study has reported a significant difference in tibial plateau angle (TPA) between dogs with and without CrCL disease, data from multiple studies contradict this, and there is no definitive evidence that either TPA or patellar tendon-tibial plateau angle is a significant risk factor for cruciate disease in dogs. When either of these angles is considered high based on reference intervals in dogs, theoretical considerations suggest there are increased CrCL strain and an increased shear component of total joint force. Thus, these components may contribute to the process of organ failure, but do not appear to be primary causal factors based on current best evidence. Inherent instability is another potential abnormality that could be involved in the development of cruciate disease. Instability can be the result of dysfunction of passive stabilizers, dynamic stabilizers, or both. In the canine stifle, passive stabilizers include the cruciate ligaments, menisci, collateral ligaments, joint capsule, and articular contours. The dynamic stabilizers are primarily the quadriceps-patellar mechanism components and hamstring muscles, but also include other associated muscles and tendons. Collectively, all of the stabilizers work to help maintain stifle joint kinematics. It is naive to view and treat CrCL disease as a singular issue of cranial caudal instability. Whereas failure of any of the stabilizers can lead to loss of normal kinematics and stifle joint organ failure, compensation for failure of 1 stabilizer by others can occur so that functional kinematics can be maintained. Instability from various causes as well as anatomic abnormalities of all types, joint incongruity, neuromuscular problems, tissue composition abnormalities, and changes to articular contact areas and pressures all alter stifle joint kinematics and are responsible for cruciate disease. These may occur because of genetics, nutrition, single or repetitive traumatic events, activities and training, infectious or metabolic disorders, and/or various surgical manipulations of the limb. It is therefore imperative that these considerations are included in investigations to determine etiopathogenesis, diagnostic approaches, breeding plans, and treatments for canine patients. The nature and complexity of this multifactorial disease process invokes comparisons with canine hip dysplasia and elbow dysplasia. This combination of anatomic, biomechanical, genetic, cellular, and biochemical factors involved in CrCL disease in dogs could appropriately be considered as components of a stifle dysplasia complex.
Developmental, infectious, immune-mediated, genetic, metabolic, hormonal, and primary cell and/or matrix disorders have been suggested as causal or associated factors in canine CrCL disease. Genetic components appear to be involved in certain dogs and may contribute to conformational changes associated with biomechanical causes of disease. Hormonal- and metabolic-related changes have recently been implicated in CrCL disease. Effects of early spay or neuter on growth plate function could contribute to conformational changes associated with cruciate disease. Cell and matrix disorders can involve a myriad of different tissues, processes, and mechanisms. The current major areas of focus are on the CrCL and its synovial sheath. A critical component to these disease mechanisms is that the CrCL is intra-articular but extra-synovial. This means that, in health, the CrCL is protected from the intra-synovial environment, and the intra-synovial environment is protected from the CrCL. Intra-synovial structures such as the articular cartilage, synovium, and menisci constantly communicate with the CrCL, but this communication is filtered by the synovial sheath. When this protective filter is lost, as it is in cruciate disease, the CrCL is exposed to the intra-synovial environment and tissues, and vice versa. Whether this exposure is of biological or biomechanical cause or both is not known, but it is clear that this does occur in the disease process and that it can have severe consequences for both ligament and joint health, including upregulation and release of inflammatory mediators and degradative enzymes, proliferation of cells, recruitment of inflammatory and immune system cells, and production of anti-collagen antibodies in many cases.
Abnormal biology and biomechanics definitely potentiate and exacerbate one another. Instability, anatomic abnormalities, muscle weakness, and altered contact areas and pressures can directly lead to inflammation, necrosis, and tissue degeneration. Tissue composition changes, cellular responses, and degradative enzyme production and release can directly result in altered kinematics, neuromuscular dysfunction, and malarticulation. Some of these competing forces result in positive responses that help to ameliorate or retard the detrimental effects of the other abnormal processes. Osteophytosis, muscle hypertrophy, and periarticular fibrosis are biologic responses that help counteract abnormal biomechanics because of dysfunction of passive stabilizers, tissue loss, and anatomic abnormalities. Articular and meniscal cartilage as well as subchondral bone can remodel to help compensate for changes in tissue structure and architecture from abnormal matrix turnover. Unfortunately, these adaptations do not appear to be sufficient to allow for healing or even functional compensation for the associated abnormal biology and biomechanics of the CrCL.
Cruciate disease in dogs involves a spectrum of potential causal factors, patient types, clinical presentations, risk factors, disease mechanisms, and rates of progression. Treatment strategies should address abnormal biology and biomechanics with the overall goals of decreasing pain, improving function, and retarding disease progression. Although there is not a currently available methodology for restoring joint kinematics to normal in dogs with cruciate disease, it is clear that addressing craniocaudal instability alone will never be sufficient for full return to long-term function.
The strategies that have supporting evidence as potential aids in augmenting the productive responses outlined above include joint lavage, complete assessment of joint pathology with comprehensive and accurate debridement, pharmaceutical and nutraceutical interventions, and physical rehabilitation modalities. Whereas none have sufficient evidence in support of blanket statements regarding their use, joint lavage, or washout, has been reported to provide benefits in terms of dilution of nociceptive, inflammatory, and degradative mediators. The utilization of platelet-rich plasma (PRP) is a new technology, which focuses on enhancing the healing response after injury of different tissue types. In recent years, several studies have described a complex regulation of growth factors for normal tissue structure and reaction to tissue damage and have demonstrated an important role for growth factor application in the healing of damaged tissue. PRP is a natural concentrate of autologous growth factors (platelet derived growth factor, transforming growth factor, platelet derived epidermal growth factor, vascular endothelial growth factor, insulin like growth factor, fibroblastic growth factor, epidermal growth factor) and cytokines, which aids in the regeneration of tissues with low healing potential. Platelets have a major role in the initiation of wound healing. They adhere, aggregate and release numerous growth factors, adhesive molecules and lipids that regulate the migration, proliferation, and function of fibroblasts and endothelial cells. PRP has been shown to accelerate tissue repair in soft tissues via mechanisms involving the further synthesis of signaling proteins that participate in cell mitosis and angiogenesis. Another important consideration is that in addition to stimulating the growth of new tissue, PRP application has been shown to decrease pain and inflammation in the degenerate area in which it is applied. The utilization of PRP has the capacity to optimize the healing environment. Because of its autogenous origin, easy preparation and excellent safety profile, PRP has tremendous potential to speed recovery in cases of tendon, ligament, muscle, and cartilage disorders. As all of these tissues are compromised to varying degrees in cases of cruciate ligament disease, the administration of PRP has the ability to improve stifle stability, diminish pain, and accelerate physiologic healing and reparative tissue processes involving the patellar tendon, cruciate ligament, and meniscus. The incorporation of PRP into the medical protocol for management of cruciate ligament pathology may affect the current debate regarding the debridement and removal of partially injured cruciate ligaments and menisci given its ability to stimulate healing in these notoriously refractory tissues.
Full exploration and assessment of the joint increases the likelihood of accurate and complete diagnosis of degree of synovitis, articular cartilage damage, meniscal pathology, and cruciate ligament pathology. Debridement of damaged and pathologic meniscal tissue can improve joint biomechanics, ameliorate pain, help to minimize further articular cartilage loss, remove a potential source of inflammatory and degradative mediators, and help prevent subsequent meniscal pathology. Therefore, complete debridement of diseased cruciate ligament may act to remove a nidus of inflammation and degradation, remove a potential source of pain, and improve observation and access to the menisci. Medications can have beneficial effects on inflammation, degradation, nociception, and synovial fluid rheologic and biologic properties. Physical rehabilitation can improve range of motion, muscle mass, and weight-bearing function in dogs with CrCL disease. These factors used in conjunction can augment the positive adaptational responses noted in canine CrCL disease, and some anecdotal evidence suggests that they may obviate the need for stabilization procedures for certain cohorts in the CrCL disease spectrum of patients. Certainly, these components should be considered for inclusion as part of a comprehensive management plan for all patients and clients. In conclusion, canine CrCL deficiency is a whole-joint disease, which should be considered organ failure in most affected dogs. Patients with CrCL disease are fighting biological and biomechanical factors that induce and perpetuate osteoarthritis and the clinical signs of pain, lameness, and limb dysfunction.
An unstable joint is thought to initiate cartilage damage and the subsequent degradation and inflammation disease mechanisms characteristic of secondary OA. Whereas biomechanics may be involved, the biology of intra-articular structures, including the metabolism of synovium, adipose tissue, tendon, and ligament, may also contribute to the initiation and progression of OA. Diseased CrCL is one possible contributing factor that is easily removed at the time of surgery. The normal CrCL is intra-articular but extra-synovial so that direct exposure and communication to synovial fluid and other joint tissues does not occur in health. Current evidence suggests that pathology of the synovial lining of the CrCL and exposure of ligament to the joint environment could be early events in canine cruciate disease. This evidence lends further support to the theory that the CrCL may be one of the primary initiators and perpetuators of OA and for this reason CrCL debridement deserves careful consideration as a component of comprehensive treatment. With the introduction of proximal tibial osteotomies (TPLO, TTA) for the treatment of cruciate disease, recommendations have been made to perform small arthrotomies for meniscal release alone, perform arthrotomy or arthroscopy with or without debridement of the CrCL or meniscal release, and avoiding exploration of the joint altogether. Some of these approaches leave the CrCL in the diseased joint and exposed to the intra-articular environment. Whether to provide complete debridement of the CrCL at the time of surgery or to leave the ligament in situ is debated among surgeons because the current best evidence in the literature neither clearly supports nor unequivocally dismisses the need for ligament debridement. Ligament pathogenesis is the complex series of events that change a normal, healthy ligament into a diseased, nonfunctional, and potentially torn ligament. Resulting changes have been evaluated in both the ligament cells as well as extracellular matrix and characterized on molecular, biochemical, histological, and gross levels. Many of the degradative molecules thought to be responsible for ligament pathogenesis are the same molecules that are known to be involved in the initiation and progression of OA. These molecules may have the potential to diffuse from the ligament and synovium into the synovial fluid in sufficient concentrations to contribute substantially to the overall disease process. The amount of matrix metalloproteinases (MMP) released and the time frame of exposure needed to produce disease in the ligament and other joint tissues is not completely understood, but both ligament and synovium appear to be contributors to synovial fluid MMP concentrations. It is very possible that MMP from CrCL could be involved in the initiation of OA in cruciate disease in dogs. There are numerous studies that implicate MMPs in ligament pathogenesis. Collagenases have been identified in CrCL at both the gene and the protein level. Gelatinases have also been characterized in a similar manner as have cathepsins and other related degradative enzymes. If these degradative enzymes can be released when ligament tissue is exposed to the joint environment, then they could play important roles in osteoarthritic processes in addition to enhancing further ligament degeneration. Also, if these molecules contribute to OA, then removal of ligament remnants may ameliorate disease progression. Some studies support the theory that intact and partially torn ligaments left within the stifle joint and exposed to the intrasynovial environment may serve as a nidus of degradation. While it cannot be definitively concluded that ligament is the major intra-articular structure contributing to the release of these enzymes, diseased ligament is, however, one potential contributing factor that can be easily removed through debridement at the time of surgery. This provides some initial evidence supporting complete debridement of the CrCL as a component of comprehensive treatment of cruciate disease in dogs. The variables in favor of debridement include removal of the inflammatory and/or degradative nidus and elimination of ligament nociceptors. Additionally, removal of the ligament improves examination, probing, and access to menisci. The variables against debridement include preservation of ligament mechanoreceptors and proprioceptors, avoidance of morbidity to other joint structures during debridement, and potential maintenance of some CrCL function. The difference observed between normal and intact ligaments suggests that large amounts of MMPs may be produced during the process in which normal ligaments become diseased. CrCL remnants exposed to the intra-articular environment have the potential to release degradative enzymes known to be involved in the initiation and progression of OA and debridement of these remnants as a component of treatment for cruciate disease in dogs deserves consideration. None the less, a separate study evaluating the subjective arthroscopic appearance of CrCL that were left partially intact at the time of surgery in a numerous canine patients treated by tibial plateau leveling osteotomy suggested that CrCL tissue remained visibly intact over a range of postoperative evaluation time points. Additionally, there was a decreased incidence of meniscal injury and articular cartilage damage associated with leaving the ligament intact. Unfortunately, no data regarding the functional capabilities of these CrCL or the status of their cell and matrix composition or activities was provided and all peer-reviewed studies, which have examined these factors, have reported that functional healing does not occur, degradation and degeneration inevitably progress, and that subjective appearance of the CrCL is a poor indicator of disease status. It is obvious, however, from these two studies that additional research needs to be performed before firm recommendations regarding the removal of CrCL remnants can be made. What is known, however, is that CrCL remnants exposed to the intra-articular environment have the potential to release degradative enzymes known to be involved in the initiation and progression of OA and debridement of these remnants as a component of treatment for cruciate disease deserves consideration.
The presence of different tissue types and their superimposition limit successful diagnostic imaging of the stifle joint with a single modality. Radiographic signs of cruciate ligament disease include intraarticular swelling, cranial displacement of the tibia in the mediolateral view with tarsal flexion applied, and in chronic cases, OA changes. The tibial compression stress radiograph has been reported to be useful in the diagnosis of partial CrCL rupture. This radiographic projection requires the stifle to be in 90 degrees of flexion with manual flexional forces applied to the tarsus. Flexion of the hock joint allows the tibia to move cranially, so it can be evaluated with during this stress view.
Ultrasonography is useful for assessing cartilage abnormalities, meniscal tears as well as muscle, tendon, and ligament abnormalities. Diagnosis of CrCL rupture can be made by demonstration of the fluttering edges of the ruptured ligament. If the infrapatellar fat pad obscures observation of the ruptured CrCL, saline solution can be injected into the joint to create an anechoic window. OA changes appear as hyperreflective regions with irregular borders on the bone surface. The entire meniscus, however, is difficult to observe. Normally, the meniscus is inhomogeneous and congruent with the margins of the femoral and tibial condyles. Meniscal injury results in hyperreflective with hyporeflective areas that are irregular in shape and displaced. There are substantial limitations to the routine use of ultrasound in evaluating the stifle joint. Ultrasound images generally have low resolution and soft tissue contrast, which may make other imaging modalities such as MRI more useful.
The major advantages of MRI are its excellent image resolution, superior soft tissue contrast, acquisition of images in any plane, and use of a magnetic field rather than ionizing radiation. MRI evaluation of the internal architecture of the stifle joint affords many advantages over arthroscopy or arthrotomy and is the primary imaging modality when assessing for cruciate, meniscal, and articular pathology in people. Because the stifle is a complex joint with various tissue types, differing image planes and sequences are typically used for complete evaluation. As mentioned previously, CrCL rupture is the most common cause of stifle OA in dogs and is frequently associated with damage to the medial meniscus. Complete evaluation of the menisci is impossible even with arthrotomy or arthroscopy because of anatomic constraints. Using either technique, the tibial surface of the menisci remains hidden from view, as does the integrity of internal meniscal structure. Additional meniscal surgery after surgical stabilization for CrCL deficient stifle joints may be needed because of undiagnosed meniscal pathology at the time of the initial surgery. Therefore, avoiding invasive inspection and handling of unaffected menisci at time of CrCL stabilization probably results in decreased postoperative morbidity, reduced incidence of surgically related complications, and less progression of osteoarthritis. However, missing a meniscal tear has been reported to result in persistent or recurrent lameness after CrCL stabilization, highlighting the need for accurate diagnosis of meniscal integrity at surgery. Because most meniscal tears are treated surgically, any positive MRI finding would result in an invasive intraarticular procedure to confirm the tentative diagnosis and to perform subtotal meniscectomy. Therefore any diagnostic test that replaces invasive inspection of the menisci has to be highly sensitive to reduce the incidence of late meniscal tears, and at the same time it must be of reasonably high specificity, because any false-positively scored meniscus will be inspected surgically, undoing the potential benefit of noninvasive preoperative diagnostics. In a recent study, low field MRI did not reach anticipated diagnostic accuracy for meniscal tears. The primary interest of this study was in evaluating low field MRI as a preoperative, noninvasive screening tool for triage of stifles as affected by meniscal tears requiring further invasive meniscal inspection and probably meniscal surgery and those where meniscal pathology could be excluded, preventing unnecessary invasive procedures. Currently, we cannot recommend low field MRI as a highly sensitive screening tool for meniscal tears in the context of CrCL surgery. Although less expensive and potentially more cost effective, low-field-strength MRI systems suffer from several technical limitations, including long acquisition times, poor signal-to-noise ratio, inability to obtain thin slices, and poor spatial resolution. The trend toward increased magnet strength (at least 3.0 T) to improve signal to noise ratio has continued in veterinary medicine despite increased purchase as well as cryogen and maintenance costs, because of the superior resolution and shorter scan times in an attempt to overcome this diagnostic dilemma.
