|Year : 2016 | Volume
| Issue : 2 | Page : 76-81
Surgical decompression of the peroneal nerve in the correction of lower limb deformities: A cadaveric study
Monica Paschoal Nogueira1, Arnaldo José Hernandez2, César Augusto Martins Pereira3, Dror Paley4, Anil Bhave5
1 Department of Orthopedics and Traumatology, State Public Hospital (HSPE), São Paulo, Brazil
2 Department of Orthopedics and Traumatology, Institute of Orthopedics and Traumatology, University of São Paulo, SP, Brazil
3 Institute of Orthopedics and Traumatology, LIM 4 - Biomechanics Laboratory, University of São Paulo, SP, Brazil
4 The Paley Institute, St. Mary's Medical Center, West Palm Beach, Florida, USA
5 Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore, Baltimore, Maryland, USA
|Date of Submission||19-Apr-2016|
|Date of Acceptance||21-Jul-2016|
|Date of Web Publication||16-Sep-2016|
Monica Paschoal Nogueira
426 Maracatins Avenue, Apt. 402, São Paulo 04089-000, SP
Source of Support: None, Conflict of Interest: None
Background: The peroneal nerve is often stretched during limb lengthening and deformity correction. If the nerve becomes entrapped under the peroneal muscle fascia and/or anterior intermuscular septum, decompression is indicated to treat nerve compromise.
Purpose: The purpose of this study was to quantify peroneal nerve tension after varus osteotomy of the proximal tibia and before and after nerve decompression.
Methods: A device, which consisted of a force transducer connected perpendicularly by a hook to the nerve and integrated to a personal computer, was able to indirectly measure the nerve rigidity in 14 lower limbs (seven cadaveric specimens). The nerve was neither cut nor disrupted from its anatomic tract by the rigidity measuring device. We measured the amount of peroneal nerve rigidity before varus angulation, after varus angulation of a proximal tibial osteotomy, and after peroneal nerve decompression in the varus angulation position.
Results: Peroneal nerve rigidity increased significantly after limb was angulated into varus (P = 0.0002) and was reduced significantly after decompression (P = 0.0003). No significant difference was noted between measurements obtained before varus angulation and measurements obtained after nerve decompression (P = 0.3664).
Conclusions: Varus osteotomy of the proximal tibia significantly increases peroneal nerve rigidity. Peroneal nerve rigidity after decompression is not significantly different from nerve rigidity before varus correction.
Clinical Relevance: This study provides biomechanical evidence of the efficacy of nerve decompression in two specific anatomic sites (peroneus longus muscle fascia and lateral, intermuscular septum) in relieving the increase in peroneal nerve rigidity that occurs in association with procedures that stretch the nerve such as limb lengthening and deformity correction.
Keywords: Cadaver, decompression, lower extremity, peroneal nerve, surgical
|How to cite this article:|
Nogueira MP, Hernandez AJ, Pereira CA, Paley D, Bhave A. Surgical decompression of the peroneal nerve in the correction of lower limb deformities: A cadaveric study. J Limb Lengthen Reconstr 2016;2:76-81
|How to cite this URL:|
Nogueira MP, Hernandez AJ, Pereira CA, Paley D, Bhave A. Surgical decompression of the peroneal nerve in the correction of lower limb deformities: A cadaveric study. J Limb Lengthen Reconstr [serial online] 2016 [cited 2020 Jun 1];2:76-81. Available from: http://www.jlimblengthrecon.org/text.asp?2016/2/2/76/190708
| Introduction|| |
Peroneal nerve entrapment and injury are well-known complications of acute deformity correction and of limb lengthening. ,,,,,,,,,,, The primary entrapment described is at the neck of the fibula. Peroneal nerve decompression is a well-recognized technique for the treatment of peroneal nerve palsy and entrapment. , For prophylactic use, the indication for peroneal nerve compression is a nerve at risk (e.g., acute valgus correction of tibia of more than 5°, acute valgus correction of the femur of more than 5°). For therapeutic decompression, the indication is when there are signs or symptoms of nerve problems (e.g. referred pain to the dorsum of foot, hypersensitivity or hyposensitivity, weakness, or paralysis of muscles). The potential complications of nerve decompression are nerve injury, infection, and hematoma. Nogueira et al.  found that peroneal nerve decompression is efficacious for the treatment of peroneal nerve injury secondary to acute and gradual deformity correction and lengthening.
