Lower Extremity Nerve Entrapment

DEFINITION

Care of peripheral nerve problems requires knowledge and understanding of nerve pathology, anatomic nerve variations, patterns of nerve damage and entrapment that follow trauma and common operative procedures, and specialized surgical techniques for manipulation of the damaged peripheral nerve.

Unlike other surgical disciplines, a large proportion of peripheral nerve pathology is secondary to postoperative neuropathy, with subsequent treatment reoperative in nature.

Lateral Femoral Cutaneous Nerve

The lateral femoral cutaneous nerve (LFCN) compression is termed meralgia paresthetica and can cause symptoms of pain, numbness, or paresthesias in the anterolateral thigh, as shown in FIG 1.

Compression can be spontaneous or iatrogenic, most commonly following procedures in proximity to the anterior superior iliac spine (ASIS), the inguinal region, or the anterior thigh.

Saphenous Nerve

Saphenous nerve compression or irritation is an often unrecognized cause of knee pain that can mimic other knee conditions and lead to unnecessary, unsuccessful surgical intervention.

 

 

 

FIG 1 • Sensory innervation of the LFCN.

 

 

Compression most commonly occurs in the upper leg are at the adductor (Hunter) canal and injury most commonly occurs from iatrogenic injury at the level of the knee.

 

Pes anserinus bursitis and space-occupying lesions are other causes of saphenous nerve compression that have been reported.5

Common Peroneal Nerve

 

Common peroneal nerve (CPN) injury is characterized by weakness of ankle and foot dorsiflexion (foot drop) as well as loss of sensation over the anterolateral leg and dorsum of the foot.

 

Surgical procedures and trauma to the lateral knee both represent potential etiologies of CPN injury.

 

The nerve can become entrapped in postoperative scar tissue, stretched with knee or ankle dislocations, or inadvertently directly damaged, resulting in neuropathy.

Superficial Peroneal Nerve

 

Superficial peroneal nerve (SPN) pathology is most commonly characterized by pain at the area of compression or injury and symptoms are often activity related.

 

SPN injury can result from entrapment where the nerve exits the deep crural fascia or from iatrogenic

injury during surgery on the lower leg and ankle.

Entrapment as the nerve exits the deep crural fascia can result from a fascial defect with herniation of the peroneal musculature. Alternatively, it can occur at this level from traction injuries that occur in the setting of chronic ankle sprains.

 

 

ANATOMY

General Nerve Anatomy

 

The peripheral nerve has a significant intrinsic blood supply that permits the surgeon to lift the nerve from its anatomic bed, open the epineurium, and operate between the fascicles.11

 

The endoneurial and perineurial microvessels maintain excellent vascularity to the peripheral nerve. Segmental blood vessels enter the peripheral nerve through the mesoneurium. In addition, an extensive

number of longitudinal vessels in the epineurium, perineurium, and endoneurium supply the nerve.12

 

 

The “safe” length a nerve can be elevated from its bed (its segmental vascular supply) is a distance of about 60 times the diameter of the nerve.13 The nerve should be

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mobilized into an area free from possible external compressible, with care to ensure that the vascular supply is not compromised.

 

Extreme caution should be exercised in repeat neurolysis of a peripheral nerve due to risk of nerve devascularization.

 

Lateral Femoral Cutaneous Nerve

 

The LFCN arises from direct contributions of the L2 and L3 spinal nerve roots, passing between the psoas and the iliacus, and traveling in the retroperitoneal space before reaching the anterior thigh.

 

The nerve typically courses medially to the ASIS and traverses the groin crease deep to the inguinal ligament (on average 1 cm medial to the ASIS) as it descends to innervate the thigh.

 

The nerve course is variable, and LFCN can pass superficially to the inguinal ligament or laterally to the ASIS, running over the iliac crest where there is increased risk of iatrogenic injury.1

 

The surface anatomy and the most common sites of impingement can be seen in FIG 2.

 

Saphenous Nerve

 

The saphenous nerve is a large sensory branch of the femoral nerve that runs with the superficial femoral artery through the adductor canal (Hunter canal).

 

The adductor canal is located in middle third of thigh and connects the anterior and medial compartments. The apex of the femoral triangle marks the superior extent, and an opening in the adductor magnus, termed the adductor hiatus, marks the inferior extent. The boundaries of the canal are the vastus medialis (lateral), adductor longus and magnus (posteromedial), and a fascial band deep to the sartorius (anterior).