As mentioned previously, progressive degenerative joint disease may contribute to ligamentous deterioration and precede actual ligament rupture in clinical cases of CrCL rupture in dogs. In both clinical cases and in experimental models of CrCL rupture in dogs, the location of the MRI lesions is typically the intercondylar fossa of the femur and in the intercondylar eminence of the tibia. This is thought to be in part related to abnormal stresses born by the remaining caudal cruciate ligament and subsequent sequellae in the cancellous bone subchondral region associated with its origin and insertion. Early detection of theoretical pre-CrCL rupture lesions by stifle MRI evaluation may therefore afford surgeons an early opportunity to intervene medically before subsequent anticipated CrCL rupture.
With CT technology, images can be manipulated, with a computerized process known as windowing, to reveal various structures based on tissue characteristics. Clinical advantages of using multidetector helical CT scanners include improved patient safety, enhanced accuracy and most strikingly, the ability to perform 3D image reconstructions with the option of creating surgical models to plan surgery for complex cases. In a recent report of CT Arthrography to assess intraarticular structures in dogs with naturally occurring stifle CrCL dysfunction, sensitivities and specificities were 96–100% and 75–100% respectively for the identification of CrCL rupture. In the same report, however, reviewers were less adept at discriminating torn meniscal fibrocartilage, with sensitivities of 13.3–73.3% and specificities of 57.1–100%.
The key to successful management of the diagnostic options available is to have a thorough understanding of the anatomy and tissue properties of region being imaged and to recognize the strengths and weaknesses of the modality being selected. Ultimately, a multimodality approach will likely provide a complete assessment of complex structures using the strengths of each modality to exploit the tissue characteristics of the structure being imaged.
Dogs with CrCL insufficiency frequently sustain damage to the caudal pole of the medial meniscus. Arthroscopy can be considered a highly accurate diagnostic tool, although meniscal tears might be overlooked, especially those that do not reach the surface and those on the tibial side of the menisci. This highlights the importance of thoroughly probing both sides of the menisci when performing arthroscopy. Using a stifle distractor to improve observation and probing of the medial meniscus is believed to further increase diagnostic accuracy.
Historically, total, partial, or segmental meniscectomy has been recommended as treatment for these meniscal tears. Persistent or recurrent lameness after CrCL stabilization has been attributed to meniscal tears missed on direct inspection either using arthrotomy or arthroscopy during joint stabilization and reportedly occurs in 6.3–17.4% of operated stifles. Such tears are referred as latent meniscal tears in contrast to postliminary meniscal tears which are thought to develop despite surgical stabilization of the CrCL deficient stifle. Treatment is directed at removing the torn parts of the meniscus and has an overall good prognosis. However, the additional surgery necessary to perform meniscectomy increases the risk for surgical complications, results in additional owner cost, and delayed treatment of the meniscal tear may lower the overall functional outcome after CrCL stabilization.
Resection of the torn meniscus ameliorates pain and improves short term function; however, meniscectomy accelerates progression of degenerative joint disease in the CrCL deficient stifle. Although total meniscectomy and segmental meniscectomy result in supraphysiologic intra-articular contact pressures and articular cartilage damage, meniscectomies are still commonly performed in dogs. Conservative excision of damaged meniscal tissue by partial meniscectomy when appropriate has been recommended. To preserve meniscal function and mitigate progression of DJD, meniscal tears are often repaired in people. Meniscal repair has been described in dogs but is infrequently performed. Evaluating the ability of meniscal repair to restore meniscal function compared with partial meniscectomy would be important to help determine whether or not meniscal repair should be considered in dogs. Meniscal repair is unlikely to be beneficial if the repaired meniscal parenchyma is degenerate and has lost its internal architecture. Torn meniscal tissue that has lost its normal structure and mechanical function is unlikely to regain normal function. A recent study evaluated the mechanical behavior of meniscal tears in dogs and found that non-reducible bucket handle, flap, and degenerative tears each caused a 45% increase in peak contact pressure (PCP). Although the meniscal parenchyma of degenerative tears and flap tears is macerated, necessitating resection of the damaged tissue, vertical longitudinal tears and bucket handle tears with healthy meniscal tissue may be amenable to repair. Repair of suitable meniscal lesions in people improves joint contact mechanics. It is anticipated that repair of reducible bucket handle tears of the medial meniscus in dogs could restore the biomechanical function of the meniscus. Conserving meniscal tissue would be advantageous because degeneration of femoral and tibial articular cartilage is proportional to the amount of meniscal parenchyma excised.
Unfortunately, the meniscal parenchyma of the axial portion of bucket handle tears in dogs with CrCL insufficiency often has disruption of normal structure and material properties because the meniscus has been damaged from chronic impingement between the femoral and tibial condyles. Crushing of the meniscal parenchyma of bucket handle tears has been shown to result in an increase in PCP. Repair of chronic tears cannot be recommended because the material properties and geometry of the meniscus would be expected to be disrupted in chronic tears. Results from a recent study suggest that meniscal repair be considered for acute meniscal tears. Suture repair in dogs in this study reestablished normal PCP whereas partial meniscectomy caused a 55% increase in PCP. The repair techniques evaluated restored normal contact mechanics to the medial compartment of a stifle with a medial meniscal tear whereas partial meniscectomy caused a 35% decrease in contact area (CA), a 57% increase in mean contact pressure (MCP) and a 55% increase in PCP. Until further mechanical studies are performed on meniscal suture techniques in dog menisci, this particular study recommends a vertical or cruciate suture repair in order to prevent subsequent articular cartilage damage. Additional studies to assess the efficacy of meniscal repairs to alleviate pain and to potentiate successful healing need to be performed. Based on current results, consideration should be given to repairing peripheral tears involving the vascular zone of the meniscus if the parenchyma of the axial portion of the meniscus is normal. Partial meniscectomy should be considered for axially located tears and degenerative tears. Further work is needed to determine the optimal repair technique that should be used clinically in dogs based on fixation strength and ease of application.
Cranial cruciate ligament deficiency in dogs is a common and costly problem for which there are multiple treatment modalities. Whereas numerous techniques have been investigated, none have proven optimal in terms of technical ease, associated costs, prevention of secondary pathology, complication rate, complication types, or mid to long-term outcomes. No one technique for treatment of CrCL deficiency has been shown superior to others in terms of functional outcome. Surgical techniques for correction have focused on intraarticular repair, extraarticular stabilization, or osteotomy of the proximal tibia. In spite of the innumerable studies performed comparing the techniques currently available, none of the techniques have consistently exhibited superiority for clinical efficacy making technique selection the surgeon’s preference.
Technical modifications of the classic lateral suture stabilization (LSS) technique reflect changes in suture material, knotting, and attachment sites. Placing the suture caudal to the lateral fabella and curving distally to a drill hole in the proximal tibial crest has been the established technique but recently, attachment points craniodistal to the fabella and caudoproximal to the tibial tuberosity at the proximal aspect of the tibial plateau have been reported. These modifications are thought to improve suture isometry and thus overall impact on functional outcome after LSS. In addition, when assuming some degree of anisometry regardless of the exact type of LSS performed, loop tension pattern during range of motion might be related to the angle of stifle flexion at the time the suture is tied. In a recent study of LSS attachment sites, results indicated that irrespective of the precise point of lateral suture attachment, substantial changes in suture tension occur during a full range of stifle motion. This change in tension increases significantly with joint flexion. The study also found that tightening the suture with the stifle in 70 degrees of flexion results in the most even tension pattern within the lateral suture loop, but stabilizing the stifle using LSS at a flexed angle would probably allow persistent joint instability, as the suture loop tends to loosen at joint angles between 70 degrees and 160 degrees.
When interpreting tension within a lateral suture used to stabilize the CrCL deficient stifle, two aspects should be considered. First, any disproportionate increase in suture tension would increase the risk of premature suture failure, or if the suture does not fail, stretching of the suture loop might occur. Secondly, very high tension within the suture will probably over-constrain the joint, whereas a substantial loss of tension within the suture will certainly result in some degree of joint instability. For optimal tibial fixation, some studies suggest attaching the suture at a point just caudal or cranial to the digital extensor groove, at the most proximal aspect of the tibial plateau. However, using a bone anchor on the lateral condyle and a divergent drill tunnel just cranial to the digital extensor groove (LSS4) resulted in the highest peak to peak load (PPL) and maximal peak load (MPL) among four techniques recently investigated. Passing the suture around the lateral fabella instead of using a bone anchor at the lateral femoral condyle might allow for some soft tissue movement, potentially reducing high strains within the suture, but relaxation of the fabellofemoral ligament might occur in the long term, resulting in loosening of the LSS and recurrent joint instability. Based on data from this recent study, LSS2 might be the preferred method when attempting to stabilize the stifle with a lateral suture, as this method consistently resulted in the least change in suture tension. Even though LSS2 is only a slight modification of the traditional technique popularized by Flo, omitting the lateral branch of the suture loop may improve isometry. None of the 4 methods studied reached isometry in terms of maintaining a constant tension throughout passive stifle motion, potentially resulting in loss of suture tension at some joint angles with consequent joint instability. There is little information about the precise joint angle at which the suture should be tightened. For any suture fixation that is not isometric, securing the loop at a joint angle when the lateral suture loop is longest will result in the least increase in suture load during range of motion, but may allow some joint laxity during range of motion of the stifle. If the suture is tied at a joint angle when the loop is shortest, tightening will occur during range of motion potentially over-constraining the stifle and promoting early suture break down. Surgical texts mostly recommend tightening the suture at slight flexion of the joint or at a normal standing angle. A survey of veterinary surgeons revealed that 67% positioned the stifle at 140 degrees when the suture was tied, full joint extension was preferred by 19%, and only 5% had the stifle at 90 degrees of flexion, confirming the divergent opinions with regard to which angle might result in the best balance between MPL and maximal negative load (MNL). Clinically, tightening the suture at an angle between 100 and 135 degrees may reduce MPL on joint flexion, potentially limiting stretch of the suture-knot construct and therefore early destabilization of the joint. At the same time, this angle would preserve most of the tension within the suture when extending the joint. In summary, both the angle of flexion chosen while tightening the suture as well as the suture attachment sites when performing LSS changes the pattern of tension within the suture throughout a full range of stifle motion. However, regardless of LSS technique, a significant increase in suture tension occurs on flexion of the joint increasing the risk of suture breakage and irreversible stretch. This unwanted peak in tension on flexion of the joint might be reduced when tightening the lateral suture in a greater degree of extension.
Lateral suture stabilization (LSS) techniques performed in stifles using an 80 lb nylon leader line and a custom made crimp. (A) Traditional technique according to Flo (LSS1); (B) modification of LSS1 with 2 parallel drill holes at the tibial crest (LSS2); (C) distal attachment of the suture through 2 divergent drill tunnels at the Gerdy’s tubercle (LSS3); and (D) distal attachment at the Gerdy’s tubercle. Proximal attachment with a bone anchor placed into the caudolateral cortex of the lateral femoral condyle, at the level of the distal pole of the lateral fabella (LSS4).
In an attempt to further refine LSS techniques, an extracapsular suture stabilization technique called the TightRope CrCL technique (TR), was developed in an attempt to address perceived shortcomings of the current techniques, and to specifically incur minimal morbidity, address all aspects of CrCL deficiency, allow for repeatable placement in the most isometric position possible, and consistently result in successful functional outcomes with low overall and major complication rates in a cost effective manner. The TR CrCL extra-articular stabilization technique was developed to provide bone-to-bone fixation of the prostheses using a stiff prosthetic material. Femoral and tibial bone tunnels are used to place a fiber tape prosthesis across the lateral aspect of the stifle. The suture is anchored to the femur and tibia using toggle buttons placed at the medial orifices of the bone tunnels.
The primary stimulus for development of the TR technique was patient safety, specifically low morbidity as well as rate and severity of complications. Some studies have indicated that tibial osteotomy procedures (TPLO, TTA) are associated with higher and more severe complications in dogs undergoing surgery for CrCL deficiency when compared to other techniques. In a recent study comparing TPLO to TR, TPLO was associated with numerically higher major and total complication rates compared with TR, but these differences were not statistically significant. However, surgery and anesthesia times were significantly shorter for TR compared with TPLO, which is consistently associated with lower morbidity. The other preclinical aspect of the development of the TR technique was comparative mechanical testing. In this study, the TR device proved superior for all variables examined. The biomaterial used for the TR procedure is a Kevlar-like material which is currently used extensively in the human field for many orthopedic applications. This material has properties that make it stronger and less prone to failure than any other suture materials currently being used in LSS CrCl reconstructions. These superior mechanical properties combined with the theoretical advantages of bone tunnel fixation in both femur and tibia suggest that the TR technique may have potential advantages with respect to stifle stability and joint kinematics during formation of periarticular fibrosis compared with LSS techniques which rely on soft tissue fixation or point-fixation. However, clinical comparisons among LSS extracapsular techniques or in vivo assessment of joint kinematics after any of the surgical techniques used to address CrCL deficiency has yet to be performed. These data from this study suggest that the TR CrCL technique can be successfully performed in medium, large, and giant breed dogs with CrCL deficiency and result in 6-month outcomes which are not different than TPLO in terms of degree and level of pain and function, as well as subjective assessment of radiographic progression of OA. Duration of anesthesia and surgery was less for TR than TPLO and major and overall complication rates were lower for TR compared with TPLO. The TR technique is safe and effective and can be considered as a viable choice as part of the overall treatment plan for CrCL deficiency in dogs. The technical aspects of TR were a major consideration for clinical application from its inception. The toggle fixation mechanism and the use of guide wires placed using consistent anatomic landmarks followed by cannulated drilling allow the TR device to be safely placed such that the functional fixation points are in locations similar to those determined most isometric for the lateral aspect of the canine stifle based on radiographic assessment.
Figure 1 Illustrations of a canine stifle with the TightRope CCL implant positioned and viewed from the cranial (A) and lateral (B) aspects. T, tubercle of insertion of the biceps tendon/iliotibial band (tubercle of Gerdy); L, tendon of origin of the long digital extensor muscle.
Despite widespread use of LSS stabilization in dogs, only a few studies have evaluated the biomechanical effects of this procedure. It would be important to define contact mechanics in stifle joints after LSS stabilization to understand and refine surgical treatment of CrCL insufficiency in dogs. Tension placed on anterior cruciate ligament grafts in people is widely accepted to be an important biomechanical factor influencing procedure success. Excessive tension can cause premature failure of the prosthesis, whereas insufficient tension may not provide adequate joint stability. Appropriate suture tension should neutralize cranial tibial thrust while allowing a normal range of motion, and restore normal kinematics and contact mechanics to the CrCL-deficient stifle. Results of a recent study confirmed that over tightening an extra-articular prosthesis when performing either TR or LSS stabilization technique increased lateral compartment pressures in the stifle joint, but lateral compartment pressure normalized when an axial load was applied to the joint. Nevertheless, the significant increase in contact pressure at higher suture tensions tested in the unloaded stifles would suggest excessive tightening of an extra-capsular prosthesis might result in elevated contact pressures during the early convalescent period after surgery, when dogs typically place limited weight on the affected hind limb. Early weight bearing after extra-articular stabilization of the CrCL deficient stifle may be important to resolve abnormalities in contact mechanics and kinematics, which were evident in this study. That study also established that extra-articular stabilization induced significant excessive external rotation of the tibia. It is likely that any extra-articular reconstruction technique causes malalignment of the femorotibial joint which may be mitigated during loading the stifle; however, an in vivo kinematic analysis would be needed to confirm that stifle alignment would return to normal with weight bearing. Ideally a prosthesis mimicking the CrCL should be secured at isometric locations, so that the distance between points of attachment remains constant as the stifle moves through a range of motion. Isometry of suture placement would prevent laxity or over constraint of the joint at different flexion angles. However, an extra-capsular prosthesis can never be truly isometric because the stifle does not function as a pure hinge joint. Tightening an extra-articular prosthesis in an effort to stabilize the joint eliminates the normal motion of the femur and tibia. In addition, alterations in the instant center of rotation may change the direction of surface velocity, causing compression of the joint surfaces at their point of contact. Results of this study substantiate that excessive tensioning of the extra-articular prosthesis is detrimental to lateral compartment contact pressures. The non-isometric placement of prostheses, such as in the LSS or TR techniques, could result in excessive or ineffective prosthesis tension at different joint angles. Ligament prostheses are high load-bearing structures that are subjected to impact loading. High loads caused by excessive postoperative activity, or severe joint instability may predispose to early elongation of the prosthesis. An over-tightened prosthesis cyclically loaded outside the range of its tolerance may loosen with weight bearing and have no impact on lateral contact pressures. Many variables such as variations in weight bearing, degree of periarticular fibrosis, stifle conformation, presence of meniscal pathology and meniscal treatment, body weight, and activity level would influence the cycling of an extra-articular prosthesis. In summary, over tightening of an extra-articular prosthesis, regardless of technique, can increase lateral compartment contact pressures when the stifle is unloaded. The optimal tension for TR and LSS is difficult if not impossible to define because of the many mechanical and biologic factors that may influence the effects and properties of the tensioned suture. None the less, tensioning an extra-articular prosthesis should be done cautiously. This finding is supported by a previous study that found that dogs that had satisfactory limb function after LSS had more cranial drawer motion and a greater range of motion than dogs that did poorly. In this study, the effect of tension was eliminated by axial load, suggesting that early weight bearing may mitigate abnormalities in contact pressures caused by excessive tension of an extraarticular prosthesis.
