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Nerve Injury ComplicatingMultiligament Knee Injury: CurrentConcepts and TreatmentAlgorithm

Abstract

Multiligament knee injuries account for <0.02% of all orthopaedicinjuries, and 16% to 40% of these patients suffer associated injuryto the common peroneal nerve (CPN). The proximity of the CPN tothe proximal fibula predisposes the nerve to injury during localtrauma and dislocation; the nerve is highly vulnerable to stretchinjury during varus stress, particularly in posterolateral cornerinjuries. CPN injuries have a poor prognosis compared with that ofother peripheral nerve injuries. Management is determined basedon the severity and location of nerve injury, timing of presentation,associated injuries requiring surgical management, and the resultsof serial clinical evaluations and electrodiagnostic studies.Nonsurgical treatment options include orthosis wear and physicaltherapy. Surgical management includes one or more of thefollowing: neurolysis, primary nerve repair, intercalary nervegrafting, tendon transfer, and nerve transfer. Limited evidencesupports the use of early one-stage nerve reconstruction combinedwith tendon transfer; however, optimal management of these rareinjuries continues to change, and treatment should beindividualized.

Multiligament knee injuries(MLKIs) associated with knee

dislocations account for <0.02% ofall orthopaedic injuries; however,this may be an underestimation be-cause some knee dislocations mayspontaneously reduce at the time ofinjury and go unrecognized.1 Com-mon peroneal nerve (CPN) injury oc-curs in 16% to 40% of patients withknee dislocation.2 The prognosis fornerve recovery associated withMLKIs is generally poor and de-pends on the extent of disruption ofthe normal neural anatomy.2

Acute knee dislocations are causedby high-energy trauma such as motor

vehicle collisions and industrial inju-ries, as well as lower-energy traumasuch as that sustained during sportsparticipation and falls.3

The four primary ligamentous stabi-lizers of the knee are the anterior cru-ciate ligament, posterior cruciate liga-ment, medial cruciate ligament, andlateral collateral ligament. Disruptionof two or more of these ligaments mayoccur with knee dislocation, resultingin an MLKI. MLKIs may be associatedwith vascular injury or neurovascularinjury or both, and the clinician shouldhave a high index of suspicion for neu-rovascular deficits during the globalassessment.1,2

William Randolph Mook, MD

Cassandra A. Ligh

Claude T. Moorman III, MD

Fraser J. Leversedge, MD

From the Department ofOrthopaedic Surgery, DukeUniversity Medical Center, Durham,NC.

J Am Acad Orthop Surg 2013;21:343-354

http://dx.doi.org/10.5435/JAAOS-21-06-343

Copyright 2013 by the AmericanAcademy of Orthopaedic Surgeons.

JAAOS Plus Webinar

Join Dr. Moorman, Dr. Mook, andDr. Leversedge for the JAAOSinteractive webinar discussing“Nerve Injury ComplicatingMultiligament Knee Injury: CurrentConcepts and Treatment Algorithm,”on Tuesday, June 18, 2013, at 9 PM

Eastern. The moderator will bePeter Jokl, MD, the Journal’s DeputyEditor for Sports Medicine topics.

To join and to submit questions inadvance, please visit theOrthoPortal website:http://orthoportal.aaos.org/jaaos/

Review Article

June 2013, Vol 21, No 6 343

Injury to the CPN may be associ-ated with sensory and/or motor defi-cits. The severity of the neurologicimpairment can range from a mildstretching injury (ie, neurapraxia), tonerve rupture or laceration with anopen injury, to neurotmesis.4 Fewevidence-based guidelines exist toguide the management of these com-plex injuries, particularly in light ofthe limited ability to determine theextent of nerve injury and establish a

prognosis for nerve recovery. Carefulpatient evaluation and individualizedtreatment are paramount.