 

The saphenous nerve divides into two branches prior to becoming subcutaneous at the level of the knee. The infrapatellar branch pierces the sartorius and fascia before turning transversely and running laterally inferior to the patella. The sartorial branch pierces the fascia between the tendons of the gracilis and sartorius before continuing down the medial aspect of the lower leg (FIG 3).

 

 

 

FIG 2 • Surface anatomy of the LFCN. Note the approximate site of compression at the level of the inguinal ligament.

 

Common Peroneal Nerve

 

The CPN is one of two main divisions of the sciatic nerve, formed from contributions from the sacral plexus from L4 to S2.

 

Pathology of the CPN classically occurs when it wraps around the neck of the fibula, deep to the peroneus longus muscle just before splitting into deep and superficial branches (FIG 4).

 

The CPN, via the deep peroneal nerve branch, innervates the muscles for foot dorsiflexion as well as sensation to the first web space. The SPN branch innervates the peroneals, which perform eversion and provide sensory innervation to the anterolateral lower leg and the majority of the dorsum of foot and toes.

 

Superficial Peroneal Nerve

 

The SPN courses inferiorly down the leg most commonly in the lateral compartment, then curves anteriorly and pierces the crural fascia approximately 10 to 12 cm above the tip of the lateral malleolus.

 

 

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FIG 3 • Anatomy of the saphenous nerve. Note the anatomic relationships of the adductor canal and the division into the infrapatellar and sartorial branches at the level of the knee.

 

 

 

FIG 4 • Anatomy of the CPN. Note the proximity of the nerve to the fibula as it wraps anteriorly on the lower leg.

 

 

Variations do exist in which the nerve travels in the anterior compartment and pierces the anterior crural fascia.18

 

Distally, the nerve courses in the subcutaneous tissue and branches into the intermediate and dorsal cutaneous nerves approximately 6 to 7 cm proximal to the tip of the lateral malleolus.

 

PATHOGENESIS

 

Peripheral nerve pathology is due to any process that interferes with neuronal conduction outside of the central nervous system.

 

 

Those processes amenable to surgical intervention include nerve damage due to (1) physical compression from anatomically adjacent structures, (2) trauma, and (3) iatrogenic injury.

 

Peripheral nerve surgery encompasses repair of two common pathophysiologic entities:

 

 

Accidental nerve transection or direct crush injury that leads to nerve dysfunction and possible painful neuroma formation.

 

Scar formation from prior procedures or trauma can engulf a peripheral nerve and compress it; symptomatic relief can then be accomplished through surgical decompression of the peripheral nerve.

 

Peripheral nerve injury becomes symptomatic either when a critical function is lost or when paresthesia and pain replace normal sensory signaling.

 

Partial or complete nerve transection causes loss of sensory or motor function because of loss of nerve continuity or disruption of the nerve's blood supply. The nerve's regenerative capacity then either reestablishes neuronal continuity or forms a disorganized scar within a mature end-bulb neuroma.

 

Similarly, compression on a peripheral nerve causes ischemia and neuroma formation.11

 

 

A neuroma contains bundled, disorganized nerve endings within a collagenous mass and is an anatomic source of the localized pain and paresthesia following peripheral nerve damage.

Lateral Femoral Cutaneous Nerve

 

Many cases are iatrogenic and injury to the nerve is a known complication of both orthopaedic and nonorthopaedic surgeries. In the field of orthopaedics, a postoperative nerve palsy can occur following acetabular fracture surgery, pelvic osteotomies, iliac crest bone harvest, anterior total hip arthroplasty, and hip arthroscopy. In other fields, the injury has been noted following laparoscopic hernia repair, bariatric, and

gynecologic surgeries.8

 

LFCN injury can occur as a result of direct mechanical compression. This can be external from a belt or tight-fitting pants and can also be internal from increased intra-abdominal pressure secondary to obesity, pregnancy, or intra-abdominal tumor.

 

Metabolic factors have been shown to contribute and are often comorbidities in spontaneous cases of LFCN injury. These include diabetes, alcohol abuse, and chronic systemic inflammatory conditions such as lupus.

 

Saphenous Nerve

 

Compression of the nerve commonly occurs at the distal aspect of the adductor canal, most commonly from external compression. Other causes include iatrogenic, space-occupying lesions, pes anserinus, or idiopathic. Compression at this level was previously reported in surfers who clenched the surfboard between their legs at

the distal aspect of the femur.7 At this level, compression can also occur secondary to thrombosis of the superficial femoral artery.

