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The Journal of Bone and Joint Surgery 78:177-84 (1996)
© 1996 The Journal of Bone and Joint Surgery, Inc.

Peroneal Nerve Palsy after Total Knee Arthroplasty. Assessment of Predisposing and Prognostic Factors*{dagger}

OSARETIN B. IDUSUYI, M.D.{ddagger} and BERNARD F. MORREY, M.D.{ddagger}, ROCHESTER, MINNESOTA

Investigation performed at the Department of Orthopedics, Mayo Clinic and Mayo Foundation, Rochester.


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Thirty-two postoperative peroneal-nerve palsies in thirty patients were documented in a retrospective review of 10,361 consecutive total knee arthroplasties performed at one institution from 1979 through 1992. The mean age of the thirty patients was sixty-five years (range, twenty-eight to seventy-eight years). Four of these patients had had a previous proximal tibial osteotomy and five had had a previous lumbar laminectomy. Ten knees (ten patients) had preoperative valgus alignment of 12 degrees or more. A control group of 100 patients who had had total knee arthroplasty during the same period was computer-matched to the patients by age, sex, and operating surgeon. Comparison of this control group with the thirty patients showed that epidural anesthesia for postoperative control of pain (p < 0.03), previous laminectomy (p < 0.04), and preoperative valgus deformity (p < 0.0001) were significantly associated with peroneal nerve palsy. The relative risk for patients who had had a previous proximal tibial osteotomy was doubled, but this was not significant (p < 0.4). To determine risk factors associated with anesthesia better, a subgroup of 4388 total knee arthroplasties performed during a five-year period (1988 through 1992) was also studied. In this sample, twenty-five peroneal-nerve palsies were documented. Eighteen occurred after epidural anesthesia (p < 0.03); five, after general anesthesia; and two, after spinal anesthesia. An important finding of this study is the high frequency of delayed presentation of peroneal nerve palsy. We believe that epidural anesthesia for postoperative control of pain leads to decreased proprioception and sensation postoperatively. It is postulated that positioning of the limb in this unprotected state may be a factor in the late development of palsy. The concept of the so-called double-crush phenomenon may partially explain the palsy seen in the patients who had had a lumbar laminectomy and asymptomatic peripheral neuropathy.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Injury of the peroneal nerve has been reported in 0.3 per cent1 (twenty-six of 8754) to 4 per cent (three of seventy11 and three of seventy-seven8) of patients who have had a total knee arthroplasty1,4,7-9,11,14,17, and its association with preoperative flexion or valgus deformity has been well documented1,9,14. The mechanism of injury has been reported to be traction on the nerve as normal alignment is obtained at the time of the joint replacement11,14. Rose et al. and others4,17 speculated that compression of the vascular supply of the nerve by the fascia and direct pressure from a tight dressing caused the injury. However, in many series1,11,14,17, some patients who had a peroneal nerve palsy did not have preoperative valgus or flexion deformity or an identifiable cause of injury.

To define the subgroup of patients who are at risk better and to determine risk factors that can be avoided, a retrospective analysis of peroneal nerve palsies in a large series of patients who had had total knee arthroplasty was conducted.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
From 1979 through 1992, 10,361 consecutive total knee arthroplasties were performed at the Mayo Clinic. A retrospective review of the medical records revealed only thirty-two (0.3 per cent) documented peroneal nerve palsies in thirty patients. Two patients had a bilateral peroneal nerve palsy. The mean age of these eighteen men and twelve women was sixty-five years (range, twenty-eight to seventy-eight years). The preoperative diagnosis was osteoarthrosis in twenty-four patients, rheumatoid arthritis in three, osteogenic sarcoma in two, and post-traumatic osteoarthrosis in one. Twenty-eight primary total knee arthroplasties and four revision procedures were performed in the thirty patients. A partially constrained implant was used in twenty-four knees and a constrained implant was used in eight.

