Clinical manifestations

Presentation and course

Femoral neuropathy presents with quadriceps weakness and numbness of the medial thigh and leg, often acutely. Patients frequently complain that their leg buckles underneath them. In cases of femoral neuropathy due to iliacus or retroperitoneal hematoma, there may be severe pain experienced over the anterior thigh in addition to the back, buttock, abdomen, and groin (31). Passive extension at the hip may be painful in these cases. Otherwise, groin or thigh pain is usually mild. The neurologic examination reveals weakness of knee extension (quadriceps) with absent or depressed patellar reflex. When the femoral nerve is injured in the pelvis, hip flexion (iliopsoas) may also be weak; however, hip flexion is spared in more distal lesions. Thigh adduction should be normal as these muscles are innervated by the obturator nerve. Hypoesthesia is common, involving the anteromedial thigh and medial calf. Sensory symptoms can include pain in the inguinal region, which forces the patient to hold the hip in the antalgic position of flexion and external rotation, as well as pain or dysesthesia at the anterior thigh and anteromedial leg. In most cases, the femoral neuropathy is unilateral, although bilateral femoral neuropathies may result from the lithotomy position or pelvic surgery.

Prognosis and complications

In a case series of 154 patients with femoral neuropathy, 36% had nearly complete recovery, 27% partially recovered, and 25% had minimal or no recovery (64). These data were strikingly similar to another study of 31 patients in which 31% of patients fully recovered, 34% had a good but incomplete recovery, and 31% had minimal to no recovery (40).

The prognosis for the recovery of muscle strength after femoral neuropathy depends mostly on whether the injury is axonal or demyelinating in nature. Findings on nerve conduction studies and EMG can determine this underlying pathophysiology. Therefore, they are often helpful in predicting the prognosis of weakness in acute femoral nerve lesions, with the single most useful piece of data being the estimate of motor axon loss based on nerve conduction studies.

The femoral nerve can be stimulated at the groin and a compound muscle action potential recorded from the rectus femoris. If the femoral CMAP amplitude is low or absent in the presence of moderate or severe weakness of the quadriceps, this suggests motor axon loss. The prognosis in such cases is relatively protracted as it will depend on axon sprouting and reinnervation. If CMAP is reduced to less than 50% of the amplitude of the contralateral response, less than 50% of patients recover over the next year. In contrast, all patients in a large case series with a femoral CMAP amplitude that was more than 50% of the amplitude of the contralateral response recovered by the end of 1 year (40). The amplitude should always be compared to the asymptomatic opposite side as this response can be technically challenging to obtain, even in normal individuals. Of note, measuring the saphenous (terminal sensory branch of the femoral nerve) sensory nerve action potential is often useful diagnostically, but it has less prognostic value than the compound muscle action potential.

In contrast, if the femoral CMAP amplitude is normal, a demyelinating lesion is implied. Focal slowing of conduction velocity and conduction block cannot be demonstrated because it is not possible to stimulate the femoral nerve at more proximal sites.

An important caveat in determining the pathophysiology and, thus, prognosis, is that the time since symptom onset must be considered. Even in cases of severe axonal injury, the femoral compound muscle action potential is likely to be normal in the hyperacute period because insufficient time has passed for Wallerian degeneration to occur. It typically takes 4 to 5 days for the compound muscle action potential amplitude to reach its nadir (15). Similarly, there are findings on needle EMG that can indicate axon loss, such as the presence of fibrillation potentials and positive sharp waves. However, these may not appear until 2 to 4 weeks after onset of injury and, therefore, are frequently not useful in gauging prognosis in the acute setting.

In comparison to other peripheral nerves, femoral neuropathy carries a relatively good prognosis, even when the lesion is due to axonal loss. This is, in part, due to a relatively short distance between common injury sites of the nerve and its target muscles (eg, iliacus and quadriceps), requiring regenerative sprouting to occur over a short distance. Demyelinating lesions may recover in 2 to 3 months by remyelination (02), whereas axonal lesions often require longer. The majority of femoral neuropathies after pelvic surgery may resolve with conservative management (08). Complete recovery is common in incomplete iatrogenic nerve injuries, particularly with regard to motor deficits, although residual sensory symptoms may remain (48).