 

Iatrogenic injury to the saphenous nerve can occur at the level of the infrapatellar branch as it crosses the knee inferior to the patella. There have been reports of injury at this level following knee arthroscopy or

through open surgery using the medial parapatellar approach.15 Injury can occur along the sartorial

 

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branch of the nerve as well at the level that it runs with the greater saphenous vein. The nerve is commonly injured at this level in vein stripping or vein harvesting procedures.16

Common Peroneal Nerve

 

CPN injuries have a particularly wide range of etiologies.

 

Trauma is a common etiology of CPN injury—either direct blow to the lateral knee, ankle fracture with a proximal fibula fracture, or a high energy or sports injury causing a multiligament knee injury.

 

Iatrogenic injury can occur from arthroscopic or open knee procedures. Total hip arthroplasty and total knee arthroplasty have low but reportable incidences of CPN palsy that are often secondary to external compression from intraoperative positioning.

 

Space-occupying lesions can compress the CPN. These include intraneural ganglia and proximal tibia-fibular joint cysts.2

 

Metabolic conditions including diabetes mellitus and hyperthyroidism can result in mononeuropathies of the CPN.

 

Superficial Peroneal Nerve

 

Compression often occurs at the level where the SPN pierces the crural fascia and becomes subcutaneous. There can be focal herniation of the peroneal musculature at this level, causing compression. This pathology

can occur in isolation or can be in addition to an underlying exertional compartment syndrome.10

 

Peroneal muscle herniation and nerve compression can also occur in a fascial defect following a surgical procedure such as ankle fracture open reduction and internal fixation.

 

SPN injury can be related to traction injury from ankle inversion, commonly occurring with repeated ankle sprains in chronic ankle instability.2

PATIENT HISTORY AND PHYSICAL FINDINGS

 

History and physical examination, particularly a thorough neurologic examination, often suggest the diagnosis by demonstrating a dermatomal distribution of pain or paresthesia. Further imaging and electrodiagnostic

testing may be necessary, mainly to rule out other causes for the symptoms.3,12

 

 

Central nervous system disease, particularly spinal root impingement, shares many of the same symptoms and must be excluded.

 

Diagnostic workup must evaluate and exclude other etiologies for postoperative pain, particularly infection, loosened hardware, mechanical misalignment, spinal involvement, and neoplasm.

 

 

The timing of the sensory or motor symptoms needs to be considered when taking the history and performing the physical examination to aid in understanding the cause of neuropathy.

 

Lateral Femoral Cutaneous Nerve

 

A patient will present a history of pain, numbness, paresthesias, or dysesthesias in the anterolateral thigh.

 

They should be carefully questioned regarding any antecedent trauma, surgical procedures, recent weight gain or pregnancy, use of tight-fitting clothing as well as medical comorbidities that can predispose to peripheral nerve disease (diabetes, alcoholism, nutritional deficiency).

 

Physical examination should involve testing the sensation in the distribution of the LFCN as well as testing for a painful response to light touch in the area. One can attempt to palpate for a neuroma or to perform a Tinel sign, although the area of nerve compression or injury can be variable. The most common area of

 

compression is 1 cm medial and inferior to the ASIS.8 The patient may have increased pain with hip extension.

Saphenous Nerve

 

A patient will typically present with pain, deep aching, numbness, paresthesia, or dysesthesia at the medial aspect of the thigh or calf or the anterior aspect of the knee.

 

The patient should be questioned regarding prior surgeries (particularly vascular surgeries involving greater saphenous vein harvest or excision and orthopaedic surgeries about the knee including arthroscopy) as well as any history of trauma (particularly blunt trauma to the anterior knee).

 

On physical examination, patient may have numbness or a sensitivity to light touch in the distribution of the saphenous nerve. There can be a neuroma or a positive Tinel sign at any point along the course of the saphenous nerve, but common sites of compression are at the adductor canal, at the medial femoral condyle, and along the course of the infrapatellar branch.

 

Common Peroneal Nerve

 

A patient will present with weakness of ankle dorsiflexion and foot eversion (“foot drop”) as well as loss of sensation over the anterolateral lower leg and dorsum of the foot. Pain is variable.

