Knee Surgery, Sports Traumatology, Arthroscopy

, Volume 18, Issue 11, pp 1583–1586

Surgical treatment of peroneal nerve palsy after knee dislocation

Authors

    • Department of Orthopaedic SurgeryMayo Clinic
  • Steven A. Giuseffi
    • Department of Orthopaedic SurgeryMayo Clinic
  • Allen T. Bishop
    • Department of Orthopaedic SurgeryMayo Clinic
  • Alexander Y. Shin
    • Department of Orthopaedic SurgeryMayo Clinic
  • Diane L. Dahm
    • Department of Orthopaedic SurgeryMayo Clinic
  • Michael J. Stuart
    • Department of Orthopaedic SurgeryMayo Clinic
Knee

DOI: 10.1007/s00167-010-1204-3

Cite this article as:
Levy, B.A., Giuseffi, S.A., Bishop, A.T. et al. Knee Surg Sports Traumatol Arthrosc (2010) 18: 1583. doi:10.1007/s00167-010-1204-3

Abstract

Purpose

Numerous surgical techniques have been described for the treatment of peroneal nerve palsy after knee dislocation with less than optimal outcomes. The purpose of this article is to present a review of the literature including modern surgical treatment options for peroneal nerve palsy after knee dislocation.

Method

Review of the current body of literature relevant to the topic was undertaken and summarized accordingly. Mechanism of injury, pathology and prognosis as well as current and novel treatment options are presented.

Results

Neurolysis and nerve grafting results are dependant on nerve graft length, with documented recovery rates of only 44% for nerve grafts longer than 6 cm. Posterior tibial tendon transfer procedures have had reasonable success in allowing patients to return to ambulation without assistive devices; however, dorsiflexion strength on the affected side has been reported at only 30% that of the normal contralateral side, and return to activities more strenuous than walking has not been reported. Future concepts including partial nerve transfer of a motor branch of the tibial nerve to the peroneal nerve have been described, but no outcome data is currently available.

Conclusion

Peroneal nerve palsy after knee dislocation leads to significant functional impairment. Prior treatment strategies utilized for restoration of dorsiflexion and peroneal nerve function have yielded overall poor results. Newer surgical techniques are being developed and clinical trials are under way to evaluate their effectiveness.

Keywords

Peroneal nerve palsyKnee dislocationMultiligament knee injuryNerve transfer

Introduction

Knee dislocations are uncommon injuries that are associated with significant trauma to the ligamentous and neurovascular structures of the knee. There is a well-established association between knee dislocation and injury to the popliteal artery and/or peroneal nerve. These associated injuries can be devastating and can lead to amputation or functional loss of the limb. Therefore, a clinician must maintain a high level of suspicion and perform a dedicated neurovascular examination in any patient suspected of having a knee dislocation.

The patient population presenting with multi-ligament knee injury is notoriously heterogeneous with respect to demographics, mechanism of injury, pattern of ligament injury and associated polytrauma [13]. Consequently, the incidence of knee dislocations in the general population is extremely difficult to estimate. Previous attempts to describe epidemiology of these injuries from large academic institutions cite incidences ranging from 0.28 to 5.3 knee dislocations per year [7, 8, 15, 23], and an overall incidence of 0.02–0.2% of all orthopedic injuries [3]. However, these figures may be deceptively low when considering that a number of knee dislocations reduce spontaneously prior to clinical presentation and therefore go undiagnosed [20]. Despite timely reduction, whether spontaneous or as a result of clinical manipulation, a significant risk for neurovascular complications remains [14]. In light of this fact, many clinicians treat patients with injury to three or more knee ligaments—especially those with bicruciate injury—as having sustained a knee dislocation [2, 10].

Niall et al. [17] recently reported on 55 traumatic knee dislocations in Scotland between 1994 and 2001. This elevated incidence of knee dislocations can likely be attributed to multiple factors and may be secondary to increased prevalence of motor vehicle accidents and sporting injuries, as well as improved injury recognition and documentation [7, 10]. Indeed, King et al. [12] recently reported on 7 open knee dislocations in a 4-year period, corresponding to more severe mechanisms of injury.

Mechanism of peroneal nerve palsy

Most knee dislocations lead to bicruciate injury and multi-directional instability. Nerve injury is also common in knee dislocation and can cause significant morbidity. The common peroneal nerve is the nerve most often injured, although the tibial nerve is also at risk. Most studies have reported an incidence of 25–36% of peroneal nerve palsy in knee dislocations [10, 16, 18].