We assessed patient-dependent factors, including the preoperative alignment of the limb, a history of diabetes mellitus, the presence of neuropathy, and a history of operations on the spine or knee, as well as technique-dependent factors, including the type of anesthetic used, the duration of anesthesia, the postoperative change in alignment, and the duration for which the tourniquet was used.

In patients who received continuous epidural infusion of the anesthetic agent, a catheter was placed preoperatively and was anchored for prolonged infusion. The local anesthetic used for the operation was bupivacaine, etidocaine, lidocaine, or mepivacaine. In the immediate postoperative period, the catheter was connected to a volumetric pump for continuous infusion of bupivacaine, at concentrations ranging from 0.125 to 0.5 per cent and at a rate of four to fifteen milliliters an hour as needed for relief of pain. The duration of the continuous infusion ranged from the first night postoperatively to five days postoperatively.

Radiographic Analysis
Preoperative and postoperative anteroposterior and lateral radiographs made with the patient standing were available for all thirty patients (thirty-two knees). The anatomical axes were measured and were used to determine the over-all alignment of the lower limbs.

Clinical Assessment
The palsy was classified as complete or partial and as sensory or motor, or a combination of these, as described by Asp and Rand. A partial motor deficit was defined as any weakness of dorsiflexion of the toe or ankle, and a partial sensory deficit was defined as diminution of sensory perception in the distribution of the common peroneal nerve.

When a peroneal nerve palsy was recognized, the extent of the deficit was noted. All postoperative constrictive dressings were removed, and the limb was placed with the knee in slight flexion14. The patients were then followed, with careful clinical assessment of sensory and motor function in the areas supplied by the common peroneal nerve. Electromyographic and nerve-conduction studies were performed, depending on the severity of the palsy and at the discretion of the surgeon. The type and distribution of neurological dysfunction were noted, as was the extent of clinical resolution. Patients who had a major residual motor deficit were fitted for an ankle-foot orthosis before discharge from the hospital. Follow-up data were obtained through a review of records of return visits, correspondence, and telephone interviews. The average duration of follow-up for the thirty-two knees was three years and eleven months (range, fifteen months to ten years) (Table I). One patient (Case 27) died after the fifteen-month follow-up evaluation. Another patient (Case 30) died after the twenty-five-month evaluation.


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  		TABLE I DATA ON THE THIRTY PATIENTS WHO HAD A PERONEAL NERVE PALSY

 

Analysis of Data
A control group consisting of 100 patients who had had a total knee arthroplasty during the same time-period as the patients was obtained from our total joint registry and was computer-matched to the patients by age, sex, and operating surgeon. Odds ratios and exact confidence intervals were calculated to estimate the relative risk of palsy for various risk factors. Comparisons of proportion were made with the chi-square test. Only the first knee affected in the two patients who had bilateral palsy was used to estimate the odds ratio.

After 1988, formal complete computerized records on anesthesia became available at the Mayo Clinic. To determine risk factors associated with anesthesia better, a subgroup of 4388 total knee arthroplasties that had been performed during the five-year period of 1988 through 1992 was also studied. There were twenty-five peroneal nerve palsies. The relative rates of general, epidural, and spinal anesthesia used for the 4388 total knee arthroplasties were compared with those for the twenty-five procedures that were followed by documented peroneal-nerve palsy during the same time-period. Comparisons of proportion were made with the chi-square test.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 

Clinical Characteristics
Of the thirty-two knees associated with peroneal nerve palsy, ten were in 12 to 25 degrees (mean, 18 degrees) of valgus angulation preoperatively, seven were in varus angulation (mean, 7 degrees; range, 3 to 17 degrees), and fifteen were in 0 to 11 degrees (mean, 6 degrees) of valgus angulation (Table I). Three knees had more than 15 degrees of flexion contracture.

Two (7 per cent) of the thirty patients who had palsy had a history of non-insulin-dependent diabetes mellitus, four (13 per cent) had had a proximal tibial osteotomy, and five (17 per cent) had had a lumbar laminectomy for intervertebral disc disease (Table I).