 

In taking the history, questioning should include details of any prior surgery, especially around the knee or hip as the CPN division of the sciatic nerve can be affected in isolation proximally. It should also include any other surgery of a long duration in which positioning on the operating room table could put the nerve at risk. One should inquire about history of trauma to the knee (either direct blow or indirect trauma causing multiligament knee injury) as well as an inversion injury at the level of the ankle.

 

Physical examination will reveal loss of strength and sensation as listed earlier. Patient may walk with increased hip and knee flexion (steppage gait) in order to clear the foot. Depending on the chronicity of the injury, there may be an equinus contracture of the ankle. A knee ligamentous examination should be performed if the nerve injury is in conjunction with a traumatic injury to the knee.

 

Superficial Peroneal Nerve

 

A patient will most commonly present with pain radiating over the dorsum of the foot and ankle. It is sometimes accompanied by numbness, paresthesias, or dysesthesias. There can be muscle weakness if the injury occurs at a proximal level, but this is less common. A patient may report pain that increases with activity. They may also report that they feel a bulge at the lateral aspect of their leg at an area of peroneal muscle herniation. They should be asked about trauma (ankle sprains) and prior surgery (lower leg or ankle surgery).

 

On examination, sensation may be diminished in the distribution of the SPN. There may be a lateral compartment muscle herniation palpable. A Tinel sign may be positive but is an insensitive test for SPN injury. Pain may be reproducible

 

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with passive ankle flexion and foot inversion or with resisted active ankle dorsiflexion and foot eversion. An examination of ankle stability should be performed.

 

IMAGING AND OTHER DIAGNOSTIC STUDIES

 

Current imaging techniques—including computed tomography (CT), magnetic resonance imaging (MRI), and radiolabeled bone scans—have limited value in confirming the diagnosis of a malfunctioning nerve.

 

Electrodiagnostic studies can also have a false-negative rate as high as 36%, whereas nerve blocks, because of anatomic variations, can give a false-negative result.9

 

For these reasons, it cannot be overstated that a diagnostic workup must be interpreted cautiously.

 

Lateral Femoral Cutaneous Nerve

 

Injection of a local anesthetic is often useful as a diagnostic tool. Injection can be placed 1 cm medially and inferiorly to ASIS, at the site of maximal tenderness or under ultrasound guidance.

 

Nerve conduction study can be performed and should be interpreted in comparison to the contralateral side. Electromyography (EMG) can also be performed to rule out involvement at the level of the lumbar plexus or nerve roots. Somatosensory evoked potentials have also been used in some cases.

 

Pelvis radiographs should be done to help rule out a tumor and to evaluate for intra-articular pathology as a contributing factor to symptoms.

 

Saphenous Nerve

 

Injection of a local anesthetic is again a useful diagnostic tool. For the saphenous nerve, the injection is typically done at the adductor canal.

 

The saphenous nerve is surrounded by significant subcutaneous fat and therefore nerve conduction studies

are difficult to perform and have not been shown to be useful diagnostically.16

 

Common Peroneal Nerve

 

Given, the wide range of etiologies for CPN injury, the clinical scenario will guide the diagnostic and imaging modalities.

 

Plain radiographs of the hip, knee, or ankle should be done in the setting of trauma to the respective areas and can also be useful in evaluating for a possible mass.

 

EMG and nerve conduction study should be used to confirm the diagnosis of CPN entrapment or injury and to differentiate from lumbar spine radiculopathy.

 

High-resolution (3 Tesla) MRI can be used to visualize intraneural ganglia or other space-occupying lesion, which is particularly relevant in the setting of spontaneous nerve palsy in the absence of trauma or suspected iatrogenic injury.

 

Ultrasound is also useful for evaluating the CPN at its superficial position at the fibular head.

 

Superficial Peroneal Nerve

 

The first-line imaging modality is typically weight-bearing ankle radiographs and if there is high concern for chronic ankle instability stress views can be obtained.

 

MRI is useful if there is concern for a space-occupying lesion.

 

Nerve conduction studies or somatosensory evoked potentials may be abnormal compared to the contralateral side but these are not sensitive tests and not commonly done in the evaluation of an SPN injury.

 

Injection of an anesthetic of the SPN at the area of compression or injury can help confirm the diagnosis. An injection can also be done at an alternative site (ie, intra-articular ankle injection) to help clarify confounding sources of pain.