Anatomy

The CPN lies close to the posterolat-eral corner (PLC) of the knee jointand the proximal fibula, whichplaces the nerve at risk of injury dur-ing varus stress, local trauma, and

knee dislocation5,6 (Figure 1). In thedistal one third of the thigh, the sci-atic nerve bifurcates into the CPNand the tibial nerve. Prior to exitingthe popliteal fossa, the CPN, situatedanterior to the conjoined biceps fem-oris tendon and posterior to the lat-eral head of the gastrocnemius mus-cle, innervates the short head of thebiceps femoris muscle. The CPNcourses distally and superficially,covered by only subcutaneous tissue

Photographs of cadaver dissection of the popliteal fossa and posterolateral corner of a right knee. A, Bifurcation ofthe tibial nerve (black chevron) and the common peroneal nerve (CPN [white arrow]) in the proximal popliteal fossa.B, Branching of the CPN proximal to the fibula (F). C, Close-up view of branching of the peroneal nerve into superficialand deep divisions, the motor branches to the short head of the biceps femoris (BF) and peroneus longus (PL)muscles, and an articular branch with the PL muscle reflected from its origin. LHG = lateral head of the gastrocnemiusmuscle, MHG = medial head of the gastrocnemius muscle, P = popliteal muscle, SM = semimembranosus muscle,ST = semitendinosus muscle, white triangle = superficial peroneal nerve, black triangle = motor nerve branches to thePL, black arrow = articular branch of the common peroneal nerve, double arrow = deep peroneal nerve, whitechevron = nerve to the short head of the BF

Figure 1

Dr. Moorman or an immediate family member serves a paid consultant to Smith & Nephew; has stock or stock options held inHealthSport; has received research or institutional support from Histogenics; and serves as a board member, owner, officer, orcommittee member of the American Orthopaedic Society for Sports Medicine and the Southern Orthopaedic Association.Dr. Leversedge or an immediate family member has received royalties from OrthoHelix Surgical Designs; is a member of a speakers’bureau or has made paid presentations on behalf of Bioventus; serves as a paid consultant to OrthoHelix Surgical Designs andStryker; has stock or stock options held in Tornier; has received research or institutional support from AxoGen; and serves as a boardmember, owner, officer, or committee member of the American Academy of Orthopaedic Surgeons and the American Society forSurgery of the Hand. Neither of the following authors nor any immediate family member has received anything of value from or hasstock or stock options held in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Mookand Ms. Ligh.

Nerve Injury Complicating Multiligament Knee Injury: Current Concepts and Treatment Algorithm

344 Journal of the American Academy of Orthopaedic Surgeons

and skin, traveling lateral to theproximal fibula.

A consistent vascular supply to theCPN arises from an unnamed branchof the popliteal artery within theproximal popliteal fossa. However,more distally, at the level of the kneejoint, the vascular supply becomesmore tenuous, relying on small vasanervorum derived from the anteriorrecurrent tibial artery.7 In contrast,the tibial nerve remains protectedwithin the popliteal fossa as itcourses between the popliteus muscleand the popliteal fascia before enter-ing the deep posterior compartmentof the lower leg, and it receives pre-dictable vascular contributions fromthe popliteal and the posterior tibialarteries.7 The tibial nerve is lesslikely to be injured during knee dis-location,1,2 which may be due in partto its protected location and moreconsistent blood supply.

In approximately 80% of patients,the CPN splits into the superficialand deep divisions at or distal to thefibular neck; however, in up to 10%of persons, bifurcation of the CPNoccurs proximal to the lateral jointline.8 The superficial peroneal nerveinnervates the peroneus longus andbrevis muscles, which function pri-marily to plantarflex the first ray andevert the ankle, respectively. Thedeep peroneal nerve innervates fourextrinsic muscles (ie, peroneus ter-tius, tibialis anterior, extensor hallu-cis longus, extensor digitorum lon-gus) to dorsiflex the foot and extendthe toes. Injury to the CPN maycause a motor palsy involving thesemuscle groups; often, the clinicalpresentation involves foot drop orloss of ankle dorsiflexion, as well asa relatively unsteady gait. The termi-nal branches of the peroneal nerveprovide sensory innervation for thedorsal foot and the first web space.Patients with knee injury may experi-ence sensory disturbances in thesedistributions.

Mechanism of Injury

At the time of knee dislocation, dis-ruption of the PLC is associated withan increased incidence of CPN in-jury.1,2 Isolated PLC injuries are rarebut may result from a posterolateralforce applied to the tibial plateauwith the knee near full extension.9

Other mechanisms of PLC injury in-clude isolated severe varus bendingmoments, external rotatory torqueon the tibia, combined hyperexten-sion and external rotation forces,and both contact and noncontact hy-perextension moments.10

Nerve Injury Classification

Two nerve injury classification systemsare applicable to the diagnosis andmanagement of CPN injuries (Table 1).Seddon12 stratified peripheral nerve in-juries into three classes: neurapraxia(mild), axonotmesis (moderate), andneurotmesis (severe). Sunderland13

modified that system to account forthe variable outcomes of axonot-metic injuries. The histology of nerveinjury and the regenerative responsefollow a predictable sequence ofpathophysiologic events; the com-plexity of this biologic process high-lights the guarded prognosis for CPNrecovery following injury (Table 2).