Clinical vignette

A 69-year-old woman was admitted to the hospital because of acute chest pain. She underwent emergency cardiac catheterization and angioplasty through the right femoral artery. She was also placed on intravenous heparin. The next day, she noted severe right leg weakness with numbness in her thigh. She had moderate pain in her groin and anterior thigh. On the third day of admission, her neurologic examination revealed complete paralysis of the right quadriceps and iliopsoas. Thigh adductors and ankle dorsiflexion were normal. The right knee jerk was absent. There was a loss of touch and pain sensation over the anterior thigh and medial leg. Urgent CT scan of the pelvis revealed a large right retroperitoneal hematoma involving the iliacus muscle extending to the iliac crest. Surgical evacuation was done that day.

Her neurologic findings did not change. Nerve conduction studies administered on the tenth day revealed absent femoral compound muscle action potential and absent saphenous sensory nerve action potential on the right, with normal responses on the left. The sural sensory, tibial, and peroneal motor conduction studies were normal. Repeat nerve conduction studies on the third week were unchanged. Needle EMG revealed prominent fibrillation potentials and no voluntary motor units in the right quadriceps and iliacus. The right thigh adductors, tibialis anterior, and paraspinal muscles were normal.

Her recovery of neurologic functions was protracted. She required a knee brace (ankle-knee-foot orthosis) for ambulation. Six months later, the iliacus strength was Medical Research Council grade 4- of 5, and the quadriceps grade 3 of 5. She could not extend her knee actively beyond 160 degrees. Sensory loss was unchanged. EMG revealed nascent (reinnervation) motor unit potentials in the right iliopsoas and quadriceps. At 1.5 years, she did not require a brace, and her iliopsoas and quadriceps strengths were Medical Research Council grade 4 of 5. The right knee jerk was still absent. As a result of painful dysesthesia in the thigh and medial leg, she was placed on a tricyclic. At 3 years, she had an absent right knee jerk, mild weakness of the right iliopsoas and quadriceps (Medical Research Council grade 4+ of 5), and hyperesthesia of the medial leg.

Biological basis

Etiology and pathogenesis

Most femoral neuropathies are caused by direct trauma to, or compression of, the nerve either in the pelvis or beneath the inguinal ligament. Kim and colleagues reviewed 119 surgically treated femoral nerve injuries reported over the past 33 years and found that 52 of 89 (58%) traumatic lesions to the femoral nerve were iatrogenic in nature (36). Most frequently implicated were gynecological procedures, with others related to orthopedic operations, femoral nerve blocks, and femoral artery puncture. Common causes include the following.

Perioperative. In a case series cataloging all cases of femoral neuropathy at a single institution, 46% of cases occurred perioperatively. Of these, the authors estimate that 75% were due to stretch injury of the nerve, 11% were due to direct nerve compression, and 14% were due to lithotomy positioning. The types of procedures implicated include abdominal, pelvic, orthopedic, and gynecologic and are detailed below (64).

Femoral neuropathy during pelvic and abdominal surgery. Iatrogenic injury to the femoral nerve during pelvic surgery is well documented. In some series, the incidence of femoral neuropathy after abdominal hysterectomy and after renal transplantation has been reported to be up to 11% and 2%, respectively (41; 22; 67; 60). Various pelvic surgeries utilizing retractor blades, particularly self-retaining retractor blades, may carry specific risk (41; 32; 29; 10; 48). During these surgical procedures, the femoral nerve becomes compressed between the lateral blade of the retractor and the pelvic wall. One study reported that the incidence of femoral neuropathy after abdominal hysterectomies was significantly decreased when retractors were not used (22). A small case series highlighted the features of femoral neuropathy following kidney transplantation: self-retaining retractors were used in all cases, and patients had good motor recovery anywhere from 3 to 313 days following the onset of symptoms (37).

Misplaced sutures are also a reported cause of femoral nerve injury in urologic procedures (49). Pelvic internal fixation device placement can be associated with femoral nerve injury (24). Although not a specifically intrapelvic procedure, lateral retroperitoneal transpsoas approaches to lumbar spinal surgery have also been highlighted as a cause of femoral neuropathy. One series described that 6 of 230 patients undergoing this approach to lumbar interbody fusion developed femoral neuropathy – five of these were due to direct nerve injury, whereas one was due to hematoma. All patients had significant neurologic improvement within 1 year (01).

Femoral neuropathy due to hip replacements and other orthopedic procedures. Femoral neuropathy is a very rare complication of hip replacement surgery but may be more common with hip revision surgery and reconstructions. A large study of 27,004 primary total hip arthroplasty cases at a single institution found an incidence of 0.17% (47 cases) for motor nerve palsy of any nerve, but only three of these involved the femoral nerve (20). Peroneal and sciatic nerve palsies are far more common than femoral palsies (66; 20). A review of the literature, however, reports an incidence rate ranging from 0.1% to 2.4% following primary total hip arthroplasty (mean 0.8%) and 0.3% to 2.3% following revision total hip arthroplasty (mean 1.1%) (21).