 

NONOPERATIVE MANAGEMENT

 

Medical management of paresthesias and pain from injured peripheral nerves centers on symptom management:

 

 

Activity and lifestyle modification

 

Nonnarcotic analgesics (narcotic medications should be avoided or used sparingly)

 

Centrally acting agents such as anticonvulsants (gabapentin, pregabalin, carbamazepine, lamotrigine) or tricyclic antidepressants (amitriptyline)

 

Topically applied compounds containing combinations of local anesthetic, anti-inflammatory medication, and capsaicin

 

Physical and occupational therapy

 

Although medical management offers temporary relief in most patients, it can be complicated by increasing dosage requirements and narcotic dependence as an acute insult develops into a chronic pain syndrome.19

 

Among the first steps to focus on are eliminating possible causes of neuropathy and optimizing the patient's medical condition if comorbidities are present.

 

Local anesthetic injections at the area of nerve pathology can have therapeutic benefits in addition to the diagnostic value detailed earlier. Corticosteroid can be used in conjunction with the local anesthetic to have an

anti-inflammatory effect and provide more prolonged and sometimes permanent relief.

 

Transcutaneous electrical nerve stimulators (TENS) can be used to try to elicit descending inhibitory pain signals through nerve stimulation.

 

Nonoperative management is considered a failure when patients with neuropathy do not achieve a reasonable recovery by approximately 12 weeks.

 

 

At that point, additional evaluation by a peripheral nerve surgeon or electrodiagnostic workup is appropriate to determine whether surgical intervention or continued observation is indicated.

 

Lateral Femoral Cutaneous Nerve

 

The first line of nonoperative intervention in LFCN compression would be to remove any external cause of compression such as tight-fitting clothing. Additionally, avoiding any symptom-producing positions or maneuvers such as hip extension or prolonged standing is advisable.

 

 

Injection of local anesthetic with or without corticosteroid can be performed as described earlier. Nonoperative modalities have been shown to relieve symptoms in up to 90% of patients.20

Saphenous Nerve

 

If initial modalities such as activity modification, topical medications, and oral medications are ineffective, a local nerve injection can be attempted.

 

 

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Injection of local anesthetic with or without corticosteroid medication can be performed at the level of the adductor canal between the sartorius and the vastus medialis. Injection is typically approximately 7 cm

proximal to the superior pole of the patella. Aspiration should be performed prior to injection to avoid injection into superficial femoral artery or vein.

 

Results of injections have been variable, and multiple repeated injections are sometimes necessary.17,21

 

If there is concern for compression of the superficial femoral artery (claudication symptoms), this should be further evaluated and, if present, should be treated with decompression rather than nonoperatively.

 

Common Peroneal Nerve

 

In addition to treating the neuropathic pain with the mentioned modalities, it is important to provide support to the foot to compensate for the motor deficits involved with CPN palsy.

 

An ankle-foot orthosis (AFO) should be used at all times. A comfortable supportive orthoses such as a pressure-relief ankle-foot orthosis (PRAFO) can be used at night to support the ankle and prevent an equinus contracture from developing. For ambulation, a low-profile spring leaf AFO can be used to allow for more normal gait mechanics.

 

Injections in the vicinity of the CPN where it lies superficially at the level of the fibular head may have not only the potential benefit of pain relief but also may decrease inflammation in the area (if corticosteroid used) and decrease compression from surrounding structures.

 

Superficial Peroneal Nerve

 

Nonoperative treatment involves managing pain symptoms as well as treating inciting factors such as ankle instability.

 

Activity modification should be encouraged if symptoms seem closely related to exercise and are likely the result of focal compression of the nerve from swelling of the peroneal musculature.

 

Physical therapy for peroneal muscle strengthening and proprioception addresses the ankle instability, and an ankle brace with a lateral wedge shoe insert can help prevent inversion stress of the ankle and relieve tension on the SPN.

 

TECHNIQUES

• Lateral Femoral Cutaneous Nerve

   

  The patient is placed in the supine position, and an incision of about 6 cm is made anterior to the ASIS, extending toward the thigh.

   

  Careful dissection is then carried to deep fascia and toward the inguinal ligament (TECH FIG 1A).

   

  The use of loupe magnification as well as proper microsurgical instruments and bipolar electrocautery is essential when identifying the LFCN because of the variability in its anatomy (TECH FIG 1B).

   

  The LFCN could be encountered at any point in the dissection of the inguinal ligament and must not be damaged.