Paley  identified two sites of entrapment and described a surgical technique to decompress both tunnels [Figure 1]a-e. The first entrapment tunnel is located at the fascial arcade of the peroneal muscles over the common peroneal nerve. After passing under the fascial arcade, the common peroneal nerve splits in the lateral compartment into superficial and deep branches. The superficial branch continues unimpeded through the lateral compartment, whereas the deep branch has to pass under the intermuscular septum (second tunnel) between the lateral and anterior compartments to enter the anterior compartment of the leg. The intermuscular septum extends from the anterior fascia covering the anterior and lateral compartments to the interosseous membrane between the tibia and the fibula at its deepest extent.
|Figure 1: Paley's technique of two-tunnel peroneal nerve decompression are shown. (a) Peroneal nerve passes through two potential entrapment tunnels: the peroneal fascia and the intermuscular septum. (b) Short oblique skin incision is made in the same direction as the nerve (Step 1). (c) Superficial peroneal fascia is divided outside of the peroneal muscles (Steps 2 and 3), and the common peroneal nerve is identified. (d) Peroneal muscle fascia is cut. The underlying peroneal muscles are retracted medially exposing the deep peroneal muscle fascia, which is then divided (Step 4). (e) Transverse fascial incision is extended toward the tibia crossing the intermuscular septum between the anterior and lateral compartments of the leg. The muscle on either side is retracted, and the septum is transected under direct vision (Step 5). The deep peroneal nerve passes under this septum, but it is not visualized (Figure and legend reprinted with permission)|
Click here to view
Nerve stretch injuries are caused when distraction overcomes the nerve fibers' elastic and plastic properties. These injuries have been the subject of many studies. ,,, It has been assumed that nerve injury resulting from limb lengthening and from acute valgus to varus deformity correction is a stretch injury. The report of Nogueira et al.  has suggested that the problem may be one of the nerve entrapments instead of stretch injury.
The purpose of this study was to quantify the tension of the peroneal nerve after varus osteotomy of the proximal tibia and before and after nerve decompression. If the entrapment sites act as tether points to the peroneal nerve when it is placed under tension, then we would expect to see a reduction of tension after decompression of the two sites of entrapment. This finding would support the rationale of therapeutic and perhaps prophylactic peroneal nerve decompression when the nerve is placed under tension by surgery or injury.
| Materials and Methods|| |
A preliminary cadaveric study was conducted to develop the protocol and the device to measure nerve rigidity. Rigidity was used as an indirect measurement of nerve tension. Then, 14 cadaveric lower limbs from seven adult males were studied.
Preliminary cadaveric study
In an initial group of 20 cadaveric specimens, the relationship between the peroneal nerve and its branches to the surrounding structures was studied, and nerve decompression was performed. During decompression, the deep peroneal nerve branch that passes under the anterior intermuscular septum was identified. These cases were necessary to study the anatomy and to define the protocol. During this preliminary study, a device was developed to measure rigidity.
Description of the nerve rigidity device
The device consists of a traction assembly, control unit, signal conditioner, and an adjustable base. The mobile portion of the traction assembly contains the electric extensometer (strain gauge), nylon wire, and connection hook [Figure 2]. The mobile portion is moved through a screw and nut system that is connected to a step motor. The motor moves the mobile part of the device and pulls the connection hook that is attached to the nerve.
|Figure 2: Illustration shows device for the measurement of nerve rigidity. Inset, mobile portion of the traction assembly. A: Connection hook, B: Nylon wire, C: Force transducer blade, D: Electric extensometer (strain gauge), E: Mobile part, F: Guide rod, G: Trapezoidal screw, H: Step motor|
Click here to view
The force transducer is mounted to an aluminum blade. One end of the force transducer blade is connected to the mobile portion of the device, and the other end is connected to the hook by a 0.32 mm diameter nylon wire. Two 120-Ω electric extensometers (strain gauge model EA-06-240 LZ-120; Measurements Group, Inc., Raleigh, North Carolina) were glued to the force transducer blade (one on each side of the blade). The extensometers measure minute deformations caused by tension. When the hook pulls the nerve, the resulting blade flexion deformation is read by the signal conditioner (model P3500, Measurements Group, Inc., Raleigh, North Carolina).