Increasing interest has emerged in use of tibial osteotomies for treatment of cranial cruciate ligament insufficiency in dogs. Rupture of the CrCL causes stifle instability, which predisposes the meniscus to injury and the stifle to degenerative joint disease. Loss of integrity of the CrCL results in an unrestricted cranial femorotibial shear force causing tibial subluxation during weight bearing. Tibial osteotomies impart dynamic stability by altering the geometry of the stifle and thereby neutralizing the cranial femorotibial shear force. Dynamic stability can be achieved by decreasing the slope of the tibial plateau or by advancing the tibial tuberosity. Tibial plateau leveling osteotomy (TPLO) imparts craniocaudal stability by reducing the tibial plateau angle (TPA), whereas tibial tuberosity advancement (TTA) eliminates cranial tibial thrust by advancing the insertion of the patellar tendon and modifying the angle between the medial tibial plateau and the patellar tendon, which defines the patellar tendon angle (PTA). Despite widespread use of these osteotomy techniques, a perspective of how they affect both TPA and PTA has not been established. In 1983, Slocum described the internally generated femorotibial shear force that causes cranial tibial translation as cranial tibial thrust. Slocum’s theory suggests that the magnitude of cranial tibial thrust is dependent upon the angle between the tibial plateau and the joint compressive force, which was purportedly directed parallel to the tibial axis. Slocum proposed that the tibiofemoral shear force or CrTT was an internally generated force that caused the tibia to translate cranially (and is opposed by the CrCL). Slocum proposed that the CrTT in the normal stifle joint was primarily controlled by the caudally directed forces of the hamstring muscles. In this theory, the compressive forces across stifle joint were proposed to be parallel to the tibial axis, but because of the caudally directed TPS, compression between the joint surfaces resulted in cranial tibial translation. This theory was developed as the active model of the stifle; CrTT is created by compression between the femur and tibia, which acts through the functional axis of the tibia, and is dependent upon the amount of compression and the TPS. Axial compression of the limb is thought to generate a compressive force across the joint, and this resultant force can be reduced to 2 orthogonal components, one perpendicular and one parallel to the tibial plateau, the latter representing the CrTT . The CrTT is a result of the tibial plateau oriented at an angle to the axial compressive force. If the angle of the tibial plateau is reduced to zero, the joint compressive force and resultant force become the same, as the CrTT becomes zero, as this force vector is eliminated. Clinically, however, the plateau is not returned to 0 degrees, but has approximately 5 degrees of remaining slope. This concept relies on the hamstring muscles, which contribute to neutralizing this small remaining force. More recently, some researchers have suggested that the sum of the forces acting around a weightbearing stifle is directed parallel to the patellar tendon. Cranial tibial thrust, according to this model, is thus dependent on PTA. This model demonstrated that the tibiofemoral compressive force was approximately of the same magnitude, and oriented in the same direction, as the patellar tendon force, which resulted in a variable tibiofemoral shear force. This force was either anteriorly or posteriorly directed dependent upon the angle of knee joint extension or flexion, respectively. The point of neutral tibiofemoral shear force was termed the crossover point in this model, which occurred at a patellar tendon angle (angle between the tibial plateau and the patellar tendon; PTA) of 90 degrees. Therefore, it was proposed that the direction and magnitude of the tibiofemoral shear force was determined by the PTA. Methods for measuring PTA have been reported using anatomic landmarks of the plateau segment (PTATP) or by estimating a tangent to the femoral and tibial condyles at their point of contact (PTACT). The method using the common tangent is stated to be more accurate because it estimates the inclination of the tibial plateau at the contact point between the femoral and tibial condyles. The common tangent is an estimation of the inclination of the plateau at the point of articulation between femur and tibia. Factors that may influence PTACT include the point of contact of the femoral condyle relative to the tibial plateau as well as the surface geometry of the plateau, which are ignored when making TPA measurements. Previous theoretical analysis demonstrated the importance of the radius of curvature of the tibial plateau in predicting forces along the cruciate ligaments. As previously suggested, PTACT may be a better measure for pre-operative planning of tibial osteotomies. Further clinical studies are needed, however, to evaluate the applicability and repeatability of using the PTACT to determine plateau rotation during TPLO, and to determine if TPLO rotation based solely on the PTACT will yield functional stability.
Schematic representation of the tibiofemoral forces in the stifle joint, according to Slocum, before (A) and after (B)
tibial plateau leveling osteotomy (TPLO). The resultant compressive force (large white arrow) across stifle joint is parallel to the tibial axis. Using the tibial plateau slope (TPS) as the baseline, whereby the femur can move along this surface if the cranial cruciate ligament (CrCL) is deficient, the resultant force can be broken down into its 2 orthogonal components (small shaded arrows), one perpendicular and one parallel to the tibial plateau. The latter represents the tibiofemoral shear force (resulting in cranial tibial thrust [CrTT]). If the angle of the tibial plateau is reduced to zero, the tibiofemoral shear force vector becomes zero, and the joint compressive force and resultant force become one and the same.
The CrCL-deficient stifle is stabilized at a PTA of 90 degrees achieved with TTA when the stifle is positioned at a standing flexion angle of 135 degrees. This model takes into consideration both extensor mechanism anatomy and the geometry of the articulating surfaces of the stifle and therefore differs from Slocum’s theory in that the direction of the joint reaction force is dependent on the inclination of the patellar tendon. The primary difference between the 2 proposed mechanisms is the direction of the tibiofemoral compressive force. With TPLO, the force is proposed to be parallel with the tibial long axis, whereas with TTA it is proposed to be parallel to the patellar tendon. Variations in morphology of the proximal aspect of the tibia, and specifically patellar tendon insertion angle, may be relevant for preoperative planning of tibial osteotomies. Recently, it has been suggested that the proposed theoretical mechanism of action of the TTA can also be used to explain the mechanism of action for TPLO. Understanding how TPLO affects both TPA and PTA may provide insight about the mechanism of action of TPLO. In a recent study, the planning of TPLO rotation using the preoperative TPA or PTATP would have resulted in similar magnitude of plateau rotation. Variations in tibial tuberosity morphology in certain breeds, such as chondrodystrophic dogs, however, could influence the surgical planning of plateau rotation based on PTA. In addition, this study indicated that a PTACT of 90 degrees is achieved at a TPA of 12 degrees with the stifle in 135 degrees of flexion. This finding may help to explain the observation that dogs with TPA less than or equal to 14 degrees after TPLO had clinically acceptable results. Based on the calculation of PTACT, the point where the femorotibial shear force is neutralized corresponds to a plateau rotation lower than previously recommended. This result would support the speculation that TPLO to a TPA of 6 degrees overcorrects the cranial tibial thrust because of excessive rotation. The excessive rotation may explain the abnormal femorotibial contact mechanics that results after TPLO which may predispose to osteoarthritis. Performing TPLO rotations based on calculations using PTACT might result in less plateau rotation and mitigate the adverse alterations in femorotibial contact pressures previously reported.
Schematic representation in the stifle joint of the tibiofemoral forces before (A) and after (B) tibial tuberosity advancement (TTA). The resultant compressive force (large white arrow) across stifle joint is parallel to the patellar tendon. Using the tibial plateau slope (TPS) as the baseline, whereby the femur can move along this surface if the cranial cruciate ligament (CrCL) is deficient, the resultant force can be broken down into its 2 orthogonal components (small shaded arrows), one perpendicular and one parallel to the tibial plateau. The latter represents the tibiofemoral shear force (resulting in cranial tibial thrust [CrTT]). If the angle of the tibial tuberosity is advanced cranially until the patellar tendon angle (PTA, angle between the tibial plateau and the patellar tendon) is reduced to 90 degrees, the tibiofemoral shear force vector becomes zero, and the joint compressive force and resultant force become one and the same.
Presence and progression of radiographic changes of OA in the stifle joint of the CrCL deficient dog has been reported after conservative treatment and after extracapsular or intracapsular substitution techniques, TPLO, and TTA. Radiographic soft tissue changes include joint effusion/capsular thickening, lateral and medial soft tissue thickening, intraarticular osseous fragments, and meniscal mineralization. Bony changes include osteophytosis and enthesiophytosis, subchondral sclerosis, subchondral cyst formation, and joint space narrowing, generally placing emphasis on presence and growth of marginal osteophytes. Patellar ligament thickening and patellar tendinosis have also been observed. Surgical techniques that change the geometry of the proximal aspect of the tibia, such as TPLO and TTA were specifically developed to restore functional stability of the stifle, prevent deterioration of the medial meniscus, and reduce the degree of secondary OA in the stifle joint with CrCL rupture. The initial hope that progression of OA could be minimized using these techniques has not been consistently realized. Whereas progression of OA is less in dogs after TPLO and TTA than after extracapsular stabilization, in general, progression of OA has been observed after both TPLO and TTA. Several studies have reported or suggested a lack of significant correlation between the radiographic appearance of OA and clinical evaluation of limb function. A recent study evaluating the presence of OA and limb function found that limb function, characterized by force plate analysis, improved markedly after TPLO and TTA in spite of the fact that OA characterized by bony changes progressed in approximately 55% of the treated stifles. The degree of radiographically visible OA and the progression of bone and soft tissues changes after TPLO or TTA did not correlate with functional outcome assessed by ground reaction forces. Therefore, radiographic scoring systems may not necessarily reflect the true severity of OA. Historically, much emphasis has been placed on the presence and degree of osteophytosis in evaluation of the clinical status of canine joints and the presence and progression of OA has been suggested as a true test of the value of the treatment of the injured CrCL. For this reason, control of OA has been listed as one of the primary surgical goals of repair of CrCL injury. However, achieving this goal remains elusive and this and many other reports note progression of OA after stabilization despite an acceptable clinical outcome.
Despite the differences in proposed mechanisms of action, clinical results appear comparable between TPLO and TTA. As previously mentioned, an argument could be made that the proposed mechanism of action for TTA can also explain the mechanism for TPLO. This can be observed after reduction of TPA via radial osteotomy and rotation of the proximal tibial fragment, as this also reorients the patellar tendon angle to less than or equal to 90 degrees. Obviously, different techniques are used to approach this mechanism from 2 different perspectives: (1) a radial cut of the proximal tibial plateau segment for TPLO, and (2) an osteotomy of the tibial crest performed in the frontal plane for TTA. For TPLO, the tibial plateau is moved to meet the force; alternatively, for TTA, the force is moved to meet the tibial plateau. In either case, it appears that the end result is the same: the tibial plateau and the patellar tendon become oriented at approximately 90 degrees to each other.
Success rates with CrCL repair are reported to be greater than 90% regardless of the surgical technique used. Historically, selection of a surgical technique has been based primarily on surgeon preference rather than definitive evidence that one technique might be better than another. Unfortunately, there is no study that demonstrates that TPLO is a better procedure than, for example, the extra-capsular stabilization; this despite much anecdotal opinion that the TPLO is a superior technique, especially for active, athletic dogs. Likewise, there are no data for functional evaluation of TTA other than similar anecdotal evidence that it is an effective technique in similar types of affected dogs. There are no peer-reviewed reports comparing the outcome of TPLO to TTA; however, anecdotal comments have been presented. The question that is raised is whether one or the other of these techniques (TPLO or TTA) might be a better choice for repair of the CrCL-deficient stifle joint, and if so, under what conditions would one choice perhaps be better than the other.
If it is accepted that tibiofemoral shear force is dependent upon the PTA (for either technique), then altering the direction of the patellar tendon force is the mechanism for obtaining dynamic joint stability. Based upon the proposed directions of the total joint force, either parallel to the patellar tendon (TTA) or to the functional axis of the tibia (TPLO), there may be a difference of as much as 10–15 degrees in endpoint after surgery. Based on this argument, it would appear that the TPLO overcorrects for the cross-over point compared with TTA. This proposed difference between the 2 techniques might be less than 10–15 degrees because of the craniocaudal translation of the femoral condyles and the contact point with the tibia during flexion/extension. During extension, the femorotibial contact point moves cranially; similarly, during flexion, it moves caudally. The effect of this varied positioning is yet to be evaluated, but a suggestion has been made that it should be considered when assessing the joint forces. These anatomic changes further minimize the difference between the calculated endpoints between the 2 techniques, perhaps only 5–10 degrees. The difference in endpoints after surgery raises the question as to whether it has any potential adverse effects. Because the primary stabilizer of the joint becomes the CaCL after either TPLO or TTA, could this theoretical difference put the CaCL at greater risk for subsequent injury with TPLO? It has been reported that the CaCL undergoes marked morphologic changes in CrCL-deficient joints, which may result in compromised material properties. Regardless, there is no clinical evidence that the CaCL is at risk for failure after either TPLO or TTA. There is only anecdotal information as to the risk to the CaCL with over-rotation of the tibial plateau with TPLO. From a theoretical standpoint, TTA would be correcting the tibiofemoral shear force closer to a neutral tibiofemoral shear force at full extension (approximately 135 degrees) during weight bearing, thus there may be less stress placed on the CaCL. It should be mentioned, however, that there is still no documentation as to the ideal point at which tibiofemoral shear is neutralized with either TPLO or TTA, and which of these techniques comes closer to this theoretical point. More information is needed about the possible risks to the CaCL over time, especially in its new role as the primary stabilizer to the joint.
Another point to consider is whether or not an anatomic alteration of the tibial plateau angle when performing a TPLO makes a functional difference with regards to altering the gait and/or placing additional stress upon the menisci because of this change in joint orientation. The tibial plateau remains unaltered with TTA, whereas with TPLO, the tibial plateau is effectively placing the joint in approximately 15–20 degrees of increased flexion. Based upon kinematic gait analysis, stifle and hock mechanics remain unaltered with TPLO during weight bearing; however, some changes can be seen in the swing phase of the gait. Therefore, gait seems to be unaltered with TPLO, assuming that the alterations observed in the swing phase have no functional or clinical ramifications. This assumption appears to be reasonable based upon the absence of weight bearing during this time frame. It has been theorized that because TTA does not alter the orientation of the articular surfaces, there would be no effect on gait; however, to date there has been no similar evaluation of gait with kinematics. Any alteration of the point of insertion of the patellar tendon into the tibia and any effect on gait mechanics remain to be investigated. After TPLO, the femoral and tibial articular surfaces are placed in a relatively increased flexed position. Altered flexion of these surfaces during weight bearing results in changes in the pressure distribution to the caudal compartments of the joint (medial greater than lateral), possibly affecting the menisci (especially the medial meniscus); this altered positioning may also reduce the space for the meniscus. Both factors may place the meniscus at a greater risk for injury. This was the rationale to perform a medial meniscal release when performing a TPLO. More recently, however, it also has been shown that performing the meniscal release, or caudal pole hemimeniscectomy, in a CrCL-deficient stifle joint with a TPLO further changes and increases the pressure distribution in the medial compartment of the joint, an argument that would perhaps favor leaving the meniscus intact. Although there is no evidence that the increased stifle joint flexion predisposes the menisci to damage, it was proposed that TTA might provide less risk for such damage because of the unaltered joint position. This led to the original recommendation to leave the intact menisci in situ when performing TTA. To summarize, some studies seem to suggest that the caudal pole of the medial meniscus is at risk for trauma after TPLO, whereas not after TTA because the TTA does not change the geometry of the joint and the pressure distributions essentially remain unchanged. Debate remains as to whether or not to perform a medial meniscal release in both TPLO and TTA.
