Ivica Ducic and Jeffrey M. Jacobson
BACKGROUND
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 surgery attempts to correct neuropathy in the postoperative patient and, therefore, is reoperative in nature.
Lateral femoral cutaneous nerve (LFCN) neuropathy can be encountered in the orthopedic patient after injuries or procedures in proximity to the anterior superior iliac spine (ASIS), the inguinal region, or the anterior thigh.
The symptoms are limited to pain or paresthesias in the distribution shown in FIGURE 1, because this nerve carries only sensory signals.
Surgical procedures and trauma to the lateral knee both represent potential for common peroneal nerve (CPN) injury.
The nerve can become entrapped in postoperative scar tissue, stretched with knee or ankle dislocations, or inadvertently directly damaged, resulting in neuropathy.
ANATOMY
Lateral Femoral Cutaneous Nerve
The LFCN arises from the lumbar plexus through contributions from the dorsal divisions of the L2 and L3 spinal roots. In most people, the nerve courses medial to the ASIS and traverses the groin crease under the inguinal ligament as it descends to innervate the thigh.
The nerve is prone to iatrogenic injury when its anatomy is aberrant; the surgeon should be aware that the LFCN can run through the inguinal ligament and against the ASIS or over the most medial portion of ASIS rather than in its usual course.
The surface anatomy and the most common site of impingement can be seen in FIGURE 2.
FIG 1 • Sensory innervation of the lateral femoral cutaneous nerve
Common Peroneal Nerve
The CPN is a branch of the sciatic nerve, formed from contributions from the sacral plexus from L4 to S2.
Pathology of the CPN classically is seen as it wraps around the neck of the fibula, deep to the peroneus longus muscle just before it splits into its deep and superficial branches (FIG 3).
The CPN innervates the muscles for foot dorsiflexion and eversion and provides sensory innervation to the anterolateral lower leg and the majority of the dorsum of foot and toes.
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.1
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.2
Maki et al3 have demonstrated that 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. Therefore, the surgeon should consider primarily the need to move the nerve into an area that is free from forces that might externally compress it and, thus, cause symptomatic neuropathy but also should acknowledge internal vascular properties of the nerve when effective mobilization is considered.
FIG 2 • Surface anatomy of the lateral femoral cutaneous nerve. Note the approximate site of compression at the level of the inguinal ligament
FIG 3 • Anatomy of the common peroneal nerve. Note the proximity of the nerve to the fibula as it wraps anteriorly on the lower leg.
Extreme caution should be exercised in repeat neurolysis of a peripheral nerve, because of repeated nerve devascularization.
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 physical compression related to various metabolic conditions and surgeries around or adjacent to a nerve.
Peripheral nerve surgery encompasses repair of two common pathophysiologic entities:
Accidental nerve transection or direct crush injury leads to nerve dysfunction and possible painful neuroma formation.
Scar formation from any surgery 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 re-establishes neuronal continuity or forms a disorganized scar within a mature end-bulb neuroma.
Similarly, compression on a peripheral nerve causes ischemia and neuroma formation.1
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.
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 evaluate other causes for the symptoms.2,4
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, because that can aid in understanding the cause of neuropathy.
When encountering potential neuropathies in the knee or lower leg, the clinician must consider that, although the common peroneal nerve is the major peripheral nerve affected following knee surgery, neuromas of sensory nerves supplying the knee and its surroundings may develop when they are severed or encased in scar tissue.
These smaller peripheral nerves can be the source of chronic postoperative knee pain and can be mistaken for CPN neuropathy or mask the CPN involvement.
Therefore, the examining physician should be aware of the different possible causes of pain in this anatomic area and should be able to distinguish deep and superficial paresthesias and pains in the knee area.
The most commonly affected sensory nerves involved in deep knee pain are the lateral retinacular nerve, the medial retinacular nerves, and the articular branch of the common peroneal nerve, whereas superficial knee pain is caused mainly by involvement of the infrapatellar branch of the saphenous nerve and the medial and anterior cutaneous nerves of the thigh.
If any of these smaller nerves is suspected as the cause of a patient's symptoms, referral to a peripheral nerve surgeon is suggested.
IMAGING AND DIAGNOSTIC STUDIES
Current imaging techniques—including CT, MRI, and radiolabeled bone scans—have limited, if any, value confirming the diagnosis of a malfunctioning nerve.
Electrodiagnostic studies also can have a false-negative rate as high as 33%, whereas nerve blocks, because of anatomic variations, can give a false-negative result.
For these reasons, it cannot be overstated that a diagnostic workup must be interpreted cautiously.
NONOPERATIVE MANAGEMENT
Medical management of paresthesias and pain from injured peripheral nerves centers on symptom management:
Activity and lifestyle modification
Narcotic and nonnarcotic analgesics
Centrally acting agents such as gabapentin and pregabalin
Nerve blocks
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.5
Among the first steps to focus on are eliminating possible causes of neuropathy and optimizing the patient's medical condition if comorbidities are present.
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.
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 anterior superior iliac spine, 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 occurs (TECH FIG 1C).
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.
TECH FIG 1 • A. Exposure for dissection of the lateral femoral cutaneous nerve (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
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 1 to 2 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).
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).
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.
TECH FIG 2 • A. Schematic for skin incision to access the common peroneal nerve. B. Exposure of CPN through surgical incision. C. Identification of CPN. D. Identification of compressive band of peroneus longus muscle fascia over CPN.
POSTOPERATIVE CARE
Wound healing concepts should be applied to the peripheral nerve.
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.7
Therefore, in operation on the peripheral nerve, it is essential that the postoperative regimen include some movement of the joints during the first week and splinting be reserved mainly for cases involving nerve grafting.
REFERENCES
1. Lundborg G, Rydevik B. Effects of stretching the tibial nerve of the rabbit: a preliminary study of the intraneural circulation and the barrier function of the perineurium. J Bone Joint Surg Br 1973;55B: 390–401.
2. Mackinnon SE, Dellon AL. Physical examination. In: Surgery of the Peripheral Nerve. New York: Thieme, 1988.
3. Maki Y, Firrell JC, Breidenbach WC. Blood flow in mobilized nerves: results in a rabbit sciatic nerve model. Plast Reconstr Surg 1997;100: 627–633.
4. Dellon AL. Physical examination in nerve compression. In: Gelberman R, ed. Operative Management of Peripheral Nerve Injury. Philadelphia: JB Lippincott, 1991.
5. Vernadakis AJ, Koch H, Mackinnon SE. Management of neuromas. Clin Plast Surg 2003;30:247–268.
6. Ducic I, Taylor NS, Dellon AL. Decompression of the lateral femoral cutaneous nerve in the treatment of meralgia paresthetica. J Reconstr Microsurg 2006;22:113–117.
7. 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;11B:117–119.