The tourniquet was used for fifty-nine to 229 minutes (mean, 129 minutes). The tourniquets were all inflated to a pressure of 300 millimeters of mercury (40.00 kilopascals). One patient (one knee) did not have a tourniquet because of peripheral vascular disease, and the tourniquet used for another patient (one knee) was deflated after only seventeen minutes (Table I). These two patients were not considered in the calculation of the mean duration of tourniquet use.

Hematomas in the knee and leg developed postoperatively in one patient (Case 13) because of platelet-related coagulopathy and in another (Case 10) because of anticoagulation therapy. The compressive dressing was removed from the latter patient, and the knee joint was aspirated.

Anesthetic Characteristics
Of the thirty-two peroneal-nerve palsies (which include the twenty-five identified from 1988 through 1992), eighteen (sixteen patients) occurred after epidural anesthesia; ten (ten patients), after general anesthesia; and four (four patients), after spinal anesthesia. Fifteen of the eighteen palsies that occurred after epidural anesthesia were in patients who had received continuous infusion of local anesthetic for postoperative control of pain. Only two of the eighteen knees in patients who received epidural anesthesia had had a preoperative valgus deformity of 12 degrees or more, compared with seven of the ten knees in patients who received general anesthesia.

Neurological Involvement
The peroneal nerve palsy was diagnosed on the day of the operation in one knee, on the first postoperative day in twelve, on the second postoperative day in six, on the third postoperative day in five, on the fourth postoperative day in three, and on the ninth postoperative day in one. In four knees, the diagnosis was made after the patient had been discharged from the hospital. Twenty-five knees had a combined motor and sensory deficit, four had a pure motor deficit, and three had a pure sensory deficit. Of the thirty-two peroneal-nerve palsies, fifteen were classified as complete and seventeen, as partial (Table I).

Electromyography and nerve-conduction studies were performed for twenty-one of the thirty-two knees. For two knees, the studies were performed within the first four weeks after the diagnosis to determine the extent of the lesion. For the remaining nineteen knees, the studies were performed three to seven months after the diagnosis to assess reinnervation. Both the peroneal and the tibial nerve were involved in six knees. Clinical and electromyographic examination of these knees showed much greater involvement of the peroneal nerve. The tibial lesion was at the level of two of the six knees and was proximal to four. The two patients with bilateral peroneal-nerve palsy had electromyographic evidence of mild sensorimotor peripheral neuropathy.

At the latest follow-up evaluation, sixteen knees had complete clinical recovery and sixteen had incomplete recovery. Thirteen of the seventeen partial peroneal-nerve palsies recovered completely, compared with three of the fifteen complete palsies (Table I). Of the twenty-five knees that had a combined motor and sensory palsy, five had a residual sensory deficit, seven had varying degrees of sensory and motor deficits, and one had a residual motor deficit. Compared with the motor deficits, the residual sensory deficits were found to be more noticeable by the patients and were a frequent source of complaints and inquiries. One of the three knees that had had a pure sensory deficit had a residual sensory deficit, whereas two of the four knees that had had a pure motor deficit had a residual motor deficit (Table II). In one patient who had a complete peroneal-nerve palsy, the course of the common peroneal nerve at the level of the knee was dissected out to determine continuity at three months, as electromyography had showed no evidence of reinnervation, and it was found to be thickened and continuous. At the time of the latest follow-up examination, the patient had little recovery from the neurological deficit.


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  		TABLE II DATA ON RECOVERY*

 

Risk Factors
Of the 100 controls, forty-seven had received general anesthesia, twenty-nine had received epidural anesthesia, and twenty-four had received spinal anesthesia. Three of the patients had had a lumbar laminectomy for a herniated nucleus pulposus, four had had 12 degrees or more of valgus deformity preoperatively, and six had had a proximal tibial osteotomy.