An important argument to preserve the menisci has to do with the important biomechanical functions of the meniscus and the role of this structure to stabilize the joint. The meniscus functions as a load-bearing structure to distribute the femoral condyle forces more uniformly over the tibial plateau. Meniscal release eliminates this function and results in increased areas of localized stress to the articular cartilage. As previously noted, there are studies that indicate that preserving the meniscus with either TPLO or TTA better preserves joint mechanics in the CrCL-deficient stifle joint and these studies suggest leaving the meniscus intact if it is uninjured. Alternatively, as the meniscus acts as a secondary joint stabilizer in the CrCL-deficient joint, with any persistent passive laxity the caudal pole of the meniscus may be more easily injured with a failure to fully neutralize the tibiofemoral shear forces. Sparing this structure from injury by performing a meniscal release has been suggested. However, it has also been noted that performing a meniscal release does not completely eliminate the possibility of subsequent meniscal tears. It has been reported that after TPLO with meniscal release, there is cartilage damage present on the tibial plateau and medial femoral condyle, confirming that subsequent articular cartilage damage does occur. These changes have been attributed to both iatrogenic surgical injury when performing the meniscal release as well as to loss of normal meniscal function. However, it has also been stated that there is little outward evidence of clinical dysfunction as a result of these changes, which is consistent with most clinical impressions. Despite the progressive effects of osteoarthritis in these dogs, clinical dysfunction is considered minor as opposed to that occurring with an injured meniscus; therefore, this argument supports the meniscal release in favor of possible future meniscal impingement. The question is the unknown frequency of meniscal injury at initial surgery, and the number of undetected tears at that time as opposed to tears occurring after surgery. These meniscal injuries have been defined as either latent (undetected) or postliminary (subsequent) tears. A recent study evaluating the rates of meniscal injuries in a consecutive series of 1000 dogs receiving TPLO surgeries indicated an incidence of primary meniscal injury (PMI) of 33.2%, and subsequent meniscal injury (SMI) of 2.8%. In this study, complete CrCL rupture was associated with higher incidence of PMI than partial CrCL rupture as previously reported. This supports a mechanically protective effect of the remaining portion of CrCL in partial tears. Meniscal release was not performed for menisci of normal appearance and texture in this case series because it was considered that the relative risk of SMI was more acceptable than potentially subjecting all dogs to more severe focal cartilage wear that might be anticipated after MMR or partial meniscal resection. Many recent studies have independently confirmed that medial meniscal release eliminates the function of a crucial articular structure and therefore is in contradiction with the principles of surgical stabilization of CrCL deficient stifles as it is likely that a combination of inflammatory and degradative mediators originating from the transected meniscus and biomechanical abnormalities from the surgically induced loss of meniscal function play a key role in the development of cartilage degeneration after MMR.
There is also the question as to whether the altered anatomy created by either of the procedures could result in other anatomic or functional changes within the joint. There have been a number of reports of patellar tendon thickening, or even patellar tendinitis after TPLO. It has been proposed that by rotating the tibial plateau, greater stress is placed on the patellar tendon compared with decreased stress to this structure after performing a TTA. The proposed increased stress (TPLO) versus decreased stress (TTA) on the patellar tendon can theoretically be explained by the change in lever-arm lengths to the patellar tendon after the osteotomies. If one considers that the CaCL becomes the primary stabilizer to the joint after either TPLO or TTA, the lever arm to the patellar tendon is the distance between the femorotibial contact point to the point of attachment of the patellar tendon to the tibial tuberosity. For TPLO, it is thought that this lever arm can shorten by as much as 10% compared with the intact joint, whereas, with TTA this lever arm can lengthen by as much as 10%. A shorter lever arm requires more force to move an object the same distance; conversely, a longer lever arm requires less force to similarly move an object. In this case, the object is the tibial tuberosity and the force is the quadriceps muscle pull on the patellar tendon. In other words, more force is required to extend the joint with a TPLO, and less force is required with a TTA. Regardless, there are no known clinical ramifications in dogs with mild to moderate patellar tendon thickening after TPLO, although a small percentage of dogs with severe patellar thickening have clinical signs consistent with patellar tendinitis. Regardless, there are no specific studies that have investigated this issue, clinically or experimentally, much less comparing the different techniques and their potential ramifications.
Both the TPLO and TTA are complex procedures, requiring appropriate preplanning and accurate execution of the details of the procedure. Preoperative planning for the TPLO must include a proper assessment of the angle of the TPS, such that precise surgical execution results in the desired postoperative TPA of 5-6.5 degrees. Preoperative planning for a TTA must include a proper assessment to ensure that advancement of the tibial tuberosity results in a PTA of 90 degrees. It is suggested that there is some variability in the postoperative outcomes with the TPLO and TTA despite an attempt to obtain precise preoperative measurements. With both TPLO and TTA, there probably is some amount of postoperative variability that will be tolerated, but the ideal clinical postoperative PTA or TPS is unknown.
As described, TPLO is a relatively invasive procedure where there is abundant circumferential dissection of the entire proximal aspect of the tibia, and a greater potential for injuring some vital structures around the joint. The substantial soft tissue dissection and limited coverage in the area of the proximal tibia may contribute to dead space and may predispose dogs to incisional complications. In addition, there are a number of surgical technical errors that can occur with TPLO. Placing the osteotomy too far cranial and/or distal will result in a higher than expected TPA postoperatively, and inadequate neutralization of the CrTT. Such malposition of the osteotomy also results in a small tibial tuberosity fragment, creating the possibility of a tibial tuberosity fracture. Placing the temporary holding pins (after initial rotation of the tibial plateau) too far distally into the tibial tuberosity may result in a stress-riser in this fragment, again predisposing this bone to fracture. Fibular fractures can result in excessive stresses placed on this structure during the rotation, or may occur as a result of stress-risers from drill holes into this structure.
The TTA is considered by many to be a simpler procedure than the TPLO. Similar comments regarding soft tissue dissection and limited coverage in the area of the proximal tibia may be made for TTA; however, the surgical dissection is confined to the cranial portion of the bone. There is much more limited possibility for iatrogenic surgical injury with TTA, but damage to the long digital extensor tendon is one potential consequence. There are a number of surgical technical errors that can occur with TTA. These issues include too small of an osteotomy fragment, shifting the patella distally, or predisposing to a patellar luxation with improper tibial tuberosity repositioning. A small osteotomy fragment does not allow adequate fork purchase as there is insufficient bone available. Another potential error is patellar malposition. Patellar luxation can result if attention is not paid to the plate contouring, ensuring that the tibial tuberosity is advanced cranially without changing the orientation within the sagittal plane. Any shift either medially or laterally could result in a malalignment of the quadriceps mechanism, and thus the resultant patellar luxation. Other issues may include poor plate position, either rostrally along the tibial crest or distally along the tibial diaphysis. When comparing TPLO to TTA, the difference in implants could be considered: commercially pure titanium is the norm with TTA versus stainless steel with TPLO. Pure titanium is touted as a more biocompatible implant with tissues as compared with stainless steel. Furthermore, the plate profile with TTA is very thin and provides less overall bulk in a position on the limb where soft tissue covering is limited to a thin muscle layer and skin. This may play a role in limiting soft tissue complications. The use of locking screw technology compared with conventional screw technology in TPLO has recently been investigated. A distinct advantage of locking screws is their ability to function as an internal fixator and maintain accurate osteotomy reduction without having a perfectly contoured plate. With conventional screws, if the plate is not accurately contoured at the time of screw placement, osteotomy reduction can be disrupted as the screws are tightened to achieve bone–plate friction. Less initial tibial plateau disruption has been reported with locking screws compared with conventional screws. Locking screws better maintain initial rotation of the tibial plateau segment if small gaps occurred between bone and plate. According to this study, locking screw technology resulted in improved radiographic healing and TPA was better conserved when compared with similar fixation using conventional screw technology.
Some factors specific to the anatomic configuration of the limbs being operated need to be considered, from the standpoint of conformational issues that would make one procedure perhaps the better choice than the other. These include angular and torsional limb deformities, patellar luxation, and excessive TPS. Furthermore, the size of the dog may also play a factor. When performing a TPLO, rotation of the tibial plateau segment only to the level of the patellar tendon insertion on the tibial tuberosity has been suggested to ensure its role as a buttress support for the tibial tuberosity segment. Therefore, dogs with high patellar tendon insertion point would run the risk of the rotation of the tibial plateau segment to a point below the patellar tendon insertion, thus potentially leaving the tibial tuberosity more prone to fracture because of an absence of buttress support. Alternatively, in dogs with a low patellar tendon insertion point, much greater rotation could be obtained while continuing to preserve the caudal buttress behind the tibial tuberosity. In contrast, the tibial tuberosity may be at more risk for possible fracture with TTA in cases with a low patellar tendon insertion point, as a smaller plate is applied to the tibial crest and the usual position of the interspersed cage is above the most proximal position of the plate with little bone present for support. In dogs with a high insertion point, a larger TTA plate can be applied to the tibial crest, and the interspersed cage is placed within the gap, which remains buttressed with adequate bone and a larger plate that disperses all the forces to the tibial crest. It is suggested that cases with a high patellar tendon insertion point are more conducive to a TTA, whereas cases with a low patellar tendon insertion point are better suited for a TPLO. In any case, there are no experimental or clinical studies reported that support these assumptions.
Cases where there is excessive TPS are not conducive to TTA, because the procedure requires that the advancement produce a PTA of 90 degrees, which likely would result in a required amount of advancement beyond that obtained with the currently available implants. Additionally, there is a conformational deformity of the joint with excessive TPS that places it in a relative angle of hyperextension despite the limb itself not being in the extended position. TTA does not address this malformation, whereas the TPLO can correct it. The question remains, however, as to the maximal angle of the TPS that should be used as a guideline to consider whether to perform a TTA, although it has been proposed that angles greater than 27 degrees probably are not well suited for a TTA.
Angular and torsional limb deformities may be treated with either TPLO or TTA; however, TPLO may be better suited to make these corrections simultaneous with the rotational osteotomy. The concept of modification of tibial plateau leveling osteotomy as a widely recognized management modality for canine CrCL insufficiency to include simultaneous correction of frontal plane deformity and/or torsional deformity of the tibia has been previously introduced. Such modifications are routinely used in dogs with preoperative tibial deformity in order to prevent subsequent development of postoperative gait abnormality or exacerbation of limb deformity during the TPLO procedure when the medial cortex of the calcaneus and the central patellar axis are not collinear in the sagittal plane. With minor angulation or rotation, these deformities can be addressed after rotation of the proximal tibial fragment, after it has been temporarily secured with a pin or K-wire, and before plate fixation. At this point in the procedure, an angular correction (stifle varus or valgus) can be performed by shifting the jig position along either the proximal or distal jig pin (a translation of the jig along the pin) so as to obtain limb realignment. Similarly, a rotational correction can be performed by bending one of the jig pins (usually the distal pin) while the jig is securely fixed to these pins. A recent study successfully utilized a TPLO with a medial opening crescentic osteotomy (TPLMOCO) in dogs with genu varum attributable to proximal tibia vara and/or tibial torsion. If a TTA was performed to correct the CrCL-deficient joint, a separate osteotomy would still be required. The disadvantage is that the medial side of the bone already has the plate positioned for TTA in the proximal one third of the medial tibial surface, which will interfere with subsequent additional medial plate fixation. Although a standard plate could be applied over the thin TTA plate, this is far from ideal and generally not recommended.
Patellar luxation requiring tibial tuberosity transposition, on the other hand, may be better suited for a TTA, as any desired transposition could be simultaneously performed with the advancement. In this case, the TTA plate is slightly over-bent to conform to the new laterally (or medially) transposed tibial crest. The limitation with the tibial tuberosity transposition and TTA, however, would be cases of patellar luxation that also had a significant angular/torsional deformity that also needed to be corrected at the same time. In the latter instance, TPLO would again be the better choice. In this instance, if there was a simultaneous rotational deformity this correction could result in appropriate alignment of the tibial tuberosity after the repositioning.
Both TPLO and TTA have been performed in dogs as small as 5 kg and as large as 92 kg. Size limitation for these techniques is dependent upon the availability of the appropriately sized implants. Both devices are produced in a variety of sizes such that they can accommodate almost any sized dog. One current limitation of the TTA may be the large distance of TTA that is required for some large breeds of dogs (not necessarily the heavier dogs, but rather the taller dogs, e.g., Great Danes). The widest cage currently available to support the osteotomy gap is 12mm. Whereas the cage can be moved further distally to increase the width of the gap, this must be done judiciously, as the tibial tuberosity above the cage may become prone to fracture because of a large stress-riser created above the cage.
Early diagnosis of a CrCL injury and treatment by either TPLO or TTA may be protective against further CrCL disruption lending stability to the joint and decreasing the incidence of meniscal injury and articular cartilage damage. One study has indicated that in joints where initially there was only partial CrCL tear with most of the CrCL appearing normal, that the CrCL remained intact after TPLO and the intraarticular structures appeared normal or near normal. By contrast, joints that initially had either complete disruption or a partial tear with the remaining CrCL judged incompetent developed a range of pathologic changes including mild fraying or complete rupture of the caudal cruciate ligament, postliminary bucket handle tears of the caudal horn of the medial meniscus and visible cartilage lesions. These findings suggest that TPLO has a protective effect on injured CrCL when there is some initial fiber disruption but most of the CrCL is intact and appears functional. The protective effect may result from decreased stress on the CrCL after rotation of the tibial plateau and subsequent transformation of cranial tibial thrust to a caudal tibial thrust. The elimination of cranial tibial thrust would likely lower strain within the CrCL reducing the possibility of further fiber tearing. As the remaining CrCL maintains the relationship of the femoral condyles relative to the tibial plateau, i.e., centers the femoral condyles within the confines of the menisci, the effect is a decreased incidence of meniscal injury and articular cartilage damage. These findings support the notion of early surgical intervention for cruciate ligament disease and against debridement of CrCL fibers in early injuries because of good functional outcome and the apparent protective effect of surgery on the remaining CrCL.
In conclusion, there are a number of apparent advantages/disadvantages in both TPLO and TTA procedures. TTA may correct the tibiofemoral shear force closer to the neutral point compared with TPLO, which might protect the CaCL from additional stress as the primary joint stabilizer. Another advantage of the TTA is the unchanged joint geometry and superior cartilage pressure distribution compared with TPLO. TTA may also be a less invasive, simpler surgical procedure with fewer potential technical issues with adverse effects. TTA may be more suitable in cases of patellar luxation. On the other hand, TPLO is a more versatile procedure than TTA in cases with excessive TPS, and in cases with a variety of angular and rotational limb deformities, including cases with concurrent patellar luxation. At this time, there are only a few studies that present reasonable scientific support for either procedure. A number of experimental and clinical studies are necessary to attempt to shed more light on these repair methods.
In summary, the stifle joint of dogs is an organ comprised of multiple tissue types that must work in concert to maintain joint health and function. Cruciate disease in dogs is caused by a spectrum of causal and risk factors that result in a final common pathway of abnormal biomechanics and abnormal biology causing osteoarthritis of the stifle and the clinical signs of lameness, pain, and limb dysfunction. It is vital to understand the components of the biologic and biomechanical pathologies to improve our understanding of cruciate disease in dogs so that we can improve preventative, diagnostic, and therapeutic strategies for our patients. As veterinary surgeons, it is important to consider and address as many aspects of the disease as possible and educate clients well with respect to the nature and progression of CrCL disease, preoperative, operative, and postoperative treatment components and options, and their roles in achieving a successful outcome for their dog. While surgical intervention is recommended in dogs afflicted by CrCL insufficiency, there is no evidence to support the notion that any one technique is clearly superior to the others at this point in time. Not only is it unclear as to which surgical technique is superior, it is also unclear as to whether or not the remnants of the diseased cruciate ligament should be debrided and removed from the intrasynovial environment. It is equally unclear as to whether or not aggressive manipulation, inspection and release or removal of meniscal tissue should be performed. When analyzed collectively, the innumerable studies presently available for review on cruciate ligament and meniscal disease fail to definitively prove which one surgical approach has the best short term and long term success rate with consistent return to full, pain free function. As with many surgical procedures, it is at the discretion of the surgeon to select the technique that he believes is the most appropriate for the specific task at hand and their own experience/expertise.
3 different views of Post Op TPLO
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Primary pulmonary neoplasia was diagnosed in 14 dogs presented to the California Animal Hospital for medical and surgical management of respiratory tract disease.
Locations of the primary tumor were the right caudal (six), left caudal (five), right accessory (two), and right middle (one) lung lobes. Complete lobectomy of the affected lung lobe using a mechanical stapling device was performed in all cases. The tumor types observed were adenocarcinoma (six), bronchoalveolar carcinoma (six), anaplastic carcinoma (one), and epidermoid carcinoma (one). Of the 14 dogs undergoing exploratory thoracotomy, two died within a 72 hour postoperative time period. The remaining 12 dogs were monitored from two to 24 months (mean= 10 months) postoperatively to determine surgical complication and recurrence rates. No evidence of recurrence of pulmonary neoplasia has been observed in these dogs through the follow-up period.
