TPLO Information

The science behind the evaluation and surgery of dogs with cranial cruciate insufficiency continues to be dynamic within the field of veterinary medicine. Beginning with Paatsama in 1952, the pathogenesis of cruciate pathology in the dog was described, and surgical techniques were developed and utilized for stifle stabilization including Fascial Strip (Paatsama, 1952), Lateral Retinacular Imbrication (DeAngelis, 1970), Fibular Head Transposition (Slocum, 1971), Posterior Capsulorrhaphy (Hohn, 1973), Modified Lateral Retinacular Imbrication (Flo, 1975), Over-the-Top (Arnoczky, 1979), Ligament Transplants (Milton, 1982), Under-and-Over (Hulse, 1983), and Fibular Head Advancement (Smith, 1984). Both intra-capsular and extra-capsular techniques utilizing various modifications and materials for cruciate instability, although most often better than conservative management, have been inconsistent in returning dogs to preinjury status regardless of size, breed or activity. In 1983, Slocum described cranial tibial thrust as a primary force in the canine stifle. Subsequently in 1993, he introduced an alternative biomechanical and surgical approach to cruciate ligament insufficiency based on cranial tibial translation.(1) Tibial Plateau Leveling Osteotomy (TPLO) is a relatively new and very innovative surgical procedure for cranial cruciate insufficiency. As all new procedures, there is only early objective scientific published data.(,2,3,4,5,6,7) The intent of this presentation is to provide basic understanding of the procedure, objective data that is available, and author's experience with the clinical results of the procedure over the past 6 months.

Historical and current surgical techniques are based on the traditional or passive model of stifle joint stability, and rely on stabilizing the stifle against cranial drawer movement. (Fig. 1. The stifle joint passive restraints against cranial drawer (C )include the cranial cruciate ligament (A) and the medial meniscus (B)).Based on this model, the femur rests on top of the tibial plateau, the cranial and caudal cruciate ligaments, joint capsule and menisci act as passive restraints to cranial tibial translation, stifle hyperextension and excessive internal rotation of the tibia. Passively, internally generated forces only flex and extend the stifle joint. This model incompletely explains cranial cruciate insufficiency (Fig. 2. Cranial cruciate ligament rupture (A) with the tibia (B) in a morecranial position due to translation or movement forward of the tibia inrelation to the femur. As cranial translation occurs, the caudal cruciateligament (C) becomes lax) in the absence of trauma, the actual mechanism responsible for cranial cruciate ligament trauma and impingement of the medial meniscus, or the inconsistent surgical outcomes utilizing techniques that re-create passive constraints . Basically, the cranial drawer sign is a passive force created by the veterinarian and now may be considered a diagnostic tool with new understanding of the biomechanics of the stifle.