The relative risk of palsy was 2.8 times greater (95 per cent confidence interval, 1.1 to 7.0; p < 0.03) for the patients who had received epidural anesthesia than for those who had received general or spinal anesthesia (Fig. 1). The relative risk of palsy was 6.5 times greater (95 per cent confidence interval, 1.1 to 43.6; p < 0.04) for the patients who had had a laminectomy (Fig. 2) and 12.0 times greater (95 per cent confidence interval, 3.0 to 56.2; p < 0.0001) for those who had had preoperative valgus deformity (Fig. 3). The relative risk of palsy was doubled in the patients who had had a proximal tibial osteotomy, but this was not significant (p < 0.4) (Fig. 4).



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  		Graph showing the type of anesthesia used in the thirty patients compared with that in the 100 controls. The percentages are given, with the numbers of patients in parentheses.

 


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  		Graph showing the prevalence of previous lumbar laminectomy in the thirty patients compared with that in the 100 controls. The percentages are given, with the numbers of patients in parentheses.

 


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  		Graph showing the prevalence of preoperative valgus deformity of 12 degrees or more in the thirty patients compared with that in the 100 controls. The percentages are given, with the numbers of patients in parentheses.

 


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  		Graph showing the prevalence of previous proximal tibial osteotomy (PTO) in the thirty patients compared with that in the 100 controls. The percentages are given, with the numbers of patients in parentheses.

 
Of the 4388 anesthetic procedures that were performed for total knee arthroplasty from 1988 through 1992, 1921 were general, 1555 were epidural, and 912 were spinal. During this same period, we documented twenty-five peroneal-nerve palsies. Eighteen occurred after epidural anesthesia; five, after general anesthesia; and two, after spinal anesthesia. Again, the risk of peroneal nerve palsy was significantly higher with epidural anesthesia than with general or spinal anesthesia (p < 0.03).


   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
Peroneal nerve palsy after total knee arthroplasty is rare. It is well documented that preoperative flexion contracture and valgus deformity increase the likelihood of this complication1,9,14. In many series1,11,14,17, the cause of peroneal nerve palsy in patients who had no known risk factors has been an enigma. The purpose of the present study was to determine other potentially important risk factors that could be prevented. We identified epidural anesthesia, a previous lumbar laminectomy, and preoperative valgus deformity as potential risk factors for peroneal nerve palsy after total knee arthroplasty.

The etiology of peroneal nerve palsy after total knee arthroplasty is multifactorial. Direct pressure from a tight dressing and compression of the vascular supply to the nerve by the fascia have been proposed as possible causes4,14,17. Pressure from a postoperative hematoma may have been the cause of the peroneal nerve palsy in two of our patients. Use of a tourniquet has also been linked to peroneal nerve palsy5,6; however, we were unable to draw any conclusion regarding its value for the prediction of peroneal nerve palsy.

Epidural anesthesia is commonly used after operations on the lower extremities because it provides better pain relief than that obtained with systemic administration of narcotics12,13. Associated with this technique is the global sensory and motor blockade produced by the local anesthetic effects2,13. In the present study, epidural anesthesia was significantly associated with peroneal nerve palsy (p < 0.03). Fifteen of the sixteen patients who had received epidural anesthesia had continuous infusion of a local anesthetic for postoperative control of pain. The diagnosis of peroneal nerve palsy was confirmed shortly after discontinuation of the epidural catheterization. In these patients, the various levels of motor and sensory blockade depended on the amount of local anesthetic that was used. These fifteen patients had localized common peroneal-nerve palsy after discontinuation of the epidural anesthesia. It is generally believed that epidural anesthesia for the control of postoperative pain decreases proprioception and sensation. We postulate that the decrease in proprioception and sensory stimuli that accompanies such anesthesia postoperatively allows the limb to rest in an unprotected state, thereby making it susceptible to neurological ischemia from local compression. However, intraoperative neurological damage may be a factor, and such damage may not be detected immediately after the operation because of the epidural anesthesia.