The control unit contains an electronic microprocessor that controls the step motor and the advancement of the mobile part with an accuracy of 0.01 mm. The value measured by the signal conditioner (i.e., microdeformation [μm/m]) is sent to a computer through a serial port. A computer program was developed to control the device, to record the data, and to plot a graph of force versus nerve deformation. The adjustable base allows the device to be correctly positioned relative to the nerve, with the connection hook and the nylon wire perpendicular to the longitudinal axis of the nerve.
Parameters developed during the preliminary study
A preliminary control was performed with twenty cadavers to determine the maximum elastic range of the nerve before permanent deformation occurred. The maximum values found were 0.78 N for force, 20 mm displacement, and 10 mm/min for velocity of displacement. Based on these findings, these parameters were not exceeded during the remainder of the study.
The transducer was calibrated with eight standard 10 g weights that were measured on a digital precision scale with an accuracy of 0.1 g (V1200; Acculab, São Paulo, Brazil). The transducer was calibrated using the standard weights in 10 g increments from 10 g to 80 g. The microdeformation measured by the transducer was correlated to the mass of the standard weight that was placed on the device. Based on these data, we were able to use a computer to calculate the force needed to cause a certain deformation of the transducer with an accuracy of 0.2 g.
Fourteen lower limbs from seven adult male cadavers were studied. The cadavers were 34-85 years of age at the time of death (average age, 56 years) and did not have any known pathologic abnormalities of the lower limb. The knee was flexed 60°, as measured with a goniometer, and the lower limb was fixed to the table with limb holders placed on the proximal thigh and foot. Care was taken to avoid compressing the sciatic nerve. An oblique, 5 cm incision was made at the level of the fibular neck. The superficial fascia was dissected under the subcutaneous fat, and the common peroneal nerve was identified just before it entered underneath the peroneal longus muscle fascia. The nerve was dissected free over a distance of 1 cm. Two horizontal, 1.5 cm collinear incisions were made just distal to the tibial tuberosity. A Gigli saw was passed percutaneously and subperiosteally according to the technique described by Paley. 
A monolateral external fixator was applied on the anteromedial face of the tibia using two proximal threaded pins placed above the tibial tuberosity and inclined inferiorly 30°, and two distal pins placed at the level between the medium and distal thirds of the limb, perpendicular to the tibia. All the threaded pins were applied in the same plane and were connected to the fixator. The two proximal pins were angulated 30° relative to the two distal ones [Figure 3]a.
|Figure 3: (a) Leg is shown before varus angulation of the proximal tibial osteotomy. (b) Monolateral fixator has been adjusted to position the leg in varus|
Click here to view
A fibular osteotomy was performed at the transition between the middle and distal thirds of the leg. A 3 cm longitudinal incision was made, and the region between the lateral and posterior compartments of the leg was dissected. The fibula was cut using the multiple drill hole technique and an osteotome; the tibia was divided with the Gigli saw.
After the monolateral fixator was applied and the osteotomy was performed, the first nerve rigidity test was performed using the traction assembly [Figure 4]. This measurement was obtained before moving the leg into varus. The tibia was then angulated 30° into varus and was fixed in that position [Figure 3]b]. Only the external fixator was adjusted to position the leg in varus. A second nerve rigidity test was then performed. The peroneal nerve was decompressed by releasing both tunnels [Figure 1]a-e. A third set of measurements was then obtained.
|Figure 4: Illustration shows the cadaver in a supine position. The nerve rigidity device is attached to the peroneal nerve. Inset, photograph shows the connection hook attached to the peroneal nerve|
Click here to view
Each nerve rigidity test was performed twice, and the mean value of the two readings was used for statistical analysis. The average rigidity measurements (obtained before angulating the osteotomy, after varus angulation of the leg, and after the nerve had been decompressed in the varus angulation position) were studied using analysis of variance to repetitive measurement. P < 0.05 was considered statistically significant.
| Results|| |
The average rigidity value before the varus angulation was 126.72 ± 33.28 N/m. The rigidity measurements of the peroneal nerve increased significantly after varus angulation were performed (average rigidity value, 155.03 ± 31.39 N/m; P = 0.0002) [Figure 5] and [Table 1]. After nerve decompression was performed, the rigidity measurement decreased significantly (average rigidity value, 120.66 ± 17.47 N/m; P = 0.0003). No statistical difference was observed between rigidity measurements obtained before the varus angulation (i.e., the initial measurement) and after the nerve decompression (i.e., the final measurement) (P = 0.3664). At least two measurements were always obtained. The time between each measurement varied from 15 to 20 min. The two rigidity measurements either remained the same or increased during this time. A decrease in rigidity was not observed unless a decompression was performed.