The active model expands upon the passive model to include biomechanics of the stifle integrating the function of forces created by muscles and weightbearing. Muscles associated with the stifle create force, moment, and equilibrium. The forces created by muscles of stifle flexion and extension participate in the balance of moments around the instant center of motion of the stifle. (Fig. 3. Forces created by the extensor (A, E, D) and the flexor (B,C) muscles of the stifle act in concert in the balance of moments around the instant center of motion (F) of the joint.)Tibial compression is created by the extensor muscles of the limb plus the force of weightbearing. (Fig 4. The components of tibial compression include the muscles of extension (A,B,C) and the forces of weightbearing (D).)The caudal direction of the tibial plateau promotes a shear force cranially during tibial compression. (Fig 5. Tibial compression can be simulated by the tibial compression test by flexing the hock (A) while supporting the femur to demonstrate the shear force created in a cranial direction (B).)Because the contact point between the femur and tibia are cranial to the center point line, to maintain equilibrium additional passive and active forces are required to prevent the tibia from projecting forward. This shear component of tibial compression, cranial tibial thrust (CTT), is balanced by the pull of the stifle flexor muscles of the thigh (active component) and the joint capsule, cranial cruciate ligament and the caudal horn of the medial meniscus (passive components). (Fig 6A. The shear force (A) or tibial thrust created by weightbearing and the action of extensor muscles in the cranial direction is balanced by the active component of the flexor muscles (B).)When the active muscle force of the flexor muscles is inadequate to prevent the cranial translation of the tibia, the passive restraint of these components counter this CTT. (Fig. 6B. When the cranial tanslation of the tibia (C) exceeds the active muscle force of the flexor muscles (D), the passive components which include the cranial cruciate ligament (A) and the medial meniscus (B) are relied upon. Damage occurs when the forces exceed the integrity of these structures.) The magnitude of the cranial tibial thrust is determined by the amount of compression between the femur and tibia, and is proportional to the slope of the tibial plateau with respect to the line between the centers of motion of the stifle and hock. (Fig. 7. The tibial plateau axis is sloped (B) which plays a major role in cranial tibial thrust. The single force (E) between the femur and tibia can be broken down into components of compression (D) along the tibial axis subsequent to weightbearing and muscle forces, and slippage across the tibial plateau (F). Cranial tibial thrust (C) is apposed primarily by active forces and if excessive can overwhelm secondary passive elements, thus cranial cruciate ligament and medial meniscal tissues can be damaged.)When the cranial tibial thrust exceeds the strength of the cranial cruciate ligament, incremental (partial tearing) or entire ligament disruption (complete tearing) occurs, as well as stress and tearing of the caudal horn of the medial meniscus. (Fig. 6-B) Excessive tibial slope (Fig 8. Excessive slope of the tibial plateau can be compared to the pull of a wagon up an incline.) predisposes the canine to cranial cruciate ligament insufficiency.

In a recently reported study, tibial plateau angles(TPA) were compared in normal dogs with dogs with naturally occurring cranial cruciate ligament (CrCL) injuries.(4) Dogs with naturally occurring CrCL injuries (mean 23.76 degrees) had a significantly (P<.01) greater TPA than normal dogs (mean 18.10 degrees) of similar age and body weight. Additionally, the TPA of the most commonly affected breeds (Labrador Retrievers, Golden Retrievers, and Rottweilers) in this study was significantly (P<.01) greater than that of dogs of the same breed without CrCL injuries. The conclusion of the study was that greater TPA increases the stress applied to the CrCL predisposing it to injury. In an report currently in review for publication, the TPA of a clinical population of dogs with diagnosed CrCL rupture undergoing TPLO were compared to a control Greyhound population.(5) TPA angles of dogs with CrCL insufficiency ranged from 15 degrees to 42 degrees with a mean of 24.96 degrees. Comparatively, tibial plateaus of the control population ranged from 16 degrees to 25 degrees with a mean of 20.84 degrees. These angles compared favorably with the results of the aforementioned study.(4) A significant (P<0.001) difference between the TPA angles of the clinical and control groups was found supporting that the conformation of the tibial plateau plays a integral role in the pathogenesis of CrCL disease.(5) Thus decreasing the slope of the tibial plateau reduces the CTT, and incrementally increases the dependence on the caudal cruciate ligament as a passive restraint to caudal tibial subluxation.(3)