Pulmonary neoplasms may be primary or secondary. Metastatic neoplasms of the lung are seen more commonly than primary tumors. The incidence rate of primary lung tumors has been estimated at 5.6 per 100,000 dogs. Although primary pulmonary neoplasia is relatively rare, as dogs continue to receive better medical attention enabling them to live longer, an increased incidence of these tumors may be observed.
The average age at the time of diagnosis is 10.5 years with the condition predominantly occurring in dogs seven years of age and older. breed or sex predisposition to primary lung tumors has not been identified. A higher incidence of primary tumors has been observed in the right lung lobes, with the right caudal lobe most frequently affected.
Any component tissue of the lung may be the site of origin of a neoplasm. The most commonly occurring primary lung tumors in the dog originate from the epithelium of the terminal bronchioli.
The majority of primary lung tumors are carinomatous. Based on histologic structure, most pathologists subdivide primary lung tumors into adenocarcinoma, bronchoalveolar carcinoma, anaplastic carcinoma, and carcinoid tumors. Other rare primary lung tumors include neoplasms arising from connective or lympathic tissue, and mesenchymal tumors.
The clinical signs associated with primary pulmonary neoplasia are usually vague and nonspecific. Symptoms observed may include loss of stamina, fatigue, anorexia and weight loss. Other clinical signs may include dyspnea, non-productive cough, hemoptysis, and lameness as a result of hypertrophic pulmonary osteoarthropathy. Occasionally, thoracic radiography reveals pulmonary lesions suggestive of neoplasia as incidental findings.
The prognosis associated with primary pulmonary neoplasia in the dog is dependent upon several factors, including (one) the severity of clinical signs, (two) the presence or absence of hilar lymphadenopathy, (three) the presence or absence of distant metastasis and (four) the tumor type.
The purpose of this paper is to describe the pathogenesis and clinical course of 14 dogs with primary pulmonary neoplasia and their responses to compete lobectomy.
Materials and Methods:
Exploratory thoracotomy was performed on 14 dogs with primary pulmonary neoplasia between January 1994 and December 1985. The dogs were elected for surgery based on the presence of a solitary mass involving a single lung lobe, with no evidence of distant metastasis or extrapleural involvement. A complete physical examination, as well as hematologic and biochemical blood analysis and urinalysis were performed in each case. Thoracic and abdominal radiographs were performed to eliminate the possibility of a primary neoplasm with pulmonary metastasis.
Complete lobectomy of the affected lung lobe using the TA 30 or TA 55 mechanical stapling deviceA was performed in each case. Examination for air leaks was made by flooding the cut surface with warm lactated Ringer’s solution. Leaks were managed with simple interrupted sutures using #2-0 polypropylene.
Following complete lobectomy, the thorax was lavaged, the remaining lung lobes were expanded to eliminate atelectasis, a chest tube was placed, and the thorax was closed. The chest was evacuated of all air and if there was no accumulation of air or fluid in the thorax over the next 24 hours, the chest tube was removed.
Representative sections of neoplastic tissue from each dog were submitted for histologic examination and classification based on the World Health Organization’s classification of pulmonary neoplasms in man.
Follow-up physical examination and suture removal were performed two weeks following surgery in all dogs. Follow-up thoracic radiography was performed at intervals of four to six months. All patients were followed from a minimum of two months to a maximum of 24 months.
The results are given in Table 1. The average age of the dogs was 10.4 years (range = 3-14 years). There was no sex (seven male, seven female) or breed predilection. Clinical signs included coughing (five), dyspnea (three), and weight loss (two). There were no abnormal findings on physical examination in four dogs.
Of the 14 lung lobes removed, nine (64 percent) were on the right and five (36 percent) were on the left. Of those tumors affecting the right lung, six (67 percent) occurred in the caudal lobe, two (22 percent) occurred in the accessory lobe, and one (11 percent) occurred in the middle lobe. All five tumors affecting the left lung occurred in the caudal lobe.
Histologic examination revealed six adenocarcinomas (43 percent), six bronchoalveolar carcinomas (43 percent), and one epidermoid carcinoma (seven percent).
Two dogs died within a 72 hour postoperative time period because of cardiac arrhythmias non-responsive to anti-arrhythmic cardiac therapy.
Three dogs were euthanized because of unrelated causes (degenerative myelopthy – two, caudal cervical vertebral instability – one) and one dog died because of unrelated causes (renal failure). Survival time of these dogs ranged from four to 24 months (mean = 11.5 months). At the time of euthanasia or death, these dogs were asymptomatic from signs of recurrent respiratory tract disease.
Eight dogs are currently alive and free from signs of recurrent or progressive respiratory tract disease at two to 24 months (mean = 9.3 months) following surgery. Thoracic radiography performed every four to six months has revealed no evidence of recurrence.
Primary pulmonary neoplasms have been reported to occur predominantly in dogs over seven to eight years of age. The results of this study support this finding. No sex or breed predisposition to primary lung tumors have been identified. In this study, males and females were represented equally. Although no one breed was affected more frequently than others in this study, all of the dogs were medium to large size breeds with the exception of case #3. Further case studies were necessary to determine if this is either a significant trend or because of the predominance of medium to large breed dogs within our referral population.
Clinical signs associated with primary pulmonary neoplasia are often vague and nonspecific. It has been reported that as many as 33 percent of primary lung tumors are discovered during a physical or radiographic evaluation for another problem. There were no abnormal findings on physical examination in four of the 14 dogs (29 percent) in this study.
The most common clinical sign (five cases, 36 percent) was a non-productive cough. This is in agreement with the findings of previous investigators. Dyspnea (three cases, 21 percent) or weight loss (two cases, 14 percent) was the primary owner complaint in the remaining five cases.
It has been reported that the absence of clinical signs in man and dogs with primary pulmonary neoplasia is a favorable prognostic indicator. Because of the small sample size and length of the follow-up period a similar conclusion could not be drawn from the results of this study.
A number of investigators have reported a majority of primary pulmonary neoplasm affecting the right lung, with the right caudal lung lobe having the highest incidence of primary tumors. The results of this study are in agreement: 64 percent of the tumors were on the right side, with the right caudal lobe affected in 43 percent of the cases.
Histologic examination of primary lung tumors in dogs has indicated that nearly all lung tumors are malignant. Adenocarcinomas have been reported to be the most commonly occurring lung malignancy (75 to 83 percent). Epidermoid (squamous cell) carcinomas (six to 12 percent) are less common, as are anaplastic carcinomas (four to nine percent). This is in contrast to man, where squamous cell carcinoma (30 to 35 percent) is more common than adenocarcinoma (25 to 29 percent).
In this study, bronchoalveolar cell carcinomas (43 percent) occurred as frequently as adenocarcinomas (43 percent). Because of the small sample size, these results must be interpreted with caution. Anaplastic carcinoma (seven percent) and epidermoid carcinoma (seven percent) occurred less frequently.
In many dogs, the confirmation of primary lung tumor may be shortly followed by premature euthanasia. It is the authors’ opinion that surgery is often indicated in the treatment of primary pulmonary neoplasia. The results of this study demonstrate that surgical excision of the affected lung lobe can lead to prolongation of good quality life.
The most frequent reason for performing a total hip replacement (THR) is relief of pain and disability caused by severe degenerative joint disease secondary to hip dysplasia.
Other reasons include hip fractures, chronic dislocation of the hip and acute dislocation of the hip that cannot be reduced because of hip dysplasia or soft tissue damage. The presence of any and all of the aforementioned conditions leads to hip joint laxity, subluxation (partial dislocation) and or luxation (complete dislocation) which ultimately leads to varying degrees of degenerative arthritic change. Contrary to what one may think, many dogs with arthritic hip joints seem to function normally while others exhibit severe crippling disease. In addition, the severity of the clinical signs does not necessarily correlate with the degree of radiographic or pathologic changes seen. Breed and individual differences in temperament may also affect the amount of discomfort exhibited. Total hip replacement is now a well-established procedure in veterinary orthopedic surgery. Although there are some variations in technique and types of implant, most involve the replacement of the acetabulum with an ultra-high molecular weight polyethylene cup and the femoral head with a cobalt chrome ball and stem which are secured in position with acrylic (cemented) or porous coated implants resulting in normal or near normal function and activity.
Clinical signs including lameness, reluctance to exercise and difficulty rising, using the stairs or jumping into and/or out of the car are often signs of hip related problems. Lameness of the hind limb varies from barely-detectable gait abnormalities to non-weight-bearing lameness. Lameness is usually especially evident after exercise periods. A “bunny-hopping” gait is often seen in affected young dogs and is characterized by simultaneous advancement of both hind limbs while running. Young dysplastic dogs often lay on their belly with limbs outstretched behind them. Pain is often elicited during full extension of the joint by a veterinarian. Hip dysplasia is not generally an acute lameness, but one of the slow progression of lameness severity. It is not uncommon for dogs with hip osteoarthritis to have in addition, other orthopedic injuries. Many times it is these other problems that are the source of the lameness that prompted the visit to the veterinarian in the first place. The most common conditions which may mimic or be confused with clinically painful hips include cauda equine syndrome, cranial cruciate ligament tears, other rear limb arthritic conditions and neoplasia. Since dogs can have profound radiographic changes with arthritis and yet have few if any symptoms, any new lameness exhibited by such a dog, or sudden worsening of what had heretofore been a mild lameness, should prompt skepticism that it is due to the hips until proven to be so. Only when other causes have been excluded or treated should attention be focused on the hips and medical and surgical treatment such as THR be contemplated.
Not all dogs with hip dysplasia or osteoarthritis require surgical treatment. The decision for performing a THR and the timing for joint replacement surgery depends on a number of factors, including the degree of clinical disability and discomfort, intended use of the dog, and the presence of other diseases or injuries. As mentioned previously the decision to perform THR is never based on radiographs alone, no matter how severe the changes appear. There can be a poor correlation between radiographic severity and clinical severity, and some dogs with terrible looking hips are yet functioning at a high athletic level with no apparent pain. So the decision to treat arthritic hips, with medicine or surgery, is always based on whatever clinical disability the patient is exhibiting.
Medical management to alleviate clinical symptoms is always attempted prior to surgical intervention as many dogs with degenerative arthritis can be kept comfortable and active with medical management. It is important to keep the patient at a normal body weight and to provide regular, controlled activity. Medical management includes the administration of steroidal or non-steroidal anti-inflammatories, muscle relaxants, poly-sulfated glycosaminoglycans (Adequan), hyaluronic acid (Legend), neutraceuticals (glucosamine, chondroitin, msm, creatine), omega 3 and 6 essential fatty acids, platelet rich plasma, Class IV laser therapy, acupuncture and physical therapy. If hip pain persists in spite of appropriate medical management, surgical therapy should be considered. The decision to intervene with surgery is based on the amount of pain, discomfort and lameness exhibited by the dog. Typically the patient has been refractory to medical therapy or has not returned to an acceptable level of performance. The decision to proceed with surgery should not wait until there is severe pain and/or loss of muscle mass as this may compromise the surgical result. Since total hip replacement results in near normal to normal function and activity, if medical treatment does not alleviate clinical symptoms, then surgical treatment is recommended.
Surgical options include femoral head and neck ostectomy (FHO) with or without a biceps sling or total hip replacement. While the purpose of this article is THR, it is appropriate to diverge and mention the FHO procedure as this has been the contemporary surgical option to treat coxofemoral pathology in smaller dogs and cats. An FHO with a biceps sling removes the femoral head and interposes muscle between the acetabulum and femoral neck so that there is no longer bone rubbing on bone in the diseased joint. While this can relieve much of the pain, the loss of the normal ball-and-socket anatomic structure of the hip may result in a limb that will not function normal mechanically. Small, light-weight dogs and cats do better than large dogs with an FHO. The advantages of FHO include easier recovery, less risky complications, and less expense. If a femoral head and neck excision was performed previously, the results of total hip replacement are generally not as rewarding as cases receiving hip replacement initially. An FHO can be converted into a total hip replacement, however, it is a technically demanding procedure with a higher complication rate than primary total hip replacement. The longer the interval from the FHO to the total hip, the more difficult the total hip replacement becomes, with the best results occurring if the total hip replacement is performed early (4-6 weeks) after the FHO. Conversion of an FHO to a THR should not be recommended, as calcar support for the prosthesis is removed by the excision arthroplasty, there is a higher risk of infection and there may be inadequate muscular support for the prosthesis.
After FHO, especially in large dogs, the hindlimb is shortened to a variable degree, biomechanical function is altered, pain relief may be unpredictable, muscle atrophy with weakness is a common long-term finding and postoperative rehabilitation is prolonged. On the contrary, published reports of objective measures taken following THR in large dogs consistently document a return to normal function. The goal of THR is a pain-free joint that mimics normal biomechanics with excellent long-term function. THR is a common procedure used to treat degenerative arthritis and other hip arthropathies in large dogs, and it should be considered in smaller patients. Total hip replacement has historically been used in medium, large and giant breed dogs. There is now a much wider range of implant sizes, so it is available for small dogs as well. Truly, the only drawback to the utilization of THR in smaller patients is its expense and the fact that these smaller implants are usually cemented rather than porous-coated.
Total hip replacement techniques fall into two categories: Cemented and Cementless. Cemented THR provides fine short term, but less satisfactory long term outcomes. Cemented implants are held in place with an acrylic, but there may be break down of the interface between the cement and bone over time. For this reason, in the past, total hip replacement was only considered in older dogs. This was due to concerns with how long the cemented implants would remain stable. With the uncemented, porous-coated implants that we now use, break-down of the interface is unlikely and the high quality of the plastic of the cup will help it last for the life of the dog. Porous-coated implants become stable by in-growth of bone into their beaded surface in the first few weeks to months after implantation. Implants can be placed in young dogs with the expectation that they will provide a lifetime of pain-free function, and are preferentially indicated for hip replacement in young dogs.
In many dogs, both hips are arthritic. In most cases, the hip with the worse function is operated on first. This results in good to excellent function in about 75 percent of dogs. The other 25 percent remain somewhat lame on the opposite hip, and total hip replacement of the other side is considered in these cases.
Both hips are never operated upon at the same time because bilateral surgery increases discomfort and the risk of complications. For this reason the two surgeries are separated by approximately 3-4 months in most cases. If function is good after the worse hip is replaced, the second hip may not need surgery and continued medical management may continue to alleviate clinical symptoms.
As there are risks inherent with any major surgical procedure, these risks should be thoroughly discussed with the client prior to surgical intervention. The current complication rate following total hip replacement is 2 to 5 percent. Complications are best treated when identified early. Significant complications include but are not limited to:
- Dislocation of the prosthetic joint is rare, and is most likely to occur in the first 4 weeks after surgery. It may be corrected manually, but another surgery is often necessary.
- Infection is a serious potential problem. If it occurs in the area of the wound, it is generally treated with antibiotics. If it occurs in the bone, removal of the prosthesis may be necessary.
- Subsidence or sinking of the stem – a small amount of settling of the stem has no effect on function of the prosthetic joint. A large amount of subsidence or stem rotation may require surgical revision of the stem.
- Fissure or Fracture of the femur – uncemented implants are hammered into place. Fissures can develop. If they are seen during surgery, wire is placed to prevent them from expanding. If they develop after surgery, they may lead to subsidence of the stem, or fracture of the bone. Another surgery would be required to manage this issue.
- Loosening of the prosthesis is an uncommon problem with uncemented prostheses. If loosening is significant or progressive, the implant may need to be replaced or removed.
Most dogs are able to stand and walk on the new prosthesis within the first few days after surgery. While hospitalized, exercise is restricted to cage confinement with 10 to 15 minute walks under leash restraint twice daily. Most animals undergoing total hip replacement are hospitalized for a total of 3 to 4 days.
During the first month at home, the dog must have very limited activity. During this crucial period the joint capsule, muscles and tendons are healing, and helping to stabilize the hip. This means that dogs are allowed short walks only, and only on a leash. Otherwise the dog should be kept confined. Dogs should not run, play, jump, or climb flights of stairs. During this time, care should be taken to avoid activity on slippery surfaces, and stairs should be climbed only while the dog is under the direct control of the owner. Going up and down one or two steps to get outside is acceptable. Management at home will require strict supervision, and activity must be restricted in order to optimize surgical recovery. Adherence to postoperative restrictions can minimize potential complication. One month after surgery, supervised exercise can be gradually increased over the next 4 weeks. During this second month dogs are still limited in their activity, but can start increasing the length of their walks outside. At the end of 8 weeks, more normal activity is allowed. Between the second and third month activity is gradually increased so that by the end of the third month the dog is nearly back to normal function and activity. Vigorous, rough play or hard work is allowed after gaining strength and conditioning. Radiographic evaluation and orthopedic examination are necessary at 3 and 6 months after surgery, and every 2 years thereafter. This provides a history of the patient’s progress and may help to detect potential complications.