Clinical Examination

Serial comprehensive examinationsshould be carefully documented anda thorough history obtained that in-cludes the mechanism of injury,postinjury interventions, and previ-ous and current symptoms. Mostknee dislocations are caused by high-energy trauma; thus, concomitant in-juries should be noted. Resuscitationand a global clinical assessment atthe time of initial presentation areprioritized. Lower limb evaluation in

the setting of knee trauma shouldconsider the integrity of the liga-ments of the knee joint, and detailedevaluation of the sensory and motorfunctions of the CPN is essential. In-jury to the CPN is suggested by in-ability to dorsiflex the foot or extendthe toes, ankle eversion paralysis orweakness, and/or altered sensibilityin the cutaneous nerve distributions;however, a more proximal nerve in-jury, such as from the lumbar spine,should be considered as well.

Muscle strength is graded from 0 to5 using the British Medical ResearchCouncil (MRC) scale15 (Table 3).Sensibility is evaluated subjectivelyby assessing the patient’s ability toappreciate deep and superficial pain,light touch, and two-point discrimi-nation. The presence of a Tinel sign,or percussion of the injured nervethat causes paresthesia in its sensorydistribution, can be used to trace theprogress of a regenerative CPN overtime. In the absence of indicationsfor emergent or urgent surgical inter-vention, serial examinations are con-ducted to monitor the neurovascularstatus of the affected limb.

Adjuvant Studies

ImagingStandard radiographs are routinelyobtained in the evaluation of acuteknee injuries. However, the use ofMRI and ultrasonography continuesto evolve for evaluating the macro-scopic anatomy of neurologic injuryand the relative zone of injury thatmay influence decisions regardingmanagement. Enhanced resolutionmay improve the ability to correlateimages with nerve function and, ulti-mately, with prognosis for neuro-logic recovery.

RadiographyStandard radiographs of the knee areindicated in the initial evaluation of

William Randolph Mook, MD, et al

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a patient with known or suspectedMLKI. These are used to evaluate forassociated bony injuries (Table 4)

and to confirm concentric joint re-duction. PLC injuries should be con-sidered in the presence of local bony

avulsion injuries (Figure 2), and theCPN should be carefully evaluated.During preoperative planning, dy-

Table 1

Nerve Injury Classifications and Electrodiagnostic Findings11

Seddon SunderlandHistopathologic

Features

Expected RecoveryResponse and

Timeline NCV EMG

Neurapraxia(mild)

1 Normal nerve archi-tecture: local loss ofconduction

No degradation of ax-ons. Full recovery inhours to weeks proba-ble.

Usually preserved. Re-duced SAP amplitudeproximal to the injuryand normal distal tothe injury. NormalMUP.

No or few fibrillations

Axonotmesis(moderate)

2 Disrupted: axonsIntact: endoneurium,

perineurium,epineurium

Wallerian degeneration,proximal axon degen-eration within the zoneof injury, variable main-tenance of supportingstructures dependingon the mechanism ofinjury. Full recovery inweeks to months pos-sible. (Regeneration 1mm/d.)

Normal or reduced to adegree dependent onthe size of the zone ofinjury, injury type,amount of axonal de-generation, and thenerve types involved.Decreased SAP andfiring rate of MUP.

Fibrillations

3 Disrupted: axons,endoneurium

Intact: perineurium,epineurium

Same as Sunderlandgrade 2



4 Disrupted: axons,endoneurium,perineurium

Intact: epineurium




Neurotmesis(severe)

5 Complete transectionof the nerve

Spontaneous recoveryunlikely

Not measurable. SAPand MUP absent.

Innumerable fibrilla-tions

EMG = electromyography, MUP = motor unit potentials, NCV = nerve conduction velocity, SAP = sensory action potentials

Table 2

Pathophysiology of Peripheral Nerve Injury

Time Stage Characteristics

At injury Mechanical nerveinjury

Axonal disruption (axonotmesis/neurotmesis) and proximal degeneration within the zone ofinjury. Some axonotmized neurons die without target support.