The objective of traditional surgeries, based on the passive model, is the elimination of cranial drawer sign. The objective of the tibial plateau leveling osteotomy is neutralization of the cranial tibial thrust and not complete elimination of the drawer sign. The stifle is redesigned (Fig. 9. The rotation of the proximal tibia (arrow indicates the direction of rotation) makes the tibial axis (B) perpendicular to the tibial plateau axis (A) which neutralizes cranial tibial thrust. The rotation is held by a special plate (C).) so that the cranial cruciate ligament is no longer necessary for stifle stabilization while under active muscle force conditions, and there is minimal reliance on the caudal cruciate ligament as a passive restraint. (Fig. 10. Redesigning the stifle creates a balance between weightbearing and active muscle forces (A,B) eliminates the need for passive components for stability. The special plate (C) holds the rotational osteotomy in place until bone healing.) In essence, the cranial translation during functional loading and activity is neutralized. In an in vitro study assessing the CTT in the CrCL deficient stifle placed under axial tibial loading before and after TPLO resulted in caudal drawer movement following plateau leveling. Increasing tibial loads in the tibial plateau leveled CrCL deficient stifle increased caudal tibial thrust.(6) The cranial drawer sign may still be present after TPLO surgery. According to Slocum, a certain amount of drawer sign is built into the procedure to protect the integrity of the caudal cruciate ligament. However, as the in vitro study suggests, over rotation of the tibial plateau may predispose the caudal cruciate to excessive stress. (Fig. 11. A technical error of over rotation would create an imbalance between flexor muscle forces (B), and active weightbearing and extensor muscle forces (B). The resulting caudal tibial thrust may predispose the caudal cruciate ligament (D) to excessive stress, and further meniscal (C) trauma.

The success of the TPLO procedure has been based on the return of full flexion of the stifle, muscle mass and limb function, and the apparent lack of joint inflammation or progressive degenerative joint disease within the joint. The persistence of cranial drawer after a TPLO is not a valid test for stifle stability and is not a SIGN OF FAILURE. The procedure has provided performance dogs the ability to return to normal function handling the highly competitive demands of their sport or work. Thus, the family pet is even better able to participate in normal daily activities without restriction of activities or residual lameness as often experienced with traditional surgical procedures.

The procedure involves specific radiographic positioning prior to surgery for critical calculations (Fig. 12. Preoperative radiographs are taken to measure the tibial plateau angle.) necessary to determine the degree of rotation required to level the tibial plateau ensuring that cranial tibial thrust is neutralized and the caudal cruciate ligament is not stressed. Generally, a standard arthrotomy of the stifle is not performed. Inspection of the joint, debridement of the ligament fibers, and medial meniscal release can be performed by arthroscopy. Alternatively, only a small incision in the caudal joint capsule is required to release (sharp bisection of the caudal horn) the medial meniscus which prevents future impingement, or torn sections to be removed in the event of existing tears. Biradial saw blades, a specially designed jig, oscillating saw specific for the blades, and a TPLO plate are required to perform the patented procedure. Postoperative radiographs utilizing the same positioning used prior to surgery are necessary to evaluate technique and measure the new angle created. (Fig. 13. Postoperative radiographs are taken to measure the tibial plateauangle after the rotational osteotomy.) Postoperatively, a soft padded bandage is applied for the first 3 days to limit swelling and edema.

In a recent report of 125 TPLO procedures on 112 dogs, the mean preoperative tibial plateau slope was 25.1 degrees (range 15-33).(7) The mean postoperative tibial plateau slope was 7 degrees (range 1-14) with a mean change in slope of 18.1 degrees (range 9.5-29). Major complications occurred in 4% of the cases. Four of the five complications developed in the first 37 procedures performed. These complications included tibial crest fracture (n=3) and osteomyelitis (n=2). Potential risk factors for the development of postoperative complications included surgeon inexperience, technical errors, small tibia size relative to blade size, bilateral pelvic limb pathology, and inadequate protection of the surgical wound from the patient during wound healing.(7)