We are aware of one previous instance of peroneal nerve palsy associated with epidural anesthesia3. In that report, the patient had intact neurological function after uneventful induction of general anesthesia. Palsy developed one day postoperatively, after continuous epidural catheterization for pain. This young patient had no risk factors. The authors thought that pressure on the nerve postoperatively caused the peroneal nerve palsy.

In the present series, the diagnosis of peroneal nerve palsy was usually made on the first, second, or third postoperative day; however, one patient was diagnosed in the recovery room. This is in direct contrast to the findings in the study by Rose et al., in which the peroneal nerve palsy in most patients was diagnosed in the recovery room. The delay in diagnosis or the late presentation of the peroneal nerve palsy in the current study may have been the result of postoperative injury of the nerve or of intraoperative nerve damage that was masked by the postoperative epidural anesthesia. One of the patients who received continuous epidural infusion of a local anesthetic and in whom peroneal nerve palsy developed was noted to have the limb in marked external rotation on a continuous-passive-motion machine on the morning after the operation. The patient was completely unaware of the awkward position of the limb.

In a comprehensive study of 115 patients who were evaluated with electromyography, Upton and McComas hypothesized that the susceptibility of peripheral nerves to injury is increased if there was a previous proximal lesion. Five patients who had had a lumbar laminectomy for pain and radiculopathy associated with intervertebral disc disease had subclinical preoperative electromyographic findings indicative of chronic lumbar radiculopathy. In addition to these findings, there was a complete lesion of the peroneal nerve in three and a partial lesion in two at the level of the knee.

The functional integrity of an axon and its target structure depends on the continued supply of special trophic substances that are synthesized in the neuronal perikaryon and transported down the axon16. A proximal insult in the nerve root or spinal canal produces a decrease in axoplasmic flow, making the distal part of the nerve vulnerable to injury. The presence of a distal lesion further decreases axoplasmic flow to the point that it is below the safety margin that prevents denervation, and clinical palsy ensues. This is the so-called double-crush phenomenon16.

Neuropathy is a major cause of morbidity in patients who have diabetes mellitus. The most common manifestation is symmetrical sensory loss in the distal part of the lower extremities. The most common symptoms are numbness or a burning sensation that is worse at night. Most patients who have diabetes mellitus are asymptomatic despite impaired conduction velocity, loss of stretch reflexes, and absence of pain and vibratory sensations. In the present series, diabetes mellitus or diabetic neuropathy was not significantly associated with peroneal nerve palsy (p = 1.00) (Fig. 5). In part, the reason for this was poor identification and documentation of neuropathy. Also, the lack of preoperative electromyography or nerve-conduction studies made it difficult to identify patients who had asymptomatic neuropathy or radiculopathy.



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  		Graph showing the prevalence of diabetes mellitus in the thirty patients compared with that in the 100 controls. The percentages are given, with the numbers of patients in parentheses.

 
The results of total knee arthroplasty after an osteotomy of the proximal part of the tibia have been reported to be comparable with those of primary total knee arthroplasty15. In a series reported on by Staeheli et al., the intraoperative and postoperative rates of complications were similar to those of primary total knee arthroplasty. Katz et al. compared the results of twenty-one consecutive total knee arthroplasties in patients who had had a previous proximal tibial osteotomy with those in a matched control group of patients who had had a primary total knee arthroplasty. They documented two postoperative peroneal-nerve palsies in the patients who had had a previous osteotomy. Technical difficulties in exposing the proximal part of the tibia were also noted in three patients. In our series, four of the thirty-two knees were in patients who had had a previous proximal tibial osteotomy. With the numbers available, the risk of peroneal nerve palsy was not significantly increased by a proximal tibial osteotomy but it was double the relative risk associated with a primary total knee arthroplasty. This slight increase in risk could be attributed to direct contusion of the nerve from excessive soft-tissue dissection and the removal of staples at the time of the total knee arthroplasty.