Neuron cell bodychromatolysis

Peripheral migration of surviving neuron nuclei. Production of reparative structural molecules.

48–160 h11 Walleriandegeneration

Degeneration of distal axon–Schwann cell activation and macrophage recruitment. The nerve-blood barrier is disrupted, which allows for clearance of inhibitory nerve outgrowth factors.Distal Schwann cells may become less able to support regenerating axons with time.14

Weeks tomonths

Growth coneformation/elongation

Motile tip of the regenerative axon that responds to neurotrophic/neurotropic stimulation pro-vided by end-organs and Schwann cells that have organized along the path of the distal axon

Reinnervation If the growth cone fails to reach its target organ, motor end plates are lost, muscles atrophy,and muscles eventually fibrose along the path of the distal axon. Nerve growth occurs at arate of approximately 1 mm/d.



namic varus stress radiographs maybe useful to supplement MRI in de-termining the degree of PLC laxity.19

MRIMRI is useful in evaluating potentialligamentous injury, detecting neuro-logic injury, and determining thesoft-tissue response to injury (Figure3). In conjunction with other studiesand physical examination, MRIhelps to confirm the presence and lo-cation of CPN injury.4,20 MRI may beuseful in determining surroundingfat planes, localized edema, presenceof contusion, nerve fiber disruption,and encasing hematoma.4,20 Increasedsignal intensity within the nerve fol-lowing injury is seen on T2-weightedimages at and distal to the site ofnerve injury. In subacute images,chronic neuropathic changes maymanifest as muscle edema or fatty in-filtration within the anterior and lat-eral compartment musculature.21

More recently, magnetic resonanceneurography has been used in bothanimal models and retrospective caseseries of peripheral nerve injuries.22

This modality involves the use ofshort tau inversion recovery se-quences to image peripheral nervesdirectly. Its precise role in the evalua-tion of peroneal nerve injury has yetto be defined; however, it seems tohave the potential to accurately de-

tect the early extent of nerve lesionsand monitor their regeneration.

UltrasonographyUltrasonography is a dynamic imag-ing modality, and knee orientationcan be manipulated to evaluate thecontinuity of the CPN (Figure 4).High-resolution ultrasonography canbe used rather than MRI to detectthe location and determine the sever-ity of nerve injury.4,23

Ultrasonography has been used toaccurately discern the specific loca-tion and length of CPN injury, thediameter of an injured but continu-ous CPN, and the presence of an ob-structing hematoma or scar.5 It is anefficient diagnostic tool for differ-entiating incomplete injury (ie,neurapraxia, axonotmesis) fromcomplete injury (ie, neurotmesis).4,23

This imaging tool is highly user de-pendent,5,23 but it is promising whenused by experienced clinicians.

Electrophysiologic TestingElectromyography (EMG) and nerveconduction velocity (NCV) studiescan be used in the assessment of theseverity, location, and prognosis ofnerve injury.4,5 Baseline NCV andEMG studies are obtained approxi-mately 6 weeks following injury if afunctional neurologic deficit re-mains. These studies may be used for

subsequent comparison at 3 and 6months if neurologic recovery is in-complete and surgical reconstructionis being considered. Pertinent EMGfindings corresponding to acutenerve injury include positive sharpwaves and fibrillation potentials.4

Chronic denervation is marked byfasciculations and complex repetitivedischarges.11

Severity of nerve injury may corre-late with NCV findings4,8 (Table 1).In an incompletely damaged nerve,conduction velocity is slowed,whereas a completely severed nervemay lack motor control (measured in

Table 3

British Medical Research CouncilScale for Evaluating MuscleFunction15

Grade Description

0 No muscle contraction1 Trace contraction2 Contraction with resis-

tance of gravity re-moved

3 Muscle contractionagainst gravity resis-tance only

4 Muscle contractionagainst some resis-tance

5 Normal muscle contrac-tion against full resis-tance

Table 4

Avulsion Fractures That May Indicate Underlying Injury to the Lateral Knee Soft Tissues

Lesion Injured Structure Radiographic Appearance

Segond fracture16 Tibial insertion of the middle third of the lateralcapsular ligament. Suspect for anterior cruci-ate ligament and lateral meniscal injuries.