| Discussion|| |
The goal of this study was to quantify the tension of the peroneal nerve after varus osteotomy of the proximal tibia and before and after nerve decompression at two specific sites: Peroneus longus muscle fascia and lateral, intermuscular septum. Peroneal nerve injury is a well-recognized complication that is associated with acute angular correction and with limb lengthening. Mont et al.  reported that correction of deformities of more than 15° of valgus put the nerve at risk when performing total knee arthroplasty and achieving correction in varus. When nerve decompression was performed on patients undergoing limb lengthening, intraoperative findings included hemorrhage, nerve flattening, narrowing of the nerve at the entrance of the fascial tunnel, and reduction of the paraneural vascularization at the site of compression. These findings are typical of nerve entrapment and not of stretch injury. Paley and Herzenberg  used peroneal nerve decompression both prophylactically and therapeutically when performing acute valgus to varus deformity corrections about the knee. Intraoperative potential nerve monitoring was used in some cases, and a sudden loss of nerve potentials was observed minutes after acute valgus to varus correction. Immediate decompression of the nerve leads to restoration of normal potentials. 
Nogueira et al.  documented that when peroneal nerve injuries are caused by limb lengthening, acute deformity correction, or gradual deformity correction, the timing of decompression affected the rate of nerve recovery. Performing an early decompression resulted in patients experiencing an early recovery, and performing a late decompression resulted in patients experiencing a late recovery. However, this study failed to find a relationship between nerve injury and the amount or percent of lengthening, suggesting again that entrapment and not stretch injury is the cause.
Nerve entrapment might also be a factor when stretch or compression injury occurs. Injury leads to inflammation. The peroneal tunnels are normally very tight, leaving little space to accommodate additional swelling. Consequently, a secondary injury might follow the original stretch injury when the nerve swells against the nonexpandable walls of the peroneal tunnels. For this reason, early decompression is warranted while the initial injury is recoverable; the secondary injury might make the situation irrecoverable. This is suggested by the observation that the longer the interval between the injury and the decompression, the longer the interval until recovery of the nerve.  Therapeutic decompression is the standard of care for the median nerve of the hand. The carpal tunnel is much more capacious than the peroneal tunnels. Prophylactic or therapeutic nerve decompression within 24 hr should also become the standard of care for the peroneal nerve.
If tension can precipitate entrapment, then decompression should be able to reduce the tension on the peroneal nerve. We tested this hypothesis by creating a cadaver model of acute 30° lateral opening wedge varus osteotomy. This clinical situation is known to precipitate peroneal nerve injury. As expected, the rigidity (our indirect measurement used to estimate tension) of the peroneal nerve increased significantly after the varus angulation and showed no sign of decreasing with time if no decompression was performed. After the decompression, the rigidity of the peroneal nerve decreased and even returned to the prevarus angulation level [Figure 5]. This is direct evidence that the fascia of the peroneal tunnels tethers the peroneal nerve and that this tether can be surgically relieved.
|Figure 5: Graph shows average rigidity measurements obtained before varus angulation, after varus angulation, and after peroneal nerve decompression. The bars show the confidence intervals. A significant difference in rigidity was noted between the measurements obtained before varus angulation and after varus angulation (P = 0.0002) and between the measurements obtained after varus angulation and after nerve decompression (P = 0.0003). No significant difference in rigidity was observed before varus angulation and after nerve decompression (P = 0.3664). After the peroneal nerve decompression, the rigidity returned to normal|
Click here to view
Previous studies measured tension by removing the nerve and obtaining measurements. ,,, We wanted to measure the tension of the peroneal nerve while it was in its anatomic tract. To measure tension, sensors would have to be applied in a standard fashion. It is difficult to create a standard protocol and to maintain consistency across all cadaveric specimens that are a limitation of this study. Therefore, the measurement of tension was obtained indirectly. The rigidity was calculated by a major or minor resistance of the nerve to perpendicular traction.