The majority of dogs are found to be more comfortable and have an improved quality of life following THR. Many owners report that their pet can do things they have not done since they were a puppy. Increase in muscle mass, improved hip motion, and increased activity levels are observed in most patients. Up to 95% of the dogs whose hips have been replaced return to normal or near normal ambulatory function. More than 95% of owners feel that their dog’s quality of life is significantly improved following THR. Although the state-of the-art equipment, implants, advanced technical expertise and training which go into the THR surgery are expensive, few other procedures are capable of so dramatically changing the quality of a pet’s life. It is for these reasons that THR is the surgical treatment of choice in both juvenile and adult dogs to obtain the best functional outcome when the pain and discomfort of degenerative arthritis is refractory to medical therapy.
Thoracolumbar intervertebral disc disease is a well-recognized entity in veterinary medicine.
The clinical incidence of intervertebral disc disease has been reported to be higher in the chondrodystrophoid breeds of dogs although disc degeneration occurs in all breeds. The pathophysiologic distinction between intervertebral disc disease in the chondrodystrophoid and nonchondrodystrophoid breeds has been reported in detail.
The severity of the spinal cord lesion resulting from intervertebral disk extrusion may be influenced by (1) the magnitude of the force of impact of the extruded disk material on the spinal cord; (2) the extent of the mechanical distortion of the spinal cord; (3) the chemical, neuronal, and vascular alterations within the spinal cord; (4) the rate of onset of spinal cord compression; and (5) the duration of attenuation.
The intervertebral disk is located between two adjacent vertebrae and acts as a “shock absorber” to handle forces along the spine. There are two parts of the disk which each work differently. The center portion, called the nucleus pulposus (NP), has a high water concentration and is positioned to help absorb the forces along the spinal column. The majority of the force of a compressive load is absorbed by the nucleus pulposus. The outer portion, the annulus fibrosis (AF), is more like a ligament. When forces impact the intervertebral disk, the nucleus pulposus spreads and transmits forces outwards to the annulus fibrosus, which also spreads. The annulus fibrosus, while flexible, is more rigid and maintains disk structure. When the forces along the intervertebral disk cease, the elasticity of the annulus fibrosus allows return to the normal shape of the disk. From the second to the tenth thoracic vertebra, the intercapital ligament between opposite rib heads lies ventral to the dorsal longitudinal ligament and dorsal to the disks. This thick ligament is thought to be the reason disk extrusion is uncommon in the cranial thoracic area. The paired vertebral sinuses lie in a ventrolateral position along the floor of the vertebral canal. Hemorrhage from the vertebral sinuses can accompany disk extrusion or can obstruct visualization during surgical decompression.
The intervertebral disk is found between all but the first two cervical (neck) vertebrae. Individually, an intervertebral disk is the largest organ in the body that does not get direct blood supply bringing nutrients and oxygen to and removing waste products from the cells of the disk. These functions are maintained mostly by diffusion from the end of the vertebral bones. This is a relatively inefficient process in relationship to the high metabolic activity of the cells that make up the intervertebral disk.
Disk degeneration is primarily a result of a breakdown in the process of diffusion leading to an environment in which the cells cannot maintain normal health and function. There is no clinical treatment that can prevent the degenerative changes, but daily controlled exercise can promote disk health by promoting diffusion in the spine.
Degeneration of the intervertebral disk leads to a change in function and chemical properties of the disk, which can result in progressive injury and failure (or rupture) of the disk. When the intervetebral disk fails, it usually does so in an upward direction into the spinal canal and this can lead to compression of the spinal cord.
Because most of the nervous system is inaccessible for direct examination, diagnosis of neurological problems depends on obtaining a good history, consideration of the species, breed, age, and gender of the patient, and conducting a thorough neurological examination in order to establish a neuroanatomic diagnosis.
There are two major types of disc disease in dogs. HansenType I disk degeneration is an early degeneration of the disk that is most commonly observed in chondrodystrophic breeds of dogs including the Dachshund, Shih Tzu, and Beagle. In this type of disk disease, as the disk ages, areas of the nucleus pulposus show signs of cellular necrosis, disintegration of the matrix, and calcification. The biochemical alterations associated with the degeneration of the nucleus pulposus are primarily a loss of water and proteoglycan molecules as well as an increase in collagen content. The poor biomechanical properties of the degenerating nucleus result in disruption of the lamellae of the annulus, which progresses until the calcified nuclear material erupts dorsally through the outer layers of the annulus and impacts on the spinal cord. In this type of disk disease, it is not uncommon for the NP to extrude out of the center of the disk to result in rapid concussion as well as compression to the spinal cord. The age range of presentation is usually between two and twelve years of age, but peak incidence of dogs presenting with this type of disk disease is between 4-8 years of age, with an average age of 5.5 years of age.
Hansen Type II disk degeneration is associated with normal aging changes. This is most often seen in middle-aged to older large breed dogs including but not limited to the German Shephard. The changes in Type II disk degeneration include alterations in the NP causing it to become similar in cellular properties and chemistry to that of the AF. In this type of disk disease, the primary physical change is tearing in the fibers of the AF and bulging or protrusion of the annulus fibrosus into the spinal canal. The degree of compression to the spinal cord can vary from minimally to severely compressed within the spinal canal. The onset usually involves more gradual progression of weakness, and often, the owner does not know exactly when it started. However, an acute and large disk extrusion is occasionally seen with this type of disk degeneration.
Whether the onset of disk extrusion is rapid or chronic, the compression to the spinal cord leads to neurological dysfunction. This can range from mild gait change and ataxia (incoordination of the limbs behind the spinal cord region affected) to weakness or even paralysis. It is not uncommon to see pain as the only presenting sign even when there is significant spinal cord compression. The extent of the clinical symptoms exhibited depends upon the length of time the disc has been herniated, the degree of compression of the spinal cord, the force of impact that the degenerated disc has on the spinal cord, and the rapidity of disc herniation and the resultant spinal shock and contusion to the spinal cord.
The most common sites for intervertebral disk extrusions in the dog occur between T11-12 and L2-3 (approximately 85% of all disc herniation), the cervical intervertebral disc C2-C3, and the L7-S1 intervertebral disc space in the lower back. Males are more commonly affected than females. Lumbosacral disc disease, a cauda equina disease at L7/S1, occurs most frequently in large breed dogs (e.g., Shepherd dogs) and is associated with Hansen type II disc disease, vertebral instability, and spinal stenosis, and the complex is called degenerative lumbosacral stenosis, a situation similar to sciatica in people.
Clinical Signs of Disc Disease
Clinical signs of intervertebral disc disease (IVDD) include spinal pain and varying degrees of neurologic deficits. Acute intervertebral disk extrusions are often characterized by the sudden onset of dysfunction of the spinal cord and pain. Chronic intervertebral disk extrusions are more common in large-breed dogs. With the latter form of disc compression, slow, progressive dysfunction without pain is common. The slow, progressive dysfunction associated with chronic intervertebral disk extrusions often times worsens in a rapid fashion as the compensatory limits of the spinal cord are exceeded. Spinal pain without paresis may cause the animal to be agitated, aggressive, or more vocal. Some animals will lie quietly refusing to walk whereas others will walk constantly or pace. Thoracolumbar IVDD may cause animals to walk with an arched back whereas dogs with cervical disk disease will be reluctant to elevate their heads or shake their ears. If there is compression on a nerve root, the animal may hold the affected limb up and have decreased weight bearing. Clinical signs of L7-S1 IVDD include pain upon rising, reluctance to jump up and down or negotiate the stairs, hesitancy to jump into or out of the car, and difficulty defecating. Some animals will have spinal pain as their only clinical sign. Clinical signs of spinal pain in our patient may improve, remain static, or progress depending on the disease progression. The clinical signs of spinal cord compression have been attributed to direct mechanical derangement of nerve tissue and hypoxic changes resulting from pressure on the vascular system in the spinal cord. Other causes for the neurologic signs include ischemia, edema, and reperfusion injury that may result in more severe spinal cord degeneration and hemorrhagic myelomalacia. Progression of neurologic clinical signs is correlated to increasing compression of the spinal cord. The larger, heavily myelinated fibers that mediate proprioception are affected first, followed (in descending order) by the intermediate sized fibers involved in voluntary motor function; the slightly smaller fibers that mediate superficial pain sensation; and, finally, the small unmyelinated fibers that mediate deep pain sensation. The spinal cord heals in the reverse direction with deep pain perception returning first, followed by superficial pain, voluntary motor control, and proprioception. Therefore, increasingly severe clinical signs occur in the following order: spinal pain, ataxia, paresis, paralysis, and loss of deep pain sensation. The ability to perceive superficial pain is typically lost at the same time that voluntary motor control is lost. Ataxia is the loss of coordination and is characterized by a broad-based stance and incoordination of the trunk or limbs in IVDD. Clinically, we may see crossing over of the limbs when walking or an over-reaching gait. Postural reactions may be diminished or absent with an ataxic animal. Paresis (weakness) and paralysis are measures of an animal’s voluntary motor ability. Gradation is arbitrary and may be characterized as mild, moderate, or severe. It is more helpful to describe if the animal can support weight or advance the limbs. The last modality lost is the perception of deep pain. An animal that has lost deep pain perception has a guarded prognosis and for the best possible outcome should be considered an emergency surgical candidate. Deep pain sensation is cerebral recognition of the painful stimuli and is different from the flexor reflex. An animal with no deep pain may retract their leg, but does not cry out, attempt to bite the examiner, or move away from the stimuli.
Diagnosis of intervertebral disc disease is based on the clinical presentation, history, and ultimately, the imaging findings. Survey radiography, myelography (contrast-assisted radiographs where a radiological contrast agent – dye – is injected into the spinal fluid to permit visualization of the otherwise radiographically invisible spinal cord on x-rays), contrast-assisted computed axial tomography (CAT Scans), and magnetic resonance imaging (MRI) are utilized to diagnose intervertebral disk disease and accurately localize the compressive spinal cord lesion. Radiographic findings suggestive of IVDD include collapse or wedging of the intervertebral disk, deformities of the intervertebral foramina, and the presence of radiopaque material in or around the spinal canal. While routine spinal radiographs may give us the suspicion of disk disease, the spinal cord and canal are not adequately visualized and significant spinal cord compression and injury are not identified in the majority of cases. The most accurate methods of diagnosis of spinal cord compression caused by IVDD require imaging of the spinal cord with myelography, computed tomography (CT), or magnetic resonance imaging (MRI). All of these methods require general anesthesia.
MEDICAL AND SURGICAL TREATMENT
Neurological grading in canine IVDD is valuable to follow the progression of neurological deficits in time (improvement or worsening), to choose the mode of therapy, for prognosis, and for assessment of outcome after medical or surgical treatment.
NEUROLOGICAL GRADING IN CANINE INTERVERTEBRAL DISC DISEASE:
- Grade 5: normal.
- Grade 4: cervical or thoracolumbar pain, hyperaesthesia.
- Grade 3: paresis (muscle weakness) with decreased proprioception, ambulatory (able to walk).
- Grade 2: severe paresis with absent proprioception, not ambulatory (not able to walk).
- Grade 1: paralysis (not able to stand or walk), decreased or no bladder control, conscious deep pain perception present.
- Grade 0: paralysis, urinary and fecal incontinence, no deep conscious pain perception.
There is a diversity of opinion regarding treatment options for dogs with IVDD, but general guidelines can be used for selecting therapy. Decisions regarding when and if surgical versus medical treatment for the spinal compressive disease is indicated depend primarily upon the severity of the neurological signs and the chronicity of the problem. In addition, treatment is modified in relation to the presumptive diagnosis, owner finances, and concomitant medical problems.
Patients with pain only (Grade 4) or pain with minimal neurologic deficits (Grade 3) can often be managed conservatively. It should be mentioned, however, that improper management of the dog with spinal pain with or without minimal neurologic deficits may result in the progression of clinical signs and a worse overall prognosis.
Ideally, any significant spinal cord compression (Grade 2-0) should be relieved surgically. While medications and time may improve the animal’s comfort and neurological function, compression on the spinal cord of these magnitudes most likely will remain and result in continued spinal cord injury and prevent complete return to normal function. Removal of the extruded nuclear material and hemorrhage crushing the spinal cord is necessary to allow for revascularization, removal of toxic by-products within the spinal cord, and resolution of swelling or edema. Decompression is based upon the location of the extruded nuclear material and hemorrhage based upon myelographic, CT, or MRI findings. For the majority of dogs, if done early, surgery will result in a good to excellent outcome. The outcome for decompression of spinal cords that have been compressed for months to years becomes more difficult to predict. Some factors that will affect the outcome are irreversible spinal cord injury (from acute concussion or chronic compression), the animal’s overall health, and whether there are multiple levels of disk extrusion with spinal cord compression.
Proper medical therapy for the IVDD patient includes cage rest, non steroidal anti-inflammatory therapy ( deramax, metacam, rimadyl), corticosteroid therapy (dexamethasone sodium phosphate, solu medrol, prednisolone), muscle relaxants (robaxin), pain management (fentanyl patches, oxymorphone, buprenex, gabapentin, tramadol), and gastrointestinal protectants (fametodine, zantac, pepcid, tagamet). Non-steroidal and steroidal anti-inflammatory therapy should not be combined in the same treatment plan because of the increased risk of gastrointestinal ulceration. While some may consider corticosteroid therapy controversial in treating intervertebral disk disease, my personal opinion, based on over 20 years of experience as a board certified surgeon, is to give steroids. Used intelligently and judiciously, my experience is that steroids have absolutely had a positive effect on a substantial number of our spinal patients.
While physical therapy and massage therapy probably will not prevent IVDD disease, they are very useful in helping patients recover from spinal cord injury. In fact, these methods may be as important as any other factor in ensuring maximal recovery. In cases where surgery is not performed, physical therapy and massage therapy must be limited to the least aggressive methods. Massage therapy improves muscle and joint flexibility, increases blood supply (improving nutrient delivery and waste removal), and help prevent or breakdown scar tissue formation. It also helps relax muscle spasms and aids in patient comfort levels. Massage therapy for animals should be performed by massage therapist trained in animal behavior and anatomy, under the supervision of your veterinarian. Many of the basic principles can be learned by the owner under proper instruction. While acupuncture cannot prevent IVDD disease and should be used with the same caution as relieving pain by conventional measures, acupuncture provides many beneficial effects in treating IVDD disease or following surgical correction during the healing process. Acupuncture is widely accepted as a method to provide analgesia without the side-effects of drugs. More recently, Class IV laser therapy may be employed in the multi-modal approach for those patients managed medically as well as surgically.
The medically managed patient must be observed frequently for deterioration of neurologic signs. Client education is an important component of the medical management regime. The client should be informed of the severity of the disease and of the fact that the signs may suddenly become progressively worse in which case surgical therapy is indicated. Recurrent episodes are frequent and are commonly more severe than the previous one. Recurrence of clinical signs after non-surgical treatment occurs in 40% of patients. Overall recovery in dogs with grade 3-4 deficits is 80% to 90%. Paraplegic dogs with grade 2-0 deficits non-surgical treatment is rarely the treatment of choice because of the low response rate, high rate of recurrence, neurological worsening during treatment, and development of complications. In dogs with grade 0 neurological deficits, the duration of absence of conscious deep pain sensation is an important prognostic parameter. Dogs with grade 0 neurological deficits should be regarded as emergencies and require surgery within 12-24 hours. When grade 0 neurological deficits persist beyond 24-48 hours the result of any treatment (surgical or nonsurgical) becomes minimal. Medical management has been shown to be as ineffective as surgical therapy in the majority of patients with sensorimotor paralysis for more than 24-48 hours. However, some clients do not consider euthanasia as an immediate alternative in these cases and may request some form of therapy.
The surgical approach taken to appropriately decompress the spinal cord is determined by the location of the herniated disc material within the spinal canal and the exact intervertebral disc space affected. In the cervical or neck region, a ventral or anterior approach is favored. The dorsal or posterior approach procedures are sometimes necessary; however, excessive muscle hemorrhage, increased surgery time, the difficulty of removing disk material from the ventral spinal canal, and prolonged postoperative care make this approach undesirable as a routine procedure. The ventral approach is less traumatic and requires less surgery time. The ventral-slot technique allows direct access to the extruded disk material and direct visualization of the affected spinal cord. The major disadvantage of the ventral-slot technique is the potential for hemorrhage associated with laceration of the venous sinuses.