Pneumatic tourniquets are routinely used during operations on the lower extremities, and the association between their use and the development of nerve palsy is well known5,6. The mechanism of injury appears to be direct mechanical pressure on local tissue and nerve ischemia due to the tourniquet effect6. In the present series, six patients had a combination of peroneal and tibial nerve palsies. Because electromyography was not performed preoperatively, it was difficult to assess the effect of the tourniquet in these patients. Additionally, five of these six palsies were in patients who had received epidural anesthesia, making it difficult to assess neurological function and to rule out intraoperative neurological damage from the tourniquet effect. The duration for which a tourniquet was used in this study, especially in operations that lasted less than 120 minutes, had no predictive value with regard to the development of peroneal nerve palsy. Even though a direct cause-and-effect relationship was not found in this review, use of a tourniquet has the potential to contribute to palsy, especially to combined tibial and peroneal lesions. A prospective, randomized controlled study may better define the importance of this variable.

A postoperative hematoma was found in two knees (two patients) in our series. One of the patients (Case 10) had involvement of the tibial nerve at the level of the knee in addition to the peroneal nerve palsy. Both of the patients had received postoperative epidural anesthesia and had been asymptomatic before the epidural catheterization was discontinued. One of the two patients had had a compressive dressing applied. It was generally thought that the increase in interstitial pressure resulted in a compromised vascular supply in these two knees, but it is also possible that an unrecognized compartment syndrome was responsible.

The association of preoperative valgus or flexion deformities with injury of the peroneal nerve after total knee arthroplasty is well known1,7,14,17. In our series, ten of the thirty-two knees with peroneal nerve palsy had valgus deformity of 12 degrees or more preoperatively; this was highly significant (p < 0.0001). The mean change in alignment after correction was 12 degrees (range, 7 to 20 degrees). Correction in these knees appeared to have stretched the nerve beyond its functional tolerance and to have produced variable degrees of neurological ischemia.

In conclusion, we believe that, of the risk factors analyzed in this study, the use of epidural anesthesia, especially for control of postoperative pain, is most important because it is within the control of the surgeon to some extent. Thus, we recommend that surgeons carefully consider and assess the risk associated with epidural anesthesia, especially in patients who have had a lumbar laminectomy. We also recommend that, if epidural anesthesia is used postoperatively, the neurological status of the patient be monitored meticulously and documented adequately by the surgeon, with frequent postoperative evaluation of clinical signs and symptoms. Also, the postoperative position of the limb in relation to the bed rail or a continuous-passive-motion machine should be assessed periodically. In the recovery room and on the first postoperative night, a pillow should be placed under the ipsilateral hip to prevent external rotation of the limb and thus markedly decrease pressure on the nerve where it courses around the head of the fibula. The amount of local anesthetic that is given should be sufficient to make the patient comfortable without producing prolonged sensory and motor blockade13. Preoperative flexion contracture and valgus deformity remain strongly associated with the development of peroneal nerve palsy, but careful preoperative neurological evaluation may effectively identify patients with peripheral neuropathy who might be at risk for nerve palsy.

The initial treatment of palsy involves removal of all constrictive dressings and repositioning of the knee in 20 to 30 degrees of flexion1,4,14. The patient should be reassured that the prognosis is uniformly good for partial peroneal-nerve palsy. A variable amount of recovery is expected with complete palsy; follow-up electromyography and nerve-conduction studies may be useful to assess reinnervation. Bilateral palsy, in our opinion, warrants a careful search for an occult generalized peripheral neuropathy or neurological disorder. We have limited experience with operative decompression of the peroneal nerve for this condition and are therefore unable to comment on its value.


   Footnotes
 
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

{dagger}Read at the Annual Meeting of The American Academy of Orthopaedic Surgeons, New Orleans, Louisiana, February 28, 1994.