AP knee: Elliptical osseous fragment parallel to thetibia, just distal to the lateral tibial plateau.

Arcuate complex avulsion(ie, arcuate sign)17

Fibular collateral, fabellofibular, popliteofibular,and arcuate ligaments

AP knee: Elliptical osseous fragment oriented orthogo-nally to the long axis of the tibia. Donor site originat-ing from the fibular styloid process.

Biceps femoris avulsion18 Conjoined tendon of the biceps femoris AP and lateral knee: Difficult to differentiate from thearcuate sign. More irregular osseous fragment foundproximal and posterolateral to the fibula. Donor site isthe fibular head. On the lateral view, found more pos-terior than the arcuate complex avulsion.


June 2013, Vol 21, No 6 347

motor unit potentials), sensation(measured in sensory action poten-tials), or both.11

Management of CPNInjuries

Management goals for CPN injuriesinclude promoting neurologic recov-ery, maximizing functional recovery,and minimizing risk and functionalloss with nerve or musculotendinousreconstructive procedures. Prognosisand management are influenced bynumerous factors, including patientage; timing of injury; mechanism ofinjury; longitudinal extent of CPNdamage; distance of injury locationfrom the nerve’s distal targets; andassociated soft-tissue, vascular, andbony injuries.

NonsurgicalNonsurgical management is pre-scribed in the presence of compelling

AP (A) and lateral (B) non–weight-bearing radiographs of the kneedemonstrating arcuate complex avulsion fracture (ie, arcuate sign). Thearrows indicate a proximally displaced elliptical fracture fragment of thefibular styloid process.

Figure 2

A, Lateral radiograph of a left knee demonstrating anteromedial knee dislocation before reduction. B, Axial T2-weighted fat-suppressed magnetic resonance image just distal to the level of the knee joint demonstrating increasedsignal intensity within the lateral gastrocnemius and popliteus muscle bellies, posterolateral corner, and lateralsubcutaneous tissue. Normally, the common peroneal nerve (CPN) would be visualized deep to the biceps femorismuscle (BF); however, normal tissue planes are obscured by edema and hemorrhage. C, Axial T2-weighted fat-suppressed magnetic resonance image at the level of the proximal fibula, distal to the image in panel B, demonstratingincreased signal intensity within the CPN (arrow), which is characteristic of injury. F = fibula, LHG = lateral head of thegastrocnemius, MHG = medial head of the gastrocnemius, P = popliteus, T = tibia, * = popliteal neurovascular bundle

Figure 3



evidence supporting the spontaneousregeneration of the CPN (eg, serialclinical examination findings con-firming improvements in sensory andmotor function, EMG recordings de-picting normal insertion activitypostinjury). Every patient with CPNmotor palsy should be fitted with anankle-foot orthosis (AFO) andshould undergo physical therapy toprevent equinovarus deformity bymaintaining range of motion of theposterior ankle capsule, preventingheel cord contracture, and strength-ening the remaining functional mus-cles.1,4 Spontaneous CPN recoveryafter injury associated with MLKIoccurs in 14% to 56% of cases.24

Younger age (ie, <30 years) at thetime of injury is the only variablethat has been shown to be predictiveof a higher likelihood of spontaneousCPN recovery.25

Surgical

Indications for NerveExploration/NeurolysisThe timing of repair or reconstruc-tion of the ligamentous structures in-jured in an MLKI is controversial26

and is dependent on numerous fac-tors, including vascular status of theinjured limb, joint stability, skin con-dition, and the status of other inju-ries. Early repair or reconstruction ofthe PLC is technically less challeng-ing, and acute intervention may yieldimproved clinical outcomes27 andpermit direct visualization of theCPN. It is the authors’ preference toreconstruct the PLC within 3 weeksof injury. Persistent CPN motor im-pairment at the time of acute recon-struction warrants exploration of theCPN and external neurolysis if it isincarcerated by hematoma, scar, orfracture. Information on the locationof the nerve injury gained from im-aging studies such as MRI and ultra-sonography is helpful in surgicalplanning. Some authors have found

the intraoperative use of ultrasonog-raphy to be invaluable in localizingnerve lesions.28