Dorsolateral hemilaminectomy is the most common surgical treatment for thoracolumbar disc disease.
Hemilaminectomy best preserves the mechanical and structural integrity of the spine while allowing for excellent access and decompression. Dorsal laminectomy is not recommended in the thoracolumbar area because it causes considerable biomechanical instability and may lead to neurological worsening. In the lower lumbar area (L7-S1), however, dorsal decompressive laminectomy is the procedure of choice.
In addition to surgically decompressing the spinal cord to allow for spinal cord recovery, preventing further extrusions by the removal of the nucleus from the offending disk and other discs which can rupture is sometimes performed in breeds with a high incidence of repeat disc extrusions. This procedure is termed a fenestration. It is not a risk free procedure and in some cases can exacerbate the already existing clinical signs of spinal cord disease. It is also not a guarantee that the prophylactically fenestrated discs will not herniate at a later date as up to 20% of nucleus may be missed with this procedure. For these reasons, it is not commonly performed at our facility. Patients that are grades 2-0 are considered immediate surgical candidates. Grade 3-4 animals that have surgery performed within 48 hours have an excellent recovery rate to useful limb function (95%). Grade 0 animals (lose the perception of deep pain) that are operated on within 12-24 hours still have a fair to good prognosis for recovery (80-90%). If an animal has lost deep pain for more than 48 hours, a guarded prognosis should be given to the owner although one recent review indicated a 50% recovery rate.
The syndrome of myelomalacia is an important consideration in prognosticating the outcome of spinal trauma. Durotomy is performed when either an edematous spinal cord or discoloration suggestive of myelomalacia is present. Durotomy is ineffective as a method of treating compressive spinal cord trauma unless performed immediately (less than 2 hours) after the trauma has been suspected. Durotomy does, however, permit direct observation of the cord to see if myelomalacia is present. Myelomalacia occurs when severe, acute spinal cord trauma results in nearly complete destruction of nervous tissue. The cause and progression of myelomalacia is not completely understood, but the ischemia-reperfusion cascade results in lipid peroxidation and necrosis of myelin, and axons is suspected. Dogs with myelomalacia that have no deep pain perception and neurologic signs may progress cranial and caudal to the original injury. The typical clinical picture is an acute onset of paralysis with loss of deep pain followed by ascending and/or descending signs of neurologic dysfunction with ascending analgesia. Oftentimes, these patients are ill, febrile, and have extreme pain at the cranial edge of the lesion. Myelomalacia carries a hopeless prognosis.
Whether managed medically or surgically, paralyzed patients need to be maintained with excellent nursing care. Bladder management prevents urinary tract infections, overdistension, and urine scalding. The bladder needs to be expressed manually every 6-8 hours. If the bladder cannot be expressed, we recommend intermittent bladder catheterization using a sterile technique. Medication that assists with the ease of manual bladder expression include phenoxybenzamine and bethanacol,. These medications can be used together. Animals must also be maintained in a clean environment to prevent decubital ulceration (pressure sores). Frequent turning (every 4-6 hours) and proper bedding of sheepskin pads or foam “egg crate” bedding helps to lessen irritation. The skin needs to be closely monitored for the development of pressure sores as they are easier to prevent than reverse.
Postoperative recovery is often aided by the aforementioned medical therapy, controlled exercise and physiotherapy, acupuncture, and laser therapy afforded the medically managed patient. The best success rates combine medical therapy and surgical intervention. Functional improvement may be noted as early as 3-5 days following medical and surgical intervention. The continued gradual improvement over the following 4-6 weeks is expected. The prognosis for functional recovery is good for dogs with grade 2, 3, and 4 lesions irrespective of the treatment choice. Dogs with grade 1 lesions have better prognosis after surgical treatment than after nonsurgical treatment. In dogs with grade 0 lesions that are treated within 24-48 hours of onset, the animal has a chance of making a functional recovery. Careful selection of surgical candidates should be based on the findings of a complete physical and neurologic examination, radiography, and specialized non-invasive diagnostic modalities (myelography, computed tomography, magnetic resonance imaging). In conclusion, the combination of medical and surgical therapy yields an optimal recovery.
MRI of Cervical Herniating Disc
MRI of Cervical Herniating Disc
MRI of Cervical Herniating Disc
The shoulder joint is the most mobile of all of the main limb joints.
While its primary motion is in a sagittal plane, the shoulder has a significant amount of abduction and adduction and internal and external rotation. Its stability is ensured by the joint capsule, the medial and lateral glenohumeral ligaments, and by large tendons located inside (tendon of origin of the biceps brachii muscle) or immediately outside the joint (supraspinatus, infraspinatus, teres minor, and subscapularis). The shoulder joint (or scapulohumeral joint) consists of a spherical humeral head articulating with a shallow glenoid fossa of the scapula. The stability of the shoulder joint is dependent on a complex interaction between active and passive mechanisms. The passive mechanisms (do not require energy expenditure by muscle) are the glenohumeral ligaments, the joint capsule, joint conformity, and the glenoid labrum. The active mechanisms (do require energy expenditure by muscle) are the muscles of the shoulder and the rotator cuff. The articular components of the shoulder are the glenoid cavity and the humeral head and they are connected by the joint capsule and the glenohumeral ligaments. It was previously believed that the rotator cuff muscles were responsible for maintaining joint stability; however, it is now established that the joint capsule and glenohumeral ligaments play a significant role in joint stability. The “cuff tendons” are four tendons that directly support the joint: the supraspinatus cranially, subscapularis medially, infraspinatus laterally, teres minor caudolaterally. The rotator cuff tendons act in concert with the joint capsule, glenohumeral ligaments and regional muscles to support the shoulder during movement. By contracting together, the cuff muscles press the humeral head into the glenoid fossa providing a secure scapulohumeral link. By contracting selectively, cuff muscles can resist displacing forces resulting from the contraction of the principal shoulder muscles.
Scapulohumeral luxation is an uncommon injury in dogs and rarely occurs in cats. The majority of luxations are medial or lateral, as cranial and caudal luxations are rarely observed. Trauma and congenital malformation are the most common causes of joint instability. Medial luxation is the most frequently observed luxation. Medial traumatic luxation may be seen in all type of dogs. It is associated with a rupture of the medial gleno-humeral capsule and ligaments and disruption of subscapularis muscle. In small breeds, medial luxation is often congenital and may be bilateral, with an important component being developmental laxity or insufficient development of the glenoid cavity, which prevents any successful reduction. Lateral luxation occurs most often in large size breeds after trauma. It is associated with a rupture of the medial gleno-humeral capsule and ligament and a rupture of the infraspinatus muscle tendon.
Affected animals may present with different degrees of lameness, which can range from mild intermittent to persistent unilateral forelimb lameness to complete non weight bearing lameness. After a traumatic luxation, the dog is usually non-weight bearing and holds the affected limb in flexion with external rotation of the foot. In contrast, dogs with a congenital luxation usually present as an intermittent to continuous lameness which is progressive in nature. Some dogs with congenital bilateral luxation however, show very little impairment in locomotion. On physical examination, the position of the greater tubercle and the acromial process are compared on both sides by bilateral palpation to reveal any sort of dissymmetry. The examination is performed with the dog in lateral recumbency and the affected shoulder uppermost. A cranial “drawer test” is performed to detect any possible cranio-caudal instability, in addition, the scapula can be immobilized with one had while the limb is abducted. Manipulation of the joint may or not be associated with crepitus, pain, muscle atrophy, possibility of reduction of the luxation, or some degree of ankylosis. The ability to abduct the limb away from the body for more than a 30 degrees angle is generally indicative of joint instability. In many cases, complete examination of the shoulder for signs of instability may need to be performed under anesthesia or heavy sedation. Flexion, extension, abduction, cranio-caudal translation, and rotational stability of the shoulder joint should be assessed. Normal range of flexion and extension are 40 degrees for flexion and 165 degrees for extension. Circumduction of the shoulder should not give rise to subluxation. Cranial and caudal translation should be similar in both shoulders. A normal abduction test is approximately 23 degrees; abnormal abduction is considered present when abduction exceeds this degree and there is a difference in abduction angle between the injured side and the normal side. When performing the abduction test, it is essential to maintain the limb in extension with the elbow in neutral position. If the elbow is externally rotated with the limb in extension, the shoulder joint will be internally rotated. The latter will give a false positive abduction test. To maintain the elbow in neutral position, the surgeon should place his thumb on the lateral surface of the olecranon caudal to the humeral epicondyle. Maintaining the thumb facing upward assures that the elbow remains in neutral position.
Radiographic examination is necessary to confirm the diagnosis. On the medio-lateral view, the displacement of the humeral head may not be easy to recognise unless it is a cranial or caudal luxation. Typically, on a medio-lateral view, the glenoid should overlap the humeral head with a medial luxation. Care should be taken to observe for possible fractures of the medial glenoid rim which would preclude conservative treatment via closed reduction. The cranio-caudal radiographic view is usually more diagnostic in cases of medial or lateral luxation. Care should be taken not to reduce the luxation by extending the limb cranially when positioning the dog for radiographic evaluation. Radiography also allows for the diagnosis of secondary degenerative joint disease lesions which have been reported to occur in 57% of all cases of shoulder instability. The existence of concurrent fracture may also be assessed. Mild cases of shoulder instability may exhibit few or no obvious evidence of radiographic change and may require bone scan, CT or MRI evaluation or arthroscopy for definitive diagnosis.
For an acute traumatic luxation, it is worthwhile to attempt closed reduction under general anesthesia. The surgeon extends the shoulder manually while lifting the humeral head into position with his free hand. If this is not accomplished easily, it may indicate a capsular flap that has fallen between the humeral head and glenoid thereby preventing reduction. In cases involving older luxations, an organized hematoma or fibrous mass may occupy the glenoid cavity preventing manual closed reduction. In either of the latter instances, open reduction will be necessary. If the reduction is stable during gentle extension and flexion, the correct positioning of the limb is confirmed with radiography and the limb is bandaged. A Velpeau sling (flexed shoulder, humerus bandaged to the chest wall, then flexed elbow and antebrachium bandaged to the thorax) is used for medial luxation, while a non-weight bearing bandage in physiologic position is used for lateral luxation. Care must be taken that the sling holds the shoulder in a stable position. Too much internal rotation of the humeral head will cause redislocation. The most stable position is that of the forepaw rotated sufficiently to be near the opposite shoulder, thus promoting lateral positioning of the humeral head. Animals should remain immobilized in this fashion for 2 to 3 weeks. Results of nonsurgical treatment of scapulohumeral luxation depend on the magnitude of soft tissue injury, success of the splintage and compliance with activity restriction. If gentle manipulation after splintage and reduction results in reluxation of the joint, surgical stabilization is necessary.
Open reduction and surgical fixation has been used successfully extensively in cases of shoulder luxation that cannot be stabilized by closed reduction. Transposition of the biceps brachii tendon is the technique preferred for treatment of lateral, medial, and cranial shoulder luxation.
In cases of medial luxation, a caudo-medial transposition of the biceps tendon is performed. Surgically, a craniomedial parahumeral incision is made, beginning 4 cm dorsal to the shoulder joint and extending to a point midway down the humeral shaft. The skin and subcutaneous tissues are then reflected, and the medial border of the brachiocephalicus muscle is separated from the superficial pectoral muscle for the length of the incision and is retracted laterally. This exposes the superficial and deep pectoral muscles, the supraspinatus muscle, and the distal communicating branch of the cephalic vein. The insertion of the superficial pectoral muscle is transected down to the border of the distal communicating branch of the cephalic vein and is retracted medially to expose the deep pectoral muscle, which is incised in a similar manner along the length of its insertion on the humerus. This muscle is then retracted medially. The fascial attachment between the supraspinatus and deep pectoral muscles is also incised to allow full medial exposure of the shoulder joint At this point, the tendinous insertion of the subscapularis muscle, crossed by the tendon of the coracobrachialis muscle, is visible, as is the medial aspect of the joint capsule. The insertion of the subscapularis is elevated and detached from the lesser tubercle and is reflected medially. The tendon of the coracobrachialis muscle lays craniomedially and is retracted with the subscapularis. The tissues over the bicipital groove and the intertubercular ligament are transected, and the dorsal aspect of the joint capsule surrounding the bicipital tendon is incised to allow mobilization of the bicipital tendon from the intertubercular groove. At this point the joint may be inspected. The biceps tendon is held in its new position by a bone screw and a spiked washer or a U-shaped surgical staple which is implanted in such way so that the tendon is not compressed. The medial aspect of the joint capsule is reefed and closed routinely. The subscapularis muscle is tightened by advancing its free end anteriorly toward the crest of the greater tubercle of the humerus. It is sutured near the insertion of the deep pectoral muscle. The deep pectoral muscle is then closed over the greater tubercle to the fascia on the lateral surface of the crest and the deltoid insertion with interrupted sutures. The superficial pectoral muscle is closed over the deep pectoral muscle in a similar manner. The brachiocephalicus muscle is closed to the superficial pectoral muscle. The subcutaneous tissues and skin are closed routinely. The leg is placed in flexion in a modified Velpeau dressing for two weeks.
For cases involving lateral luxation, the technique of greater tubercle osteotomy and bicipital tendon transplantation mimics the method used for medial luxation; however, here the biceps tendon is repositioned on the lateral side of the shoulder joint to provide lateral “collateral” support. The skin incision and retraction of the superficial tissues are the same as for medial luxation. The brachiocephalicus muscle is retracted medially, exposing the cranial aspect of the proximal humerus and the insertions of the supraspinatus, deltoideus and superficial and deep pectoral muscles. The insertion of the superficial pectoral muscle is transected down to the border of the distal communicating branch of the cephalic vein, and the muscle is retracted medially, exposing the insertion of the deep pectoral muscle. The deltoideus muscle is transected in a similar manner. The exposed insertion of the deep pectoral muscle is elevated from the humerus and retracted medially, exposing the biceps brachii muscle and the tendon in the intertubercular groove. The intertubercular ligament is incised, and the biceps tendon is freed from the surrounding fascia and joint capsule. The greater tubercle is osteotomized so as to reflect dorsomedially the intact tendon of the supraspinatus muscle. The joint capsule is incised dorsally to free the full tendon of the biceps brachii to facilitate translocating it laterally on the opposite side of the osteotomized greater tubercle. The cut portion of the greater tubercle is replaced and fixed in position with two Kirschner wires. The dorsal joint capsule is closed and the capsular attachments near the intertubercular groove are sutured. Several sutures are placed through the bicipital tendon and the tendinous insertions of the supraspinatus, infraspinatus and teres minor muscles to immobilize the tendon. The muscles are reattached routinely as in the medial luxation. The limb is bandaged for 15 days with a nonweight bearing bandage. A velpeau sling promotes lateral translation of the humeral head so its use is avoided in patients with lateral luxation.
In the case of a (much less common) cranial luxation, the biceps tendon is transposed cranially, into a groove created in the greater tubercular osteotomy site, then immobilized by returning the tubercle to its initial position and securing it with two Kirschner wires or pins. In cases of (even less common) caudal luxation, imbrication of the lateral and caudolateral joint capsule has resulted in good return to ambulatory function. In cases of recurrent surgical luxation, major degenerative joint disease, dysplasia of the glenoid cavity or extensive instability, excision arthroplasty or an arthrodesis may be required as salvage procedures required.
Open reduction and fixation using a biceps tendon transposition for medial and lateral shoulder luxations in the absence of concurrent fractures or significant joint abnormality has a good prognosis for success and return to normal to near normal function of the shoulder. Likewise successful closed reduction and fixation, when possible, has the same prognosis. Many studies report satisfactory results in greater than 90% of the cases managed with conservative medical and/or surgical intervention.
Fractures of the humerus are relatively common in the dog and cat with approximately half of all humeral fractures occurring in the distal portion of the bone.
The overwhelming majority of distal humeral fractures involve the elbow joint and are classified according to their anatomic location. Lateral condylar fractures are common and may occur from either minor or severe trauma in dogs and cats of all ages. Because of the close proximity of the thoracic cavity, additional injuries such as pneumothorax, hemothorax, pulmonary contusion, traumatic myocarditis, diaphragmatic hernia, and thoracic wall trauma can occur concurrently with humeral fractures. These potential injuries should be identified and treated appropriately prior to repair of the humeral fracture.