The biomechanical findings of this study were complementary to the clinical findings of Nogueira et al.  and reinforced that it is not necessary to discontinue lengthening or undo an angular correction if the nerve is decompressed promptly. In this study, both peroneal tunnels were decompressed to achieve the final rigidity measurement. We did not separately measure the rigidity change after decompressing only the first tunnel versus decompressing both tunnels. This would be a worthwhile follow-up study.
| Conclusion|| |
Performing an acute 30° proximal tibial varus angulation causes an increase of peroneal nerve rigidity. Decompressing the peroneal nerve reduces the rigidity to the initial level. This study supports the efficacy of peroneal nerve decompression both prophylactically and therapeutically when a corrective varus osteotomy of the proximal tibia is performed. The results of this study suggest that the mechanism of nerve injury might be nerve entrapment rather than stretch injury.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Atar D, Lehman WB, Grant AD, Strongwater A, Frankel V, Golyakhovsky V. Treatment of complex limb deformities in children with the Ilizarov technique. Orthopedics 1991;14:961-7.
Coleman SS. Simultaneous femoral and tibial lengthening for limb length discrepancies. Arch Orthop Trauma Surg 1985;103:359-66.
Coleman SS, Stevens PM. Tibial lengthening. Clin Orthop Relat Res 1978;136:92-104.
Dahl MT, Gulli B, Berg T. Complications of limb lengthening. A learning curve. Clin Orthop Relat Res 1994;301:10-8.
Eldridge JC, Bell DF. Problems with substantial limb lengthening. Orthop Clin North Am 1991;22:625-31.
Galardi G, Comi G, Lozza L, Marchettini P, Novarina M, Facchini R, et al.
Peripheral nerve damage during limb lengthening. Neurophysiology in five cases of bilateral tibial lengthening. J Bone Joint Surg Br 1990;72:121-4.
Mont MA, Dellon AL, Chen F, Hungerford MW, Krackow KA, Hungerford DS. The operative treatment of peroneal nerve palsy. J Bone Joint Surg Am 1996;78:863-9.
Noonan KJ, Price CT, Sproul JT, Bright RW. Acute correction and distraction osteogenesis for the malaligned and shortened lower extremity. J Pediatr Orthop 1998;18:178-86.
Paley D. Problems, obstacles, and complications of limb lengthening by the Ilizarov technique. Clin Orthop Relat Res 1990;250:81-104.
Rose HA, Hood RW, Otis JC, Ranawat CS, Insall JN. Peroneal-nerve palsy following total knee arthroplasty. A review of The Hospital for Special Surgery experience. J Bone Joint Surg Am 1982;64:347-51.
Strong M, Hruska J, Czyrny J, Heffner R, Brody A, Wong-Chung J. Nerve palsy during femoral lengthening: MRI, electrical, and histologic findings in the central and peripheral nervous systems - A canine model. J Pediatr Orthop 1994;14:347-51.
Velazquez RJ, Bell DF, Armstrong PF, Babyn P, Tibshirani R. Complications of use of the Ilizarov technique in the correction of limb deformities in children. J Bone Joint Surg Am 1993;75:1148-56.
Humphreys DB, Novak CB, Mackinnon SE. Patient outcome after common peroneal nerve decompression. J Neurosurg 2007;107:314-8.
Nogueira MP, Paley D, Bhave A, Herbert A, Nocente C, Herzenberg JE. Nerve lesions associated with limb-lengthening. J Bone Joint Surg Am 2003;85-A: 1502-10.
Paley D. Principles of Deformity Correction. 1 st
ed. Corr. 3 rd
Printing. Revised Edition. Berlin: Springer-Verlag; 2005.
Chuang TY, Chan RC, Chin LS, Hsu TC. Neuromuscular injury during limb lengthening: A longitudinal follow-up by rabbit tibial model. Arch Phys Med Rehabil 1995;76:467-70.
Wall EJ, Massie JB, Kwan MK, Rydevik BL, Myers RR, Garfin SR. Experimental stretch neuropathy. Changes in nerve conduction under tension. J Bone Joint Surg Br 1992;74:126-9.
Young NL, Davis RJ, Bell DF, Redmond DM. Electromyographic and nerve conduction changes after tibial lengthening by the Ilizarov method. J Pediatr Orthop 1993;13:473-7.
Daniels TR, Lau JT, Hearn TC. The effects of foot position and load on tibial nerve tension. Foot Ankle Int 1998;19:73-8.
Kwan MK, Rydevik BL, Myers RR, Garfin SR, Triggs K, Woo SL. Stretching injury of rabbit peripheral nerve: A biomechanical and histological study. Trans Orthop Res Soc 1988;13:430.
Kwan MK, Wall EJ, Massie J, Garfin SR. Strain, stress and stretch of peripheral nerve. Rabbit experiments in vitro
and in vivo
. Acta Orthop Scand 1992;63:267-72.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]