Neurolysis of the CPN at the timeof acute or subacute PLC repairmay improve functional outcomes.Thoma et al29 retrospectively re-viewed 20 patients with CPN injury,of whom 19 patients (95%) demon-strated improvement of at least oneMRC grade for ankle dorsiflexion.Ten of these 19 patients regainedmotor function of grade 3 or better.Neurolysis was delayed >7 months inhalf of the patients, which indicatesthat even delayed management of anincomplete injury may result in im-proved ankle dorsiflexion strength.Nevertheless, these authors reportedexcellent results with early interven-tion. All three patients who under-went neurolysis within 4 months ofinjury improved from MRC grade 0to at least grade 4. The natural his-tory of these specific injuries is notknown. Seidel et al30 reported that 8of 11 patients who underwent neu-rolysis for traumatic CPN injuriesachieved a good functional outcome(MRC grade ≥4). Average surgical

delay was 5 months. Although bothstudies are limited by lack of controlgroups and small sample size, thefindings indicate that surgical neu-rolysis is indicated after 3 months ifno electrical or clinical improvementis observed and the CPN is morpho-logically intact.

If acute intervention on the PLC iseither not indicated or not possible,the patient is followed clinically,with electrodiagnostic testing at 6weeks following injury and again at3 months. Serial clinical examinationfindings and EMG and NCV resultsat 3 months assist in determiningwhether neurophysiologic testing isrepeated at 6 months or if earlier sur-gical intervention is warranted. Priorto proceeding with surgery, repeatMRI and ultrasonography are rec-ommended to help define the natureand extent of the zone of injury.

Indications for DirectNerve RepairDirect epineurial repair is the proce-dure of choice when the CPN is notin continuity and the zone of injuryis small, thereby enabling end-to-end

A, Photograph demonstrating the orientation of the right leg andultrasonography transducer that corresponds to the sonographic image inpanel B. The proximal thigh is in the foreground, the popliteal fossa is to theright, and the foot can be seen in the upper left corner. B, Axial high-resolution sonogram (15.6 MHz transducer) of the split deep (arrow) andsuperficial (arrowhead) branches of the peroneal nerve, respectively, as theycourse around the proximal fibula (F). Normal atraumatic peripheral nerveechotecture is shown.

Figure 4


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repair without undue tension at therepair site. Because of the mechanismof injury associated with acute kneedislocations, the CPN fibers are of-ten severely stretched, making end-to-end repair impossible without ex-cessive tension.1,4,31 Kim et al32

reported that 16 of 19 patients whounderwent end-to-end suture repairrecovered motor function of MRCgrade 3 or higher, which obviated theneed for the use of AFOs to achievefunctional gait mechanics.

Repair can be performed up to 12months following the initial injury.However, delay of this length is con-troversial because the longer the in-terval between injury and repair, thegreater the likelihood of adverse out-comes. Reinnervation of motor endplates is more time sensitive thanthat of sensory end-organs.33 Weagree with many of the authors whosuggest that outcomes are best whenrepair is performed within 3 to 6months of injury.33,34

Indications for Nerve Excisionand Intercalary Nerve GraftingIf after at least 3 months of expec-tant management there is no clinicalor electrical evidence of CPN rein-nervation, regardless whether acuteexternal neurolysis or direct repairwere attempted acutely, the progno-sis for a reasonable functional recov-ery is poor and surgical interventionis indicated.1,34

If tension-free repair has failedand/or is not feasible, additional op-tions to promote reinnervation areconsidered. Tomaino et al35 recom-mended cable grafting in the absenceof positive EMG potentials even af-ter neurolysis. Determining thelength or zone of nerve injury is criti-cal, and advanced imaging such asultrasonography may assist in surgi-cal planning.5 If repair or intercalarynerve grafting is performed withinthe zone of injury, reinnervation maybe limited by neuroma formation or

fibrosis. Intraneural exposure withserial sectioning (ie, bread-loafing)and examination of the nerve canhelp to delineate normal fascicularanatomy. In general, an intercalarynerve graft measuring ≥4 cm isneeded to span the entire zone of in-jury in cases of failed primary re-pair.33

The influence of length of the zoneof injury has been demonstrated inseveral large series in which poorerprognoses were observed with theuse of grafts measuring ≥6 cm.30,32,34

