Management of Bone Loss: Structural Grafts in Revision Total Knee Arthroplasty

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CHAPTER SYNOPSIS:

Major bone loss around total knee arthroplasty is a frequent reconstructive challenge. Elimination of infection is critical. Contained defects can be reconstructed with morselized allograft or newer highly osteophyllic metals. Reconstruction of small uncontained lesions can be managed with metal augments. Large defects necessitate structural allograft or mega-prostheses in certain situations.

IMPORTANT POINTS:

1

Reconstruction of bone defects is required any time that revision component stability is compromised.
2

It is critical to rule out infection as an underlying cause.
3

Surgical technique depends on the size of the lesion and whether it is contained or uncontained.

CLINICAL/SURGICAL PEARLS:

1

It is critical to rule out infection cases with significant bone loss, particularly if there is clinical suspicion, very early in the life span of the implant or extreme in magnitude.
2

Careful wound assessment is very important and the potential for a soft tissue rotational flap must be kept in mind.
3

Both structural and morselized allograft bone should be available in the operating room at the initiation of the procedure.
4

Surgery should be carried out using standard revision total knee arthroplasty techniques including careful balance of flexion and extension gaps.
5

Careful wound care and status of the wound must be carefully attended to in the post-operative phase, since these knees have often been multiply revised.

CLINICAL/SURGICAL PITFALLS:

1

It is critical to diagnose and treat infection prior to reconstruction.
2

Revision implants with stems should always be used.
3

Fixation of structural allografts is accomplished by step cuts, press-fit, and screws.
4

Cement is used for the prosthesis-allograft composite but not for host bone fixation.

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HISTORY/INTRODUCTION/SCOPE OF THE PROBLEM

Dealing with bone loss can be one of the greatest challenges in revision total knee arthroplasty (TKA). Adequate bony support of implants is critically important to a successful procedure. This chapter will discuss frequently encountered sources of bone loss as well as methods of reconstruction, which overcome these deficiencies.

Etiology of Bone Loss

Osteolysis, infection, aseptic loosening and stress shielding are the most common causes for large amounts of bone loss. This bone loss is known to be particularly severe when revision from hinged or stemmed components is undertaken. Overzealous surgical bone removal, which can occur at the time of primary arthroplasty, revision arthroplasty, or debridement for infection, can also be a source of significant bone loss.

Large amounts of bone loss and destruction can directly result from an infected TKA, especially if there is concomitant mechanical loosening. Infection can also indirectly cause bone loss as a result of static cement spacers which may erode and destroy bone during the first stage of a two-stage infected TKA treatment ( Fig. 20-1 ). Significant bone loss can also occur by overly aggressive debridement and resection on either the femoral or tibial side. Although this is more commonly seen when considering surgical debridement for infection, it can also occur during primary and revision TKA as reported by other authors.

In a series by Hockman, Ammeen, and Engh, the most common etiology of TKA failure resulting in the requirement of a structural allograft was osteolysis or bony destruction due to polyethylene wear. This occurred in 16 of 24 revision TKAs in that series. Lachiewicz and Soileau found osteolytic lesions in 8 of 112 knees with a modular posterior stabilized cemented TKA. Osteolysis was diagnosed in 16% of uncemented TKAs reviewed by Peters at an average of 35 months after surgery. The most common site of bone resorption was the tibial diaphysis while a histological examination showed that most intracellular polyethylene and metal particles were less than a micron in size. Polyethylene debris was associated with micromotion between modular polyethylene inserts and metal tibial trays as well as other risk factors believed to include uncemented components, screw fixation, and thin polyethylene.

INDICATIONS/CONTRAINDICATIONS

Any patient presenting with radiographic evidence of bone loss around a TKA requires a complete investigation to define the underlying cause. The most critical diagnosis to exclude is infection.

In patients with significant bone destruction around knee prosthesis, the differentiation between a septic cause and aseptic mechanical failure is not always obvious. Chronic pain, especially at rest is more common in patients with an infected prosthesis. On the other hand, pain associated with weight bearing is more indicative for patients with aseptic loosening of the prosthesis. Persistent stiffness and joint effusion are common symptoms of a deep infection around total knee arthroplasty. The presence of symptoms in the patient’s history, such as prolonged postoperative wound drainage, the use of antibiotics for primary wound healing problems, and knee stiffness recalcitrant to rehabilitation can also suggest deep postoperative infection.

Diagnostic tools readily available that can assist in the assessment for infection is blood work including a leukocyte count, a C-reactive protein level, and erythrocyte sedimentation rate. Elevation of these blood markers can be characteristic of chronic infection. In the absence of other systemic sources, a septic knee or infected prosthesis should be suspected. Arthrocentesis is an essential part of the workup for a suspected chronic infection of the knee joint. A leukocyte count with differential, Gram stain, and culture for aerobic and anaerobic bacteria should be used to evaluate the aspirate. A series of consecutive radiographs can demonstrate new lytic lesions and periosteal reaction around the infected bone. The use of radioisotope investigations such as gallium and indium in comparison with a technetium scan can help with the differential diagnosis of infection. Even with negative results for all the above-mentioned tests, infection may still be diagnosed intraoperatively. A frozen section of deep tissue, with a polymorphonuclear leukocyte count, is a useful intraoperative tool to diagnose infection. Ten polymorphonuclear leukocytes per high-power field is generally considered indicative of infection.

Preoperative delineation of the bone defects requires imaging including routine radiographs. It is our standard protocol to obtain weight-bearing anteroposterior, lateral, and skyline radiographs in addition to a full-length standing views. It is recommended that prior to undertaking revision surgery, the precise configuration of major defects should be well understood. This may necessitate enhanced imaging beyond plain radiographs, such as a computed tomography scan ( Fig. 20-2 ).

CLASSIFICATION SYSTEM

The following classification has been developed by the authors and is used when communicating and describing specific cases of bone loss around TKAs.

Tibial Bone Loss

Contained bone loss is defined as a lesion which is surrounded by an intact cortical rim of bone. Bone loss is considered uncontained when there is no surrounding cortical sleeve.

Type I — No notable loss of bone stock . There may be erosion of the endosteal bone, but there is no involvement of the cortex. There has been no migration of the component and bone is largely intact.
Type II — Contained loss of bone stock with cortical thinning . The canal is widened, but there is still an intact cortical sleeve.
Type III — Uncontained (segmental) loss of bone stock involving less than 50% of either medial or lateral tibial plateau . Uncontained bone loss less than 50% of medial or lateral tibial platform and less than 15mm in depth.
Type IV — Uncontained (segmental) loss of bone stock greater than 50% of either medial or lateral tibial plateau . Total bone loss greater than 50% of medial or lateral tibial platform and more than 15mm in depth.

Femoral Bone Loss

Type I — No notable loss of bone stock . There may be erosion of the endosteal bone, but no involvement of the cortex. There has been no migration of the primary femoral component and bone is largely intact.
Type II — Contained loss of bone stock with cortical thinning . The canal is widened, but there is still an intact cortical sleeve.
Type III — Uncontained (segmental) loss of bone stock involving less than 50% of medial or lateral femoral condyle . Uncontained bone loss less than 50% of medial or lateral femoral condyle and less than 15mm depth.
Type IV — Uncontained (segmental) loss of bone stock greater than 50% of medial or lateral femoral condyle . Total bone loss greater than 50% of medial or lateral femoral condyle and more than 15mm deep.