   

  Once identified, the nerve is first decompressed distally approximately 4 to 6 cm and then proximally at the inguinal ligament and internal oblique and transversalis deep muscle fascia where most compression

  typically occurs6 (TECH FIG 1C).

   

   

   

  TECH FIG 1 • A. Exposure for dissection of the LFCN. B. Identification of LFCN. C. Internal oblique muscle elevated off LFCN at compression site. D,E. LFCN proximally and distally decompressed. Note the cuff of internal oblique that has been removed around the LFCN proximally.

   

   

  After this release, retroperitoneal decompression is performed by retraction of the muscle and excision of the deep fascia sitting on the top of the nerve (TECH FIG 1D,E).

   

  Great caution must be exercised dissecting in this area because of the proximity of the deep circumflex iliac artery that crosses the nerve in the retroperitoneum.

   

  Some surgeons prefer nerve transection rather than neurolysis. The disadvantage of transection is the

  resultant loss of sensation to the anterolateral thigh. Case series comparing the two treatment options have shown mixed results. In the case of a LCFN neuroma, transection is the only option.

   

  If transection is performed, traction should be applied to the nerve and the nerve should be sharply transected as proximal as possible to allow retraction into the retroperitoneum in order to avoid a painful more proximal neuroma.

   

   

  Whether performing neurolysis or transection, care should be taken to identify and address all branches of the nerve.

   

• Saphenous Nerve

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  Patient is positioned supine with a bolster beneath the contralateral hip to externally rotate the operative leg. A sterile thigh tourniquet may be used.

   

  A 6-cm longitudinal incision is made at the anterior border of the sartorius, centered approximately 10 cm proximal to the proximal pole of the patella or alternatively at the level of a positive Tinel sign.14

   

  The first interval to identify is between the sartorius and the quadriceps. The interval may be most readily identified at the distal extent of the incision.

   

  Next, the interval between the adductor magnus and the vastus medialis. There will be a fascial band overlying this interval. This fascia should be divided, and the saphenous nerve should be identified beneath it.

   

  At this juncture, the surgeon can proceed with neurolysis or alternatively neurectomy. Neurectomy is more likely to achieve pain relief but causes permanent anesthesia of the medial leg and anterior knee. Therefore, this decision is controversial.

   

  If one elects to perform neurolysis, nerve should be traced distally as far as necessary to release all palpable fascial bands.

   

  If neurectomy is performed, the nerve should be sharply divided as far proximal in the adductor canal as possible. The proximal stump should be buried in muscle to prevent formation of a more proximal painful neuroma.

• Common Peroneal Nerve

   

  With the patient in a supine position, a thigh tourniquet is placed—as long as the patient does not have previous vascular bypasses in this area—and an incision is made one to two fingerbreadths below the fibular head (TECH FIG 2A).

   

  Dissection is carried to the deep fascia under loupe magnification because proper identification of the nerve is critical (TECH FIG 2B).

   

  The nerve can easily be mistaken for yellow fat, particularly if it runs abnormally superficially or was displaced with trauma.

   

  Proximal decompression is performed first by release of the gastrocnemius fascia and its attachment to hamstring and iliotibial fascial tissues (TECH FIG 2C).

   

   

   

  TECH FIG 2 • A. Schematic for skin incision to access the CPN. B. Exposure of CPN through surgical incision. (continued)

   

   

  Distal dissection is performed by incising the peroneus longus fascia and retracting this muscle laterally.

   

  A fascial band that causes both a kink in the nerve as well as compression against the fibula can then be visualized and addressed (TECH FIG 2D).

   

  In patients with a proximal tibia-fibula cyst, it is important to roughen the proximal tibia-fibula joint with a curette to create a degree of fusion and prevent recurrence of the cyst.

   

  Closure is then performed in anatomic layers, sparing the deep fascia, which is not closed, to avoid recreating the nerve compression.

   

  Great caution should be exercised in patients with a history of previous knee trauma or dislocation because the anatomy of the nerve may be aberrant, which could lead to iatrogenic nerve injury during surgical approach and manipulation.

   

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  TECH FIG 2 • (continued) C. Identification of CPN. D. Identification of compressive band of peroneus longus muscle fascia over CPN.

• Superficial Peroneal Nerve

 

Patient is positioned supine with a bolster under the ipsilateral hip to internally rotate the leg. A thigh tourniquet may be used.