{ddagger}Department of Orthopedics, Mayo Clinic, 200 First Street S.W., Rochester, Minnesota 55905. Please address requests for reprints to Dr. Morrey.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Asp, J. P. L., and |and |Rand, J. A.: Peroneal nerve palsy after total knee arthroplasty. Clin. Orthop., 261: 233-237, 1990.
  2. Britt, B. A., and |and |Gordon, R. A.: Peripheral nerve injuries associated with anaesthesia. Canadian Anaesth. Soc. J., 11: 514-536, 1964.
  3. Cohen, D. E.; Van Duker, B.; Siegel, S.; and |and |Keon, T. P.: Common peroneal nerve palsy associated with epidural analgesia. Anesth. and Analg., 76: 429-431, 1993.[Medline]
  4. Coventry, M. B.; Upshaw, J. E.; Riley, L. H.; Finerman, G. A. M.; and |and |Turner, R. H.: Geometric total knee arthroplasty. II. Patient data and complications. Clin. Orthop., 94: 177-184, 1973.
  5. Denny-Brown, D., and |and |Brenner, C.: Paralysis of nerve induced by direct pressure and by tourniquet. Arch. Neurol. and Psychiat., 51: 1-26, 1944.
  6. Dobner, J. J., and |and |Nitz, A. J.: Postmeniscectomy tourniquet palsy and functional sequelae. Am. J. Sports Med., 10: 211-214, 1982.[Abstract/Free Full Text]
  7. Gunston, F. H., and |and |MacKenzie, R. I.: Complications of polycentric knee arthroplasty. Clin. Orthop., 120: 11-17, 1976.
  8. Hui, F. C., and |and |Fitzgerald, R. H., Jr.: Hinged total knee arthroplasty. J. Bone and Joint Surg., 62-A: 513-519, June 1980.
  9. Insall, J. N.; Ranawat, C. S.; Aglietti, P.; and |and |Shine, J.: A comparison of four models of total knee-replacement prostheses. J. Bone and Joint Surg., 58-A: 754-765, Sept. 1976.[Abstract/Free Full Text]
  10. Katz, M. M.; Hungerford, D. S.; Krackow, K. A.; and |and |Lennox, D. W.: Results of total knee arthroplasty after failed proximal tibial osteotomy for osteoarthritis. J. Bone and Joint Surg., 69-A: 225-233, Feb. 1987.[Abstract/Free Full Text]
  11. Kaushal, S. P.; Galante, J. O.; McKenna, R.; and |and |Bachmann, F.: Complications following total knee replacement. Clin. Orthop., 121: 181-187, 1976.
  12. Mahoney, O. M.; Noble, P. C.; Davidson, J.; and |and |Tullos, H. S.: The effect of continuous epidural analgesia on postoperative pain, rehabilitation, and duration of hospitalization in total knee arthroplasty. Clin. Orthop., 260: 30-37, 1990.
  13. Raj, P. P.; Knarr, D. C.; Vigdorth, E.; Denson, D. D.; Pither, C. E.; Hartrick, C. T.; Hopson, C. N.; and |and |Edström, H. H.: Comparison of continuous epidural infusion of a local anesthetic and administration of systemic narcotics in the management of pain after total knee replacement surgery. Anesth. and Analg., 66: 401-406, 1987.[Abstract/Free Full Text]
  14. Rose, H. A.; Hood, R. W.; Otis, J. C.; Ranawat, C. S.; and |and |Insall, J. N.: Peroneal-nerve palsy following total knee arthroplasty. A review of The Hospital for Special Surgery experience. J. Bone and Joint Surg., 64-A: 347-351, March 1982.[Abstract/Free Full Text]
  15. Staeheli, J. W.; Cass, J. R.; and |and |Morrey, B. F.: Condylar total knee arthroplasty after failed proximal tibial osteotomy. J. Bone and Joint Surg., 69-A: 28-31, Jan. 1987.[Abstract/Free Full Text]
  16. Upton, A. R. M., and |and |McComas, A. J.: The double crush in nerve-entrapment syndromes. Lancet, 2: 359-362, 1973.[Medline]
  17. Webster, D. A., and |and |Murray, D. G.: Complications of variable axis total knee arthroplasty. Clin. Orthop., 193: 160-167, 1985.

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