Mononeuropathies after hip surgery are usually caused by stretch injury, but at times, may be due to encasement and damage by the cementing substance used. In one case, acetabular reinforcement rings loosened leading to intrapelvic granuloma formation and subsequent femoral nerve compression (06). Femoral neuropathy can also result from the placement of anterior acetabular retractors over the femoral nerve (79). Risk factors for the occurrence of any motor nerve palsy after hip arthroplasty may include developmental dysplasia of the hip, revision surgery, posttraumatic arthritis, surgical lengthening of a leg, cement-less femoral fixation, and a posterior surgical approach (20; 66). Neurologists should also be mindful of the surgical approach used when evaluating cases of suspected femoral mononeuropathy. The direct anterior approach to hip replacement is muscle-sparing and typically offers faster recovery and less postoperative pain. A series of 1756 patients undergoing a direct anterior approach total hip arthroplasty had a low femoral neuropathy incidence of 0.34% (57). In these cases, the authors speculated that the presence of large, anterior osteophytes may have contributed to the risk of femoral nerve injury due to difficulty placing an anterior retractor on the wall of the anterior acetabulum.

Although 77% of orthopedic surgery–associated femoral neuropathies are from hip procedures (total hip arthroplasty or revision), knee surgeries can also be complicated by femoral nerve injury, particularly total knee arthroplasty. There have also been demonstrated cases of femoral neuropathy from lateral knee release and tibial tubercle osteotomy (64).

Femoral neuropathy due to operative positioning. The femoral nerve may become compressed at the inguinal ligament during lithotomy positioning for various procedures, such as vaginal delivery, urological and rectal procedures, vaginal hysterectomy, and laparoscopy (77; 02; 26). In a single-center retrospective review, the femoral nerve was the most commonly injured nerve following gynecological surgery (23 total cases among 2449 reviewed surgeries) (16). Women of thin habitus and smokers are at higher risk of lithotomy-induced femoral neuropathy (69). Prolonged lithotomy positioning due to immobility after drug overdose has also been reported to cause femoral neuropathy (74). Femoral neuropathy can also occur after prolonged hyperlordotic positioning. A case has been reported in which femoral neuropathy occurred after a prolonged dental procedure (04). The patient was placed in a hyperlordotic position to improve surgical exposure and the field of view of the surgeon.

Local compression. The vast majority of nonperioperative femoral neuropathies are due to local compression. Nerve injury occurs most commonly in the setting of retroperitoneal hematomas, but masses, abscesses, vascular catheterization, and radiation are other established causes (64).

Femoral neuropathy due to iliacus or iliopsoas hematoma. Acute retroperitoneal hemorrhage within the iliacus muscle, or less commonly the psoas muscle, can lead to a compartment syndrome, which may result in femoral nerve injury (85; 59; 81). Hematoma formation may occur after trauma, but these often occur spontaneously, typically in patients receiving anticoagulation therapy. This is a relatively common etiology of femoral neuropathy, as hematomas are estimated to cause about 21% of femoral neuropathy cases (64).

Up to 10% of patients with hemophilia may experience iliopsoas bleeding, with estimates of the proportion of these patients developing femoral neuropathy ranging from 39.3% to 57% (07; 55). Rarely, anticoagulant therapy can lead to bilateral thigh hematomas within the iliopsoas muscle and result in bilateral femoral nerve palsy (25; 78; 42; 80). Low molecular weight heparin infusions may yield similar hematomas with compression (35). Less commonly, the hematoma extends into the retroperitoneal space, leading to a more extensive injury of the lumbar plexus or entire lumbosacral plexus (33).

Femoral neuropathy due to other local compression. Inguinal lymphadenopathies, femoral vessel catheterization or cannulation, and localized hematomas rarely can cause femoral neuropathy. ECMO may be particularly likely to injure the femoral nerve. In a systematic review, 7.9% of patients with femoral ECMO cannulation developed femoral nerve injury, thought to be compressive either from the large cannula or swelling or hematoma in the surrounding tissue (30). Rheumatoid arthritis has been described to cause iliopsoas bursitis and iliopectineal synovitis, with this inflammation leading to femoral nerve entrapment (44; 72; 73; 51). Large renal cysts, as can occur in polycystic kidney disease, may rarely affect femoral nerve function (84). Infection from taenia echinococcus leading to hydatid cyst formation in the psoas muscle with femoral nerve compression has also been reported (28), as have other retroperitoneal abscesses (64). Likewise, benign and malignant tumors can cause compression femoral neuropathies (64).

