A sixty-three-year-old man presented with an acute exacerbation of chronic
pain in the left knee and subjective weakness of the left lower extremity.
Specifically, he described a progressive neurologic deficit that had developed
over a period of four months and that had resulted in a profound footdrop. He
characterized the knee discomfort as moderate pain that limited his ability to
walk one to five blocks. The patient used a cane when walking long distances
and held onto a banister for stair-climbing. He stated that he had not had a
recent traumatic episode and did not have pain radiating from the back.
Physical examination revealed that the patient weighed 86 kg and was 178 cm
tall. He walked with a steppage gait and had a varus thrust of the left knee.
The knee was in 10° of varus alignment when the patient was standing.
Palpation of the knee demonstrated patellofemoral crepitus and medial
joint-line tenderness. The range of flexion was from 10° to 120°.
Examination of the ligaments with the knee in maximal extension (a 10°
flexion contracture) demonstrated 10 mm of varus laxity with a soft end point.
With valgus stress, the knee alignment improved to neutral (0°) with a
solid end point. Motor examination demonstrated grade-0 of 5 strength of the
tibialis anterior and extensor hallucis longus muscles. There was decreased
sensation to light touch and to pinprick on the dorsum of the left foot and in
the first web space. An examination of the hip, spine, and pelvis revealed
unremarkable findings. The Knee Society clinical and functional
scores6 were 43 and
69 points, respectively.
Radiographic examination of the knee demonstrated medial compartment
osteoarthritis and varus angulation (Fig.
1). Radiographs of the lumbar spine demonstrated mild degenerative
disc disease at the L4-L5 level. Magnetic resonance imaging of the lumbar
spine showed no canal stenosis or foraminal narrowing. Electromyography and
nerve condition studies demonstrated a peroneal neuropathy at the level of the
knee.
Given the history of progressive knee pain, neurologic deficit, varus knee
alignment and laxity, and medial compartment arthritis, we recommended total
knee arthroplasty in conjunction with exploration and decompression of the
peroneal nerve. At surgery, the nerve was found to be grossly intact without
discontinuity or contusion. There was no evidence of a neuroma or a focal
compression. A primary total knee arthroplasty (Advance; Wright Medical
Technology, Arlington, Tennessee) was performed. Ligament balancing was
obtained by a medial release. Despite the restoration of anatomic alignment,
residual varus laxity (5° in extension) was present with a posterior
stabilized tibial insert. Therefore, a constrained tibial insert and cemented,
stemmed femoral and tibial components were used to minimize any persistent,
repetitive traction on the peroneal nerve.
The patient was evaluated at four weeks, four months, one year, and two
years postoperatively, over which time the knee pain resolved and the peroneal
nerve function improved. At the two-year follow-up examination, the patient
had no knee pain and no numbness or tingling of the foot. He was able to walk
unlimited distances and to climb stairs with use of the banister, and he did
not use a cane. The range of knee flexion was from 0° to 130°, with no
extensor lag or instability. The neurologic examination demonstrated grade-4
of 5 strength of the extensor hallucis longus muscle and grade-4+ of 5
strength of the tibialis anterior muscle. The sensory examination demonstrated
only a slight decrease in sensation to pinprick in the first dorsal web space.
The Knee Society clinical and functional scores were 100 and 91 points,
respectively. Radiographs demonstrated a well-fixed prosthesis with no
radiolucencies, osteolysis, or asymmetric polyethylene wear
(Fig. 2).
This patient presented with a varus arthritic knee and an associated
peroneal nerve palsy. We hypothesized that traction on the common peroneal
nerve at the level of the fibular neck secondary to moderate lateral laxity of
the knee was the cause of the neuropathy. In support of this theory,
preoperative electromyography demonstrated an injury to the common peroneal
nerve at the level of the knee. Therefore, we explored the peroneal nerve and
performed a decompression at the level of the fibular head and neck to
diagnose and treat any potential compressive lesion or tethering by soft
tissue. The absence of a compressive lesion at the time of the operation is
entirely consistent with our preoperative hypothesis that this was a
repetitive traction injury of the peroneal nerve, similar to a repetitive
traction injury of the ulnar nerve at the cubital
tunnel7.
Mild or moderate residual ligament laxity is not uncommon after primary
total knee
arthroplasty8. In
our patient, a constrained total knee design was used to minimize any residual
varus laxity, to prevent continued traction on the peroneal nerve, and to
optimize the environment for recovery of the nerve. Importantly, after a
medial release and correction of knee alignment, this patient still had mild
residual varus laxity intraoperatively. Therefore, a constrained tibial insert
was utilized.
To our knowledge, the management of a progressive peroneal nerve palsy
associated with a varus arthritic knee has not been reported. Treatment
options include bracing and measures to treat symptoms, nerve exploration and
decompression alone, conventional total knee arthroplasty with or without
nerve decompression, and constrained total knee arthroplasty with or without
nerve decompression. The efficacy of these various treatment options is not
known. Our patient had a profound peroneal nerve palsy that progressed over
the course of five months and was associated with moderate varus laxity of the
knee. We initially performed a nerve exploration and decompression to release
any source of nerve entrapment and to optimize the local environment for
recovery of the nerve. We then implanted a total knee prosthesis with a
constrained tibial insert in an attempt to minimize the risk of any continued
residual traction on the peroneal nerve at the level of the fibular neck. This
treatment strategy was associated with an excellent clinical result at two
years.