The severity of the trauma sustained has been shown to influence the resulting fracture type. While severe trauma has been shown to result in simple lateral condylar fractures and the associated injuries previously mentioned, the majority of lateral condylar fractures result from minor trauma. The high incidence of condylar fractures resulting from minor trauma in immature animals may be explained by the relative weakness of the fusion zones of the principal centers of ossification of the developing distal humerus. A substantial number of condylar fractures, however, occur in adult animals. One study found an increased risk for male Cocker Spaniels over two years of age fracturing their humeral condyle with only minor loading forces. The findings of this study suggest that certain breeds of dogs may be predisposed to distal humeral condylar fractures after sustaining minor trauma equal to or only slightly greater than the loading forces generated by the normal activity. Distal humeral condylar fractures are far more common in dogs than in cats. The rarity of condylar fractures in cats may be partially explained by their straighter condyles and relatively wider and thicker epicondylar crests.
Fractures of the lateral humeral condyle (capitulum) occur as abnormal compressive forces are directed upward through the radius. The condyle shears off the intercondylar area through the supratrochlear foramen and the lateral supracondylar ridge. Several factors are associated with the higher incidence of lateral versus medial condylar fractures. The capitulum is the major weight-bearing surface because of its articulation with the radial head. As forces are directed through the radius, they are transmitted directly to the capitulum. Fractures of the medial condyle (trochela) are less common because of its less frequent weight bearing position. In addition, the shape of the distal humerus is such that the capitulum sits off the midline of the central axis of the body, predisposing itself in injury. Finally, the lateral supracondylar ridge is smaller and biomechanically weaker than its medial counterpart.
Treatment of lateral condylar fractures should be directed at complete restoration of joint anatomy and function. Because these fractures are intraarticular, perfect reduction with interfragmentary compression is required for optimal postoperative function. Closed methods of reduction and external fixation cannot usually reduce the fracture fragments perfectly and prolonged immobilization of the joint, which is necessary for fracture healing may lead to joint stiffness. Closed reduction and stabilization using a condyle clamp to place a transcondylar screw through a stab incision is possible. The results obtained with this technique depend on the length of time since the injury occurred, the expertise and experience of the surgeon, the amount of swelling and edema present, and the amount of soft tissue interposed at the fracture site.
Open reduction and internal fixation are indicated for optimal alignment and stabilization of lateral condylar fractures and an early return to function. An early return to function will help alleviate elbow stiffness and degenerative joint disease. While several surgical approaches may be used to expose lateral condylar fractures, excellent exposure with minimal soft tissue dissection is achieved via a lateral or craniolateral approach to the elbow. The most common method employed for repair of lateral condylar fractures is a transcondylar lag screw with or without an additional crosspin for increased rotational stability.
Once the fracture site is adequately exposed, fibrin, clots, blood, and interposed soft tissue should be removed to allow perfect anatomic reduction of the articular surface. With the fracture reduced, a transcondylar hole is drilled beginning at a point just cranial and ventral to the palpable lateral epicondylar crest. The drill hole is tapped, the later condylar fragment is over-drilled to create a gliding hole, and transcondylar lag screw is placed. In order to ensure central placement of the lag screw through the condyle, an alternate technique may be employed. The lateral condylar fragment is outwardly rotated and the gliding hole is drilled from the intercondylar fracture surface out through the lateral side of the condyle. The fracture is then reduced, the medial condyle is appropriately drilled, and tapped and a lag screw is placed. An anti-rotational Kirshner wire or Steinman pin is then driven from the lateral condyle and seated into the medial cortex of the distal humeral shaft. The elbow joint should be put through a full range of motion to assess stability and to check for crepitus.
I prefer to place the limb in a modified Bobby Jones dressing to help control swelling during the immediate post-operative healing period. The owners are advised to restrict the animal’s exercise for the first 6-8 weeks after surgery while employing gentle, passive physiotherapy to help prevent elbow stiffness. When early surgical intervention, accurate anatomic reduction, and rigid internal fixation are employed a good to excellent result should be expected.
Considerable attention has been given to the topic of coxofermoral luxation in the dog primarily because hip luxation is a relatively common traumatic injury encountered in small animal practice.
Hip luxation is a relatively common traumatic injury encountered in small animal practice. Hip luxation is usually the result of blunt trauma with resultant disruption of the joint capsule and ligament of the head of the femur. The low incidence of hip luxation in dogs less than one year of age is due to the fact that the femoral capital epiphysis fuses to the femoral neck at about 11-12 months of age and that, prior to this time, trauma is more likely to cause a femoral epiphyseal separation. Numerous studies have indicated that a unilateral craniodorsal luxation is the most common injury seen.
The diagnosis of hip luxation is easily made upon physical examination and confirmed with survey radiography. While the affected limb may be held elevated, many patients will bear weight on the limb with the toes rotated laterally. Craniodorsal displacement of the greater trochante is evident as a noticeably increased distance between the trochanter and the tuber ishium, and a thumb held between these bony prominences will not be displaced laterally when the hip is rotated externally. Crepitus is usually detected upon palpation of the joint, and the affected limb will appear shorter than the contralateral limb when the dog is placed on its back and the limbs are extended caudally. Pelvic radiography will confirm diagnosis and demonstrate if there is the presence of pre-existing hip dysplasia or degenerative joint disease or concomitant injuries such as fractures of the femoral head and/or acetabular rim, all of which have a profound impact on the method of treatment selected and the ultimate prognosis.
Numerous techniques have been advocated for treatment of canine hip luxation. Closed reduction is the procedure of choice upon initial presentation of a patient with hip luxation if the luxation is not complicated by acetabular fracture, an avulsion fragment, or failed previous reduction. Closed reduction should be attempted as soon as possible after the injury, as there is a poorer prognosis for maintaining closed reduction if it is attempted more than 4-5 days post trauma. Maintenance of closed reduction may be achieved with application of a non-weight bearing Ehmer sling or insertion of a DeVita pin. Several studies have indicated a high failure rate associated with closed reduction and application of an Ehmer sling and so my personal preference is insertion of a DeVita pin. While sciatic nerve damage has been associated with this technique, in my experience, if the proper placement technique is utilized the danger of vital tissue injury is minimal. If stability is inadequate following closed reduction or if closed reduction can not be achieved, open reduction is indicated. The presence of osteochondral fragments, acetabular fractures, inversion of the joint capsule into the joint space, and the presence of debris (hemorrhage, fibrin, fibrous tissue) within the acetabulum, may preclude successful closed reduction. Another indication for open reduction is the presence of multiple orthopedic traumas where there is a need for immediate stable weight-bearing ability on the affected limb.
A number of surgical techniques have been described for management of hip luxation in the dog. These include replacement of the ligament of the head of the femur (transarticular pinning, toggle pin), extension of the acetabular rim with bone grafts or implants, reconstruction of or substitution for a damaged joint capsule (capsulorrhaphy, extracapsular suture stabilization), and the creation of extramuscular forces around the hip joint to maintain reduction (translocation of the greater trochanter). A combination of techniques may also be utilized in an effort to save the hip in difficult cases. In cases exhibiting an acetabular fracture, a significant avulsion fracture of the femoral head, pre-existing hip dysplasia, and/or the presence of degenerative joint disease, excision arthroplasty with a biceps sling or total hip replacement may be indicated. While all of these procedures have their inherent advantages and disadvantages, my procedure of choice for surgical treatment of canine hip luxation is capsulorrhaphy with trochanteric transposition. This technique is relatively simple to perform and avoids the potential complications of some of the other techniques including injury to vital structures, implant migration, pin breakage, foreign body reactions, and interference of implants with articular surfaces. Capsulorrhaphy with trochanteric transposition requires an adequate amount of intact joint capsule in which primary closure may be achieved and intact gluteal musculature to achieve internal rotation and abduction. Ideally, the joint capsule should be reconstructed and the greater trochanter advanced caudodistally to a decorticated bed while the hip is maintained in reduction, flexion, abduction, and internal rotation. In some hip luxations, the initial trauma may have resulted in extensive damage to the joint capsule and surrounding tissues such that a secure capsulorrhaphy cannot be performed. In these instances, extracapsular suture stabilization should be implemented to provide additional support during healing of the joint capsule. In most cases, a good prognosis is warranted for return of limb function when successful closed or open reductions are maintained post-operatively. Utilizing open reduction with capsulorrhaphy and trochanteric transposition as described above, early weight bearing ability is achieved and the technique offers an excellent chance of restoring a highly functional reduced hip joint without significant risk of complications or need for implant removal.
The ductus arteriosis is a normal structure that is present in the canine fetal heart.
Its purpose is to divert blood from the pulmonary artery (the vessel that brings blood from the heart to the lungs for oxygenation) directly to the aorta (the vessel that delivers blood from the heart to the rest of the body). Therefore, the ductus arteriosis is present in the fetal heart to allow the majority of canine fetal blood to flow around rather than through the lungs. This is necessary because the canine fetus lives in the fluid environment of the mother’s uterus, receiving oxygen from its mother’s bloodstream. The ductus arteriosus normally closes at the time of birth when the young animal begins to breathe, oxygen is obtained by the lungs and normal circulation is established. The problem occurs when the ductus arteriosus does not close.
With the condition patent ductus arteriosus (PDA), the ductus arteriosus does not close, causing abnormal blood flow through the heart and lungs. The result is a connecting vessel that allows blood to travel in a circular fashion from the left side of heart through the lungs and immediately back to the left side of the heart. The heart must work much harder to maintain a normal amount of blood flow to the rest of the body. This extra workload eventually causes the heart to fail. The degree to which a patient is affected depends on the magnitude of the defect. This can range anywhere from a small blind pocket off the aorta which does not cause any problems, to varying degrees of abnormal blood flow through the ductus arteriosis between the aorta and the pulmonary artery. Most commonly, there is a shunt from the left to the right side of the heart, with blood from the higher pressure aorta continuously shunted to the pulmonary artery. This means an increased volume of blood is sent to the lungs which results in fluid build-up (pulmonary edema) and volume overload of the left side of the heart. In some cases, however, the increased flow of blood into the lungs injures the pulmonary blood vessels. This can reverse the path of blood flow from right to left. In this case, un-oxygenated blood flows into the aorta. PDA is the second most commonly diagnosed congenital heart defect of dogs. It affects about 7 out of every 1000 puppies. The condition is usually inherited as a genetic trait. This condition most commonly affects the Miniature Poodle, Collie, Maltese, Shetland sheepdog, German Shepherd, Cocker Spaniel, Pomeranian, Yorkshire Terrier and Labrador Retriever. Female dogs are predisposed.
Clinical symptoms of the disease include: coughing, reduced tolerance of exercise, loss of weight, and eventually, congestive heart failure. Affected puppies initially appear normal, although they are usually smaller and play less vigorously than their littermates. Typically, there are no clinical signs until congestive heart failure develops. This leads to fluid accumulation in the lungs that causes the previously described clinical symptoms. In most cases, clinical signs develop within a year. About 60% of affected dogs will die without surgical treatment.
Patent ductus arteriosus is diagnosed by history, auscultation of a “machinary” heart murmur on physical examination, cardiac enlargement and pulmonary edema on chest x-ray, and visualization of the defect with cardiac ultrasound (echocardiagram). The majority of cases are first diagnosed upon the initial visit to a veterinarian when the characteristic heart murmur is detected on routine physical examination.
When caught early and following treatment with successful closure of the PDA, most dogs live a normal life. Unless there are complications from other heart defects or heart failure has already developed, there is rarely any future need for medication. While special circumstances can influence the prognosis, most cases are straightforward.
The conventional treatment is surgery, which should be performed shortly after the diagnosis is confirmed. Dogs as young as 8 weeks are considered surgical candidates, and it is recommended to carry out the procedure when the dog is between 8 and 16 weeks of age. There is no benefit to delaying surgery. In fact, the chances of a dog developing heart failure or suffering irreversible damage to the heart muscle only increase with time. Anesthetic and surgical risks become greater as the heart fails and the heart and lungs become irreversibly damaged. Medical therapy may be necessary prior to and immediately after surgery if significant clinical symptoms are present. Dogs with a right to left shunting PDA are to be treated medically as surgery cannot be successfully performed in these pets. The polycythemia caused by right to left shunting is treated periodically by phlebotomy, which is removing blood to control the red blood count and viscosity of the blood. When surgery is not an option, and heart failure has occurred, drug therapy with furosemide, enalapril or benazepril, and digoxin is often prescribed. A salt-restricted diet is enforced. Aspirin, indomethacin, and other prostaglandin inhibitors sometimes used to close the PDA in premature human babies do not work in dogs and should not be given to close the ductus because the canine ductus lacks the smooth muscle capable of responding to these drug therapies.
Historically, surgical ligation has been the standard method of correction. Surgery consists of performing a thoracotomy on the left side of the chest through the third or fourth intercostal space to gain access to the surgical site. The standard technique has been to dissect immediately cranial and caudal to the ductus and then carefully create a passage on the medial aspect of the ductus by blind dissection with right-angle forceps and tying off the patent ductus. Operative success should be greater than 90 percent, even in the smallest dogs, and the prognosis is excellent for a normal life if surgery is completed early. Although highly successful, surgical ligation is associated with some operative morbidity and mortality.
The least invasive treatment available is to feed a coil via a catheterized large vessel into the patent ductus arteriosis to block the flow of blood through it. However, depending on the size of the patient, anatomical and other factors, not every case is a candidate for this procedure. In these cases, open heart surgery to ligate the patent ductus ateriosus closed is necessary. If the patient is reasonably stable immediately prior to treatment, prognosis tends to be fair to good with treatment.
While traditional surgery to close the PDA has a very high success rate, more recently, thorascopic PDA occlusion using Titanium ligating clips or a custom-designed thoracoscopy clip applicator has been described. Although technically demanding, minimally invasive PDA occlusion via thorascopy is a safe and reliable technique in dogs; however, preoperative measurement of the diameter of the PDA is crucial to determine if complete closure with metal clips can be achieved. Assuming the diameter of the PDA is amenable to clip ligation, minimally invasive thorascopic PDA occlusion can be considered as an alternative to occlusion via conventional thoracotomy.
More recently, minimally invasive transcatheter techniques have been employed for PDA occlusion. Transarterial PDA coil embolization is a safe, less invasive alternative for PDA occlusion. This procedure involves catheterization of the femoral artery under general anesthesia. An angiogram is then performed to delineate PDA morphology and facilitate coil selection. Coils are commercially available and composed of surgical stainless steel with prothrombotic poly-Dacron fibers. Coil occlusion has been widely accepted as a relatively safe and effective treatment for PDA in dogs, although careful patient selection is helpful in achieving a high success rate. Important patient factors that affect successful coil occlusion include the size and morphology of the ductus and the patient’s body weight. The standard arterial approach for PDA coil embolization requires placement of a 4-French sheath introducer into the femoral artery. The estimated minimal patient body weight needed to safely introduce this device is ∼2.5 kg, although there is variability associated with operator experience as well as the breed and age of the patient. Coils are advanced through a catheter into the PDA under fluoroscopic guidance until satisfactory angiographic occlusion is documented. Patients are then recovered and released the following day. This procedure requires substantial technical expertise and specialized equipment.
Many devices are available to close a PDA, and in each case, the device that is used is determined by the size of the PDA. For narrow PDAs, a vascular coil, as described above, can be used to close the vessel. Larger PDAs can be closed by canine ductal occluders (CDO) or vascular plugs. To place any of these devices, a small incision is made allowing entry into the femoral artery and then the device is threaded through the artery to close the PDA. The Amplatz canine duct occluder (ACDO) is a nitinol mesh device with a short waist that separates a flat distal disc from a cupped proximal disc. The device is designed to conform to the morphology of the canine patent ductus arteriosus. PDA dimensions are determined by angiography, and a guiding catheter is advanced into the main pulmonary artery via the aorta and PDA. An ACDO with a waist diameter approximately twice the angiographic minimal ductal diameter (MDD) is advanced via the catheter using an attached delivery cable until the flat distal disc deploys within the main pulmonary artery. The partially deployed ACDO, guiding catheter, and delivery cable are retracted until the distal disc engages the pulmonic ostium of the PDA. With the delivery cable stabilized, the catheter is retracted to deploy the waist across the pulmonic ostium and cupped proximal disc within the ductal ampulla. Tension on the delivery cable is released, and correct ACDO positioning and stability are confirmed by observing that the device assumes its native shape, back-and-forth maneuvering of the delivery cable, and a small contrast injection made through the guiding catheter. The delivery cable is detached and removed with the guiding catheter. To assess for any residual ductal flow, an angiogram is performed at the conclusion of the procedure, followed by Doppler echocardiography. PDA occlusion in dogs with the ACDO is straightforward and extremely effective across a wide range of body weights, MDDs, and ductal morphologies.
In conclusion, prompt and appropriate diagnosis and treatment of this congenital, hereditary cardiac disorder is associated with an excellent long term prognosis. Both standard surgical and minimally invasive transcatheter techniques can be utilized at the surgeon’s discretion to achieve success.