In the largest study to date, Kimet al32 reported functional outcomesfollowing CPN injury for externalneurolysis (121 patients), direct end-to-end repair (19 patients), and graftrepair (138 patients). In the graft re-construction group, 27 of 36 patientshad a postoperative MRC grade 3 orabove when a graft of <6 cm wasused (75%). When the graft lengthwas 6 to 12 cm, only 24 of 64 pa-tients achieved an MRC of grade 3or higher (38%). In persons withgraft lengths of 13 to 24 cm, only16% had a good outcome (6 of 38patients). Recently, Cho et al36 re-ported on outcomes of sports-relatedperoneal nerve injuries. Nerve gapsof <6 cm had a favorable functionaloutcome (MRC grade 3 or above) in70% of patients, whereas gaps of 6to 12 cm had only a 43% successrate and gaps of 13 to 24 cm hadonly a 25% functional success rate.Similar findings have been reportedin other studies in which nerve graft-ing was the preferred management ofCPN injury.6,34

Autogenous nerve graft remainsthe standard for the management oflarge peripheral nerve defects that re-quire reconstruction because thisgraft type provides a nonimmuno-genic and structurally inert scaffoldfor axonal regeneration.37 Autoge-nous nerve grafts provide neuro-trophic factors, extracellular matrixmolecules, and viable Schwann cells

not found in allografts or syntheticalternatives.

The sural nerve is the most com-monly used autograft because of itspotential length, diameter, proximityto the surgical field, and relativelylow donor site morbidity.38 However,the patient should be cautioned ofthe potential graft harvest morbidity,which includes leg pain resultingfrom neuroma formation, distal sen-sory changes, hematoma, and woundhealing problems.39 PreoperativeEMG and NCV studies should in-clude an assessment of the viabilityof the ipsilateral sural nerve; thisnerve may have been injured at thetime of injury. In the case of suralnerve injury, the surgeon may needto consider using contralateral suralgraft harvest or an alternative nervegraft source instead.

Sedel and Nizard40 caution againstnerve grafting in the setting of con-comitant vascular injury about theknee, even when adequately repairedor bypassed, due to disappointingoutcomes. The use of a vascularizedsural nerve graft (VSNG) has beendescribed when vascular insult is sus-pected. Terzis and Kostopoulos41 pre-sented their long-term results of a se-ries of 12 patients treated between 3and 48 months from injury withVSNG using grafts between 6 and 35cm in length. All patients treatedwithin 6 months of injury, regardlessof graft length (≤20 cm), achieved anMRC grade 4 of ankle dorsiflexionand/or eversion. Outcomes were sub-stantially better if denervation timewas ≤6 months at the time of sur-gery. For this reason, the authorsconcluded that VSNG should be con-sidered when attempting to bridgenerve defects ≥13 cm in length, espe-cially within 6 months of injury.

Nerve allografts offer an additionalsource for nerve reconstruction. Al-lografts have the advantages of un-limited supply, ready availability inmost cases, and lack of harvest site



morbidity. However, they have a di-rect risk of infection, and they re-quire the use of temporary systemicimmunosuppression, which may pre-clude their use in patients with multi-system trauma. Giusti et al42 recentlyshowed autogenous nerve graft re-constructions to be superior to al-lograft reconstructions with regardto motor recovery in a rodent model.Based on the current evidence, weprefer the use of autogenous nervegrafts when possible.

Indications for Tendon Transfer,With or Without NerveReconstructionHistorically, tendon transfer was in-dicated only when time-dependentmyoneural degeneration had oc-curred and/or previous attempts atreinnervation had failed. The poste-rior tibialis is the most commonlyused tendon. It is transferred fromthe posterior compartment of the legto the dorsal second or third cunei-form. The procedure enables the tibi-alis posterior to function as a dorsi-flexor, resulting in improved gaitmechanics and decreased reliance onassistive devices such as AFOs.