The peroneal nerve is most susceptible to traction injury when the knee is exposed to a varus stress. Therefore, peroneal nerve injuries most commonly occur when the posterolateral corner structures are injured [19], although peroneal nerve palsy has been described in the setting of varus deformity as a result of osteoarthritis [9]. Several anatomic factors predispose the common peroneal nerve to injury. These include its superficial and relatively tethered location around the fibular head as well as relatively tenuous vascular supply and small amount of epineural connective tissue [4, 16].

Pathology and prognosis

Peripheral nerve injuries occur along a continuum from mild stretch injuries to complete transection. Seddon classified peripheral nerve injuries into neuropraxia, axonotmesis and neurotmesis [21]. Neurotmesis is complete nerve disruption and is the most severe of these injuries. Axonotmesis involves disruption of the axons with relative preservation of the axonal sheaths. Neuropraxia, the least severe, consists of a demyelination injury without axonal degeneration [16].

While neuropraxia results in transient nerve dysfunction secondary to local ischemia and demyelination, axonotmesis and neurotmesis injuries lead to Wallerian degeneration distal to the injury site. After delay of a 4–6 weeks, axonal regeneration initiates and continues at a rate that averages approximately 1 mm/day or 1 inch/month [6]. If re-innervation does not occur within 9 to 12 months, irreversible time-dependent muscle atrophy/fibrosis as well as nerve endplate degeneration occurs. It is crucial that surgical restoration of nerve integrity be performed early (i.e., between 6 weeks and 6 months) to allow re-innervation to occur prior to the time-dependent changes in the motor endplate [5, 24, 26].

Peroneal nerve injuries carry a notoriously poor prognosis, and close patient follow-up is essential. Despite more advanced and aggressive treatment methods, only 40% or less of patients who suffer peroneal nerve palsy in association with knee dislocation will experience functional recovery [16]. Patients with incomplete nerve palsy have a significantly better prognosis, and most can be expected to recover with observation alone [6].

Nerve conduction studies and EMG can provide useful information regarding patient prognosis. However, axonal degeneration takes 4 to 6 weeks to occur after injury, and the value of nerve studies is limited prior to this time [26]. In neuropraxia injuries, sensation loss is less severe, and there is an absence of muscle atrophy. EMG shows intact nerve conduction distal to the injury site, although voluntary action potentials are not present. This is in contrast to axonotmesis and neurotmesis, where sensation loss is often more severe and EMG does not show conduction distally [16].

Treatment options

Treatment of peroneal palsy in the setting of knee dislocation includes operative and non-operative techniques. Unless acute operative management is chosen, the initial treatment consists of observation, physical therapy and an ankle–foot orthosis (AFO). Physical therapy focuses on prevention of equinovarus deformity via stretching of the posterior ankle capsule and strengthening of residual anterior compartment motor function. The AFO assists in ambulation and stretches posterior ankle structures [10].

Operative interventions for peroneal palsy have included neurolysis, primary nerve repair, nerve grafting and tendon transfers.

Neurolysis and nerve grafting

Surgical exploration and/or neurolysis are often performed in cases of complete peroneal palsy that do not improve spontaneously. Recommendations regarding the timing of surgical intervention differ, but most peripheral nerve surgeons emphasize close clinical follow-up after the initial injury with physical examination and EMG at 3–4 weeks post injury [6, 10, 16]. Patients with incomplete nerve palsy can improve without surgical intervention, but need close observation and serial examination. However, those with complete palsy should undergo repeat EMG and clinical examination at about 3 months. If no recovery is noted at this time, surgical intervention is warranted [6, 10, 16].

Knee dislocation often leads to considerable traction injury (up to 20 cm in length), and surgeons must visualize the entire course of the common peroneal nerve to accurately gauge the degree of injury [22]. When exploration of the peroneal nerve reveals a nerve in continuity, intraoperative nerve conduction studies as well as intraoperative EMG can be helpful to determine the functional status of the nerve. If the nerve is noted to be in continuity and nerve action potentials are transmitted across a lesion, then there may be continuity of the nerve, and neurolysis is performed [16]. In the case of a completely transected nerve, the surgeon must decide between direct repair and nerve grafting (most often with sural nerve autograft). Direct repair is rarely possible in stretch injuries, as the zone of injury must be resected to normal nerve fascicles. In most cases, the nerve traction injury after knee dislocation is too extensive to allow direct nerve coaptation [25, 28, 29].