Radiation (46), and laceration, misplaced injection and tourniquet application (39; 64) are extremely rare causes of femoral nerve injury. Patellar dislocation has been rarely identified as a cause of femoral nerve injury more proximally at the level of the inguinal ligament (75).

Pseudoaneurysm formation can rarely complicate femoral artery access for endovascular procedures (23). Qureshi and colleagues reviewed 270 neuroendovascular procedures and found that four of their patients reported symptoms of femoral neuropathy that were typically transient and sensory predominant (61).

Inflammatory. Inflammatory femoral neuropathies comprise approximately 10% of all cases, with the other 90% being local compression/stretch/injury. As these cases are relatively rare, the relative proportion of etiologies hasn’t been clearly established. In a large case series of 10 patients with inflammatory femoral neuropathy, four were due to diabetic inflammatory mononeuropathy, two to focal CIDP, one to vasculitis, one was postviral, one was postsurgical, and one was idiopathic. These patients typically presented with subacute pain followed by weakness in the femoral nerve distribution, although one patient’s presentation was painless (64).

Table 1. Common Causes of Femoral Neuropathy

In order to understand the pathophysiology of femoral neuropathy, it is essential to review the anatomy of the femoral nerve, which is also called the anterior crural nerve. The nerve is formed when the posterior divisions of the ventral rami of L2, L3, and L4 spinal roots combine. Note that the anterior divisions of the same roots form the obturator nerve. Once formed, the femoral nerve immediately gives branches to the psoas muscle before it enters its substance. Then, covered by a tight iliac fascia, the femoral nerve passes between the psoas and iliacus muscles where it innervates the latter. After passing underneath the rigid inguinal ligament, the femoral nerve branches widen into its terminal motor branches (to the quadriceps and sartorius) and sensory branches (to the anterior thigh), including the saphenous sensory nerve, which innervates the skin over the medial half of the leg to the ankle. Experimental evidence shows that nerve injury occurs if the nerve is elongated by more than 6% of its original length; hence, females with shorter nerves are more prone to injuries with the use of retractors (21).

The primary pathological process in femoral neuropathy is either demyelinating or axonal. This determines the prognosis for recovery.

Epidemiology

Epidemiological studies exist on the incidence or prevalence of femoral neuropathies. Estimated frequencies of iatrogenic femoral nerve injury following certain procedures are as follows:

Prevention

Femoral nerve injury may be prevented during pelvic surgery by careful retraction against the iliopsoas and pelvic wall where the nerve is usually compressed. Avoiding the use of retractors cut the incidence of femoral nerve lesions after abdominal hysterectomy by more than 90% (22). If necessary, the use of handheld retractors should be encouraged, as a trend for more femoral lesions with the application of self-retractors exists (10). Additional preventive measures relating to renal artery transplantation include monitoring hemostasis parameters, short clamping time, and limiting iliac artery manipulation (76).

To prevent compression of the femoral nerve at the inguinal ligament during lithotomy, it is recommended that extreme hip flexion (not hyperflexed more than 80 or 90 degrees) and external rotation be avoided and prolonged lithotomy positioning discouraged (02; 09). Intraoperative neural monitoring for high-risk cases is one proposed method to assess nerve injury, but the ability of this method to prevent nerve injury remains unestablished.

Differential diagnosis

Confusing conditions

The most important alternative considerations in the differential diagnosis are lumbosacral radiculopathy and lumbosacral plexopathy. The hip flexors and quadriceps are innervated by the L2-L4 nerve roots, so radiculopathy at these levels or damage to the upper lumbar plexus could cause similar symptoms to a femoral neuropathy. Diabetic lumbosacral radiculoplexus neuropathy (also known as diabetic amyotrophy) is an especially relevant cause of lumbosacral plexopathy to consider as it commonly presents with severe thigh pain, weakness, and atrophy.

Three important clinical features are useful at the bedside:

(1) Weakness of thigh adductors, innervated by the obturator nerve, excludes a selective femoral lesion. When present, this suggests radiculopathy or plexopathy.

(2) A positive straight-leg test is nonspecific. It is common in lumbar radiculopathy; however, it may occur with lumbar plexopathy and femoral nerve lesion, particularly when due to retroperitoneal hematoma.

(3) In plexopathy or radiculopathy, weakness of ankle dorsiflexion is common and does not occur in femoral nerve lesions. Likewise, reduced or absent Achilles reflex does not occur with femoral neuropathy and should, therefore, raise consideration of plexopathy or multilevel radiculopathy.