Equinovarus deformity is believedto result from an imbalance betweenthe flexor and extensor muscles ofthe foot, and it is a complication ofCPN injury following acute disloca-tion.31,43 Recent studies have shownthat early surgical intervention tocorrect imbalances with concomitantnerve reconstruction or repair canpositively influence prognosis.31,43

Garozzo et al43 and Ferraresi et al44

compared combined CPN repair/reconstruction and posterior tibialtendon transfer (PTTT) with CPNrepair/reconstruction alone in patientgroups that were matched with re-gard to demographics, mechanism ofinjury, and surgical timing. Eighty-five percent of patients had improvedmotor function of the tibialis ante-rior muscle, peroneal muscles, and

common toe extensors to MRCgrade 3 or higher. Although the con-clusions are limited by the small sizeof the control group, CPN repair/reconstruction combined with PTTTresulted in improved objective recov-ery of the CPN as measured clini-cally and on EMG. No patient whofailed initial nerve repair or recon-struction and then underwent a de-layed PTTT objectively recoveredCPN reinnervation. The authors pro-posed that the early improvement indorsiflexion provided by the PTTTallows for “internal rehabilitation”to maintain the flexibility of the an-kle joint and surrounding muscula-ture and fosters passive stimulationof the denervated muscles. They feltthat this may be more effective thanthe combination of traditional physi-cal rehabilitation and use of an AFO.

Our experience with delayed man-agement of extensive CPN injury (>6cm) with nerve reconstruction alonehas been similarly disappointing,with outcomes comparable to thosereported by Ferraresi and col-leagues.43,44 We have modified ourtreatment algorithm based on thesefindings and other available litera-ture (Figure 5).

Previous studies indicate that patientswho undergo PTTT—regardless oftiming—can return to ambulationwithout an AFO.4,31 Nonetheless,there are no reports describing returnto competitive sports or participationin activity more strenuous thanwalking.34 This is likely due in partto the inability to completely restoredorsiflexion and eversion strength,which affect gait mechanics.45 It alsomay be complicated by the long-termincrease in the risk of developing apes planovalgus deformity and/orhindfoot arthrosis.46 Although earlyPTTT may prove to be more advan-tageous for nerve recovery whencombined with early nerve repair, itremains the standard of care for themanagement of equinovarus defor-

mity in the setting of chronic CPNpalsy.

Indications for Nerve TransferNerve transfer involves the coaptionof a functional but potentially ex-pendable nerve with an injurednerve. In the case of an injured CPN,a tibial nerve branch or fascicle canbe used to reanimate the tibialis an-terior muscle.47 With nerve transfer,one of these functional donor nervefascicles can be placed closer to themotor end plate than to the site oforiginal injury. This reduces the timeand distance required for the regen-erative nerve to migrate to the motorend plates.48 For this reason, the ad-vantage of nerve transfer over nerverepair or grafting may be fully real-ized in the setting of delayed surgicalintervention; however, despite en-couraging anatomic and limited out-comes studies, no evidence exists tosupport the benefits of nerve transferover traditional methods of manag-ing CPN injury.

Summary

CPN injuries associated with MLKIhave a poor prognosis for recoveryand are challenging to manage,4,6,34

although emerging evidence and out-comes studies have improved our un-derstanding of the natural history ofthese complex injuries. In the acuteand subacute settings, the inability toquantify the pathophysiology ofnerve injury despite advances innerve imaging precludes the accuratedetermination of the prognosis forrecovery and, therefore, adversely in-fluences clinical decision-making.

Important factors that influence ul-timate outcomes include the zone ofinjury, patient age, graft length, in-terval from injury to surgical repair,and severity of injury.32 Nonsurgicalmanagement options include physi-cal therapy in combination with or-


June 2013, Vol 21, No 6 351

thoses. Surgical options include oneor a combination of the following:neurolysis, primary nerve repair, in-tercalary nerve grafting, tendon

transfer, and nerve transfer. Limitedevidence exists in support of earlyone-stage nerve reconstruction com-bined with tendon transfers; how-

ever, optimal management of theserare injuries continues to change andshould be individualized to each pa-tient.44

Evidenced-based treatment algorithm to help guide decision making when managing peroneal nerve injuries followingmultiligament knee injuries. EMG = electromyography, NCV = nerve conduction velocity, PTTT = posterior tibial tendontransfer

Figure 5



References

Evidence-based Medicine: Levels ofevidence are described in the table ofcontents. In this article, references 27and 28 are level II studies. References6, 19, 20, 22, 32, and 43 are level IIIstudies. References 5, 9, 24, 29-31,36, 39-41, 44, 45, and 47 are level IVstudies. References 12-15, 17, 18, 35,and 46 are level V expert opinion. Theremaining references are cadaver oranimal studies, book chapters, ortraditional clinical reviews.

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