A longitudinal incision is made several centimeters proximal to the tip of the lateral malleolus, just anterior to the fibula.

The SPN is first identified distally in the subcutaneous tissue and trace back to the level where it pierces the crural fascia.

The nerve should be released from any structures to which it is tethered. A partial fasciotomy should be performed (at least 5 cm proximal and distal to nerve) to allow adequate room for the nerve.

An adequate decompression and neurolysis should be tested with intraoperative plantarflexion. There should be no tension on the nerve.

If there is coexisting lateral ankle instability or exertional compartment syndrome, these pathologies should be addressed at the time of surgery with lateral ligament repair/reconstruction or extensile lateral compartment fasciotomy, respectively.

Closure should include skin only. No fascial closure should be done.

Immobilization in a removable boot is recommended initially to allow wound healing. However, controlled range-of-motion exercises should begin shortly after surgery and immobilization should be discontinued once sutures or staples are removed.

 

PEARLS AND PITFALLS
	Indications ▪ Complete history and physical examination, with particular focus on the neurologic examination Document any nerve function compromise: loss of function, paresthesias, positive Tinel sign, or tenderness over nerves. Obtain electrodiagnostic confirmation of diagnosis if possible.     Lateral femoral ▪ Careful dissection with appropriate magnification and instruments cutaneous nerve ▪ Consider anatomic variations of the nerve in relation to the ASIS and the inguinal ligament. Careful retroperitoneal decompression because of the proximity of the deep circumflex iliac artery     Saphenous nerve ▪ Be sure to differentiate nerve compression from vascular compression, which will present with claudication symptoms. If neurectomy is performed, be sure to bury nerve in muscle proximal in adductor canal.     Common ▪ Careful initial dissection because nerve can easily be mistaken for fat peroneal nerve ▪ Recognize that the nerve can be more superficial than expected; with a history of trauma, it tends to be more anterior and superior. Careful dissection with appropriate magnification and instruments     Superficial ▪ Be aware of variants in which the SPN travels in the anterior rather than

 

	peroneal nerve lateral compartment. Address underlying pathology such as ankle instability or exertional compartment syndrome at time of nerve decompression.     Postoperative ▪ If a nerve decompression was performed, early mobilization should be management encouraged. If nerve reconstruction was performed, limited ambulation or immobilization is advised.

 

 

 

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POSTOPERATIVE CARE

 

Wound healing concepts should be applied to the peripheral nerve with immediate range of motion and avoidance of immobilization.

 

During the first week after surgery, the nerve will lie in an environment that is predominantly inflammatory. Collagen is not deposited into the wound until the second week, and cross-linking of the collagen does not occur until after the third week.

 

If the nerve is kept immobile during the second and third postoperative weeks, it will become adherent to the surrounding tissues.

 

 

Conversely, for the nerve to be loose and able to slide through its surrounding tissues, it is necessary to allow the nerve to move with respect to its bed following the first week of splinting.

 

The fact that a nerve will not adhere to a bed of cut muscle and fibrous tissue if it is allowed to glide early in the postoperative period was demonstrated for the ulnar nerve at the elbow in a baboon model.4

 

Therefore, in operation on the peripheral nerve, it is essential that the postoperative regimen includes some movement of the joints during the first week and splinting be reserved mainly for cases involving nerve grafting.

 

REFERENCES

1. Aszmann OC, Dellon ES, Dellon AL. Anatomical course of the lateral femoral cutaneous nerve and its susceptibility to compression and injury. Plast Reconstrc Surg 1997;100:600-604.

    

    

2. Daghino W, Pasquali M, Faletti C. Superficial peroneal nerve entrapment in a young athlete: the diagnostic contribution of magnetic resonance imaging. J Foot Ankle Surg 1997;36:170-172.

    

    

3. Dellon AL. Physical examination in nerve compression. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: Lippincott, 1991.

    

    

4. Dellon AL, MacKinnon SE, Hudson AR, et al. Effect of submuscular versus intramuscular placement of ulnar nerve: experimental model in the primate. J Hand Surg Br 1986;11:117-119.

    

    

5. Docherty JG, Morrice JJ, Bell G. Saphenous neuritis following varicose vein surgery. Br J Surg 1994;81:698.

    

    

6. Ducic I, Dellon AL, Taylor NS. Decompression of the lateral femoral cutaneous nerve in the treatment of meralgia paresthetica. J Reconstr Microsurg 2006;22:113-118.

    

    

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