The most difficult surgical decision is how to approach the non-conducting but continuous peroneal nerve. In these cases, the surgeon must perform neurolysis and then repeat intraoperative nerve conduction studies. If nerve conduction is not present after neurolysis, the surgeon must identify the nerve portion most abnormal in appearance and texture and then resect the nerve proximally and distally until normal fascicular detail is encountered. Care must be taken to avoid excision of healthy nerve tissue; conversely, failure to properly excise abnormal nervous and fibrotic tissue will predispose the resultant nerve anastomosis to failure [16].

The outcomes for neurolysis and/or nerve grafting for complete common peroneal lesions have been generally poor. A large retrospective study showed that recovery rate is related to nerve graft length, with longer graft length correlated to worse clinical outcome. These authors cited a recovery rate of 44% for nerve grafts longer than 6 cm, which comprised the majority of patients [11, 29]. Sedel and Nizard also reported results of nerve grafting for traction injury of the common peroneal nerve. Of the 17 patients who underwent grafting for nerve gaps ranging from 7 to 20 cm, only 6 had a functionally satisfactory result. The authors partially attributed the poor graft results to the significant length of traction injury (up to 15 cm) [22].

Tendon transfers

When neurolysis and nerve grafting do not provide satisfactory results, the remaining surgical options are salvage procedures such as tendon transfer or arthrodesis. Posterior tibial tendon transfer is the most commonly used procedure and involves passing the posterior tibial tendon anteriorly through the interosseus membrane to the dorsum of the foot with attachment to the medial cuneiform or tenodesis to the anterior tibial tendon [10]. This effectively converts the posterior tibialis into a dorsiflexor to compensate for the denervated tibialis anterior. Achilles tendon lengthening is often performed simultaneously [16].

Posterior tibial tendon transfer procedures have had reasonable success in allowing patients to return to ambulation without assistive devices [10]. Yeap et al. reported results of posterior tibial tendon transfers for 12 patients with common peroneal nerve palsy. Of these 12 patients, 10 no longer required an AFO after the procedure. However, dorsiflexion strength on the affected side was only 30% that of the normal contralateral side and return to activities more strenuous than walking was not reported [10, 30]. Vigasio et al. [27] reported the outcomes at minimum 2-year follow-up of 16 patients in which they had performed posterior tibial tendon/flexor digitorum longus transfers for common peroneal nerve palsy. The authors concluded that their procedure effectively restored balance to foot dorsiflexion and gait without the use of orthoses. It should be noted, however, that tendon transfer can lead to flatfoot and/or hindfoot valgus and may not fully correct associated gait problems [1].

Future concepts—partial nerve transfer

The significant morbidity associated with peroneal nerve injury as well as disappointing clinical results from traditional treatment have stimulated investigation of other avenues for surgical intervention. One of these procedures, documented in an anatomic feasibility study [1], involves direct nerve transfer of a motor branch of the tibial nerve to the tibialis anterior motor branch of the deep peroneal nerve with the goal of restoring ankle dorsiflexion. This procedure involves identification of the peroneal nerve as well as its distal branches distally beneath the lateral compartment muscles. The tibial nerve is exposed with the same incision and a portion of the tibial nerve that contributes most to lesser toe flexion is identified. This portion of the tibial nerve is divided distally and transferred directly to the motor branch of the tibialis anterior (Fig. 1a, b).
https://static-content.springer.com/image/art%3A10.1007%2Fs00167-010-1204-3/MediaObjects/167_2010_1204_Fig1_HTML.jpg
Fig. 1

a Exposure and identification of the deep branches of the peroneal nerve (black arrows) and tibial nerve (white arrow). b Direct partial nerve transfer of a motor fascicle of the tibial nerve (white arrow) to the target fascicle of the deep peroneal nerve (black arrow)

Conclusion

Peroneal nerve palsy after knee dislocation leads to significant functional impairment. Prior treatment strategies utilized for restoration of dorsiflexion and peroneal nerve function have yielded overall poor results. Newer surgical techniques are being developed, and clinical trials are under way to evaluate their effectiveness.

Copyright information

© Springer-Verlag 2010