Abstract
There is a difference between “functional instability” of a total knee arthroplasty (TKA) and a case of “TKA instability”. For example a TKA with a peri-prosthetic fracture is unstable, but would not be considered a “case of instability”. The concept of “stability” for a TKA means that the reconstructed joint can maintain its structure and permit normal motion and activities under physiologic loads. The relationship between stability and alignment is that stability maintains alignment. Instability means that there are numerous alignments and almost always the worst one for the loading condition. In the native knee, “instability” is synonymous with ligament injury. If this were true in TKA, then it would be reasonable to treat every “unstable TKA” with a constrained implant. But that is NOT the case. If the key to successful revision of a problem TKA is understanding (and correcting) the specific cause of the problem, then deep understanding of why the TKA is unstable is essential. A case of true “instability” then, is the loss of structural integrity under load as the result of problems with soft tissue stabilizing structures and/or the size or position of components. It is rare that ligament injury alone is the sole cause of instability (valgus instability invariably involves valgus alignment; varus instability usually means some varus alignment and compromised lateral soft tissues). There will be forces (structures) that create instability and forces (structures) that stabilise.
There are three categories of instability: Varus-valgus or coronal: Assuming that the skeleton, implant and fixation are intact. These are usually cases that involve ligament compromise, but the usual cause is CORONAL ALIGNMENT, and this must be corrected. The ligament problem is best solved with mechanical constraint. Gait disturbances that increase the functional alignment problems (hip abductor lurch causing a valgus moment at the knee, scoliosis) may require attention of additional compensation with re-alignment. Plane of motion: Both fixed flexion contractures and recurvatum may result in buckling. The first by exhaustion of the quadriceps (consider doing quadriceps “lunges” with every step) and the second because recurvatum is usually a compensation for extensor insufficiency. The prototype for understanding recurvatum has always been polio. This is perhaps one of the most difficult types of instability to treat. The glib answer has been a hinged prosthesis with an extensor stop but there are profound mechanical reasons why this is flawed thinking. The patient with recurvatum instability due to neurologic compromise of the extensor should be offered an arthrodesis, which they will likely decline. The simpler problem of recurvatum secondary to a patellectomy will benefit from an allograft reconstruction of the patella using a modified technique. A common occurrence is obesity with patellofemoral pain, that the patient has managed with a “patellar avoidance” or “hyperextension gait”. Plane of motion instability is a problem of the EXTENSOR MECHANISM DEFICIENCY. Flexion instability. This results from a flexion gap that is larger than the extension gap, where a polyethylene insert has been selected that permits full extension but leaves the flexion gap unstable. These patients achieve remarkable flexion easily and early, but have difficulties with pain and instability on stairs, with recurrent (non-bloody) effusions and peri-articular tenderness. Revision surgery is necessary. Flexion instability may also occur with posterior stabilised prostheses. So-called “mid-flexion” instability is a contentious concept, poorly understood and as yet, not a reported cause for revision surgery distinct from “FLEXION INSTABILITY”. Flexion instability is a problem of GAP BALANCE.
