Paul A Lotke and RG Simon

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Many patients requiring total knee arthroplasty will have a moderate flexion contracture that is fully corrected at surgery. However, when preoperative contractures are greater than 20 degrees, the deformity may become fixed and require special surgical consideration. This chapter will discuss these patients.

The deformity is a result of either a bone block and/or soft tissue contractures (Fig. 5.1). The proliferation of osteophytes in degenerative joint disease or prior trauma creates bone blocks that can occur in the anterotibial or posterofemoral condyles. They mechanically abut the intercondylar notch, or tether the posterior capsule, thus preventing full extension. The bone deformity may be slowly progressive and subsequently cause secondary soft tissue contracture of the posterior capsule and collateral ligaments.

Soft tissue contracture occurs in patients with long-standing deformities from a variety of disease states such as inflammatory arthritis, immobility, hemophilia, and neuromuscular disorders. These contractures can be static or progressive and can lead to increasing tightness in the posterior capsule, collateral ligaments, and hamstring muscles. Once the deformity exceeds 50 degrees, the collateral ligaments are inevitably involved.

Flexion of the knee is a response to inflammation, infection, or any condition that leads to joint swelling and increased intra-articular pressures. It has been demonstrated that increasing intra-articular pressure results in the knee assuming a 30- to 45-degree flexion position.1

Fixed flexion contractures decrease the patient's ability to walk. Velocity is slowed and energy costs are increased. Perry and asso-ciates2 measured a 50% increase in work by the quadriceps at a given rate of ambulation in the presence of bilateral contractures of 30 degrees. The adjacent joints also assume abnormal posturing and increase the energy requirements with a corresponding reduction in endurance. Persons who have added disability of muscle

Severe Contractures
FIGURE 5.1. (A) Patient with rheumatoid arthritis and fixed flexion from soft tissue contracture. (B) X ray of patient with osteoarthritis and severe flexion contracture secondary to bone impingement preventing full extension.

weakness from disease atrophy or paralysis may lose their ability to walk.

Persistent flexion posture eventually leads to tightening of the posterior capsule and portions of the collateral ligaments. Normally these structures help prevent hyperextension and are at full length in extension. With a flexion contracture the collateral ligament and posterior capsule shorten, thereby preventing full extension. it is undetermined if the posterior cruciate ligament contributes to the persistence of flexion contracture, because this ligament lengthens with flexion.

The secondary soft tissue shortening of the capsule and portions of the collateral ligament makes it difficult to achieve ligament balancing during total knee replacement. At surgery we attempt to achieve an equal space between the femur and tibia in both flexion and extension (Fig. 5.2). This is referred to as a balanced flexion-extension gap. in a normal knee we use "measured resections" (i.e., removing equal amounts of bone from the femur and tibia that are to be replaced with prosthetic material). The flexion and extension gaps should be equal after the bony cuts are performed. Patients with long-standing flexion contractures will have a normal flexion gap, but a narrow gap in extension. This leads to persistence of the contracture. This imbalance can be corrected by releasing the soft tissue contracture and/or resecting more distal femur, thereby increasing the extension gap. As more bone is resected from the femur, the joint line is subsequently moved proximally. This creates alterations in the kinematics of the knee and in the contact points of the patella femoral joint. occasionally it is necessary to take a few more millimeters of distal femur. However, the preferable method to achieve flexion-extension gap balance is to release the soft tissue structures.

in addition to the flexion contractures there is an attenuation in the extensor mechanism and anterior capsule.3 Although this does not create intraoperative problems, it may contribute to persistent extensor lag and some degree of persistent quadriceps weakness, and may inhibit the patient's ability to maintain full extension during the postoperative period. it is important to recognize this potential for prolonged extensor lag so that the knee can be protected from current deformity.

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