The postoperative rehabilitation is longer than extracapsular techniques due to the osteotomy. Initial rehabilitation in our practice involves physical therapy modalities that concentrate onsoft tissues such as cryotherapy, heat, passive range of motion, and programs that reduce inflammation, edema and pain (1 week)following bandage removal. Immediatelyafter surgery and once home, weightbearing activity is strictly controlled due to the immediate use of the limb for 3 weeks. Radiographs are performed at 30 day intervals to assess implants and osteogenic activity at the osteotomy site. After adequate healing (Fig. 14. Postoperative radiographs revealing the healing process of the osteotomy site.of the osteotomy site is radiographically noted (generally 4 weeks), additional physical therapy is initiated to begin rebuilding and retraining muscle groups, and promote range of motion (2 weeks). Modalities include neuromuscular stimulation, therapeutic ultrasound, treadmill activity, and swimming / under water treadmill in the therapy pool. Following physical therapy, weightbearing activities are developed over a period of months before normal activity is resumed. These involve gradually increased leash walking, sit / stay / rises, ascending inclines, and other protocols developed by our therapists for individual patients. At 12 weeks, patients begin light off-leash activities which are progressively increased until 16 weeks. At 16 weeks, patients engage in preoperative activities.

In our first 40 cases, there have been no major postoperative complications. It is our belief that attention to technical detail and established postoperative physical therapy protocols have resulted in excellent clinical results devoid of reported complications. One patient developed wound dehiscence 3 weeks postopeatively. Culture and sensitivity revealed no pathologic organisms. Surgical reconstruction of the wound resulted in complete healing. Patients are typically weight bearing the day after surgery and are very sound by 4 weeks. Lameness is not apparent by 4 -12 weeks, and patients are back to normal activity within 16 weeks. Previously operated stifles in which traditional methods of stabilization were used have undergone TPLO with results similar to those having TPLO performed initially.

Although the procedure is more involved and requires a significant investment in time training, equipment and supplies, the cost is not significantly more in our practice than traditional surgery and physical therapy because the cost is fixed to include evaluation, all preoperative and postoperative radiographs, surgery, hospitalization (24-hour care), medications, necessary follow-up through 16 weeks, and physical therapy. Considering the cost and the rehabilitation, the results certainly justify the additional expense for the procedure. Client satisfaction remains extremely high, and client awareness of and demand for the procedure are increasing. Currently dogs 45 - 50 lb. and over are potential candidates for TPLO. However, instrumentation for smaller dogs will eventually be available. The TPLO is an extremely detailed and technical procedure requiring exceptional surgical expertise, obligatory training, and a substantial orthopedic caseload for proficiency. In our practice the procedure has rapidly become the standard of care for CrCL insufficiency and is currently the ideal treatment of choice for medium - large, large, and giant breeds.

References

1.Slocum B, Slocum TD. Tibial Plateau Leveling Osteotomy for Repair of Cranial Cruciate Liagament Rupture in the Canine. Vet Clin N Amer: Smal Anim Pract. 2000,23(4):777-795.

2. Schwarz PD. Tibial Plateau Leveling Osteotomy (TPLO): A Prospective Clinical Comparative Study. Proc Ninth Annual Amer Coll Vet Surg Symposium, 1999, 379-80.

3. Warzee CC, Dejardin LM, Arnoscky SP, et al. Effect of Tibial Plateau Leveling Osteotomy on cranial and caudal tibial thrust in canine cranial cruciate deficient stifles: an in-vitro analysis. Vet Surg (abstr) 1999: 28:407.

4. Morris EH, Lipowitz AJ. Comparison of Tibial Plateau Angles in Dogs With and Without Cranial Cruciate Ligament Injuries. Abstr Proc Tenth Annual Amer Coll Vet Surg Symposium, 2000, 15.

5. Wheeler J, Taylor RA, Steinheimer DN. Evaluation of the Tibial Plateau Angle as a Predisposing Factor for Cranial Cruciate Rupture in the Dog. Unpub.

6 Hulse DA, Hauptman JG. Effect of Tibial Plateau Leveling Osteotomy on Joint Stability in the Canine Cranial Cruciate Deficient Stifle Under Axial Tibial Load: An In Vitro Study. Abstr Proc Tenth Annual Amer Coll Vet Surg Symposium, 2000, 18.

7. Palmer RS. Tibial Plateau Leveling Osteotomy. Proc Tenth Annual Amer Coll Vet Surg Symposium, 2000, 271-275.