Associated or underlying disorders

This article relates primarily to femoral mononeuropathy. Careful neurologic examination should be undertaken to exclude the presence of additional mononeuropathies elsewhere—mononeuropathy multiplex. Unless there is an obvious cause (eg, trauma, compression), this presentation should raise concern for vasculitic neuropathy. Hereditary neuropathy with liability to pressure palsies can also present with mononeuropathy multiplex.

Diagnostic workup

A thorough neurologic examination is critical for recognizing femoral neuropathy and distinguishing it from mimicking conditions. Knee extension weakness is expected, and hip flexion may be weak if the lesion is proximal to the inguinal ligament. Hip adduction, innervated by the obturator nerve, should be examined to help exclude mimics. Of note, severe pain may lead to limitation of movement separate from neurologic weakness and can be recognized by a “give-way” pattern on examination. Sensory examination may detect a deficit over the anteromedial thigh and medial leg. The patellar reflex is diminished or absent in femoral neuropathy.

Apart from urgent CT or MRI of the pelvis in patients with suspected retroperitoneal hemorrhage, EMG examination, including detailed nerve conduction studies and needle EMG, is frequently employed for diagnostic and prognostic purposes.

Table 2. EMG Diagnostic Strategy

Nerve conduction studies can be performed to examine the femoral nerve compound motor action potential recording over rectus femoris, with stimulation placed at the groin. A low-amplitude femoral compound muscle action potential is seen with axonal injury to the femoral nerve. The sensory nerve action potential of the saphenous nerve is useful for localization. This will be of low amplitude or absent in femoral neuropathy and (usually) lumbar plexopathies but is normal in radiculopathy. Both femoral compound muscle action potentials and saphenous sensory nerve action potentials can be technically difficult to obtain, even in normal individuals, so comparison with the asymptomatic side is always advised. Needle EMG is often most useful for localization to the femoral nerve and exclusion of mimics. Needle EMG abnormalities of the thigh adductors, for example, exclude femoral mononeuropathy and would suggest either plexopathy or radiculopathy. Likewise, fibrillation potentials and positive sharp waves seen in the lumbar paraspinal muscles are seen with involvement of the nerve root, thus, suggesting a lumbosacral radiculopathy.

MR neurography (MRN) for femoral neuropathy may be useful if electrophysiologic studies are equivocal or if an etiology for femoral neuropathy is not obvious from prior workup. Advantages of MRN are that benign and malignant peripheral nerve sheath tumors can be delineated and characterized further by MR imaging (13) and potentially lead to a site-directed biopsy to determine pathological diagnosis.

The utility of ultrasound in assessment of traumatic peripheral nerve lesions is increasing. High-resolution ultrasound can be used for anatomic understanding and surgical planning of femoral neuropathy. Zeidenberg and colleagues presented a case of femoral neuropathy in a patient developing pseudoaneurysm after undergoing a procedure for cardiac ablation via percutaneous femoral artery approach (86). Ultrasound was performed the same day to evaluate the patient and it showed a pseudoaneurysm dissecting and displacing the left femoral nerve. Surgery for vascular repair and neurolysis of the left femoral nerve with sural nerve grafting was performed.

Management

Most patients with femoral neuropathy are managed conservatively. A knee brace may be useful if there is significant knee extension weakness. Physical therapy may help the patient avoid falls and aid in restrengthening the affected muscles. A case report suggests early involvement of rehabilitation medicine (PM& R) may be helpful in patients with significant weakness (47). If pain is significant, neuropathic pain or anti-inflammatory medications may be trialed. A knee-ankle-foot orthosis is helpful for patients with severe weakness of the quadriceps so as to prevent falls. A case report indicates that percutaneous femoral nerve stimulation can ameliorate intractable causalgic pain (52). In a small case series, femoral nerve palsy due to traumatic or other causes may also benefit from femoral neurolysis (19), but this method is unproven. In cases where recovery was poor and weakness persists, nerve transfer has been tried to improve knee extension function (45; 58; 83).

Controversy exists regarding the indication and timing of surgical evacuation of hematoma if a compressive femoral nerve lesion is clinically apparent. In theory, surgical evacuation should occur as soon as possible, even before signs of severe femoral nerve injury and axonal degeneration occur (56; 18). Practically, limited data on the natural history of hematomas are available; therefore, decisions regarding surgical management are often made on a case-by-case basis. Good outcomes have been reported with both conservative and early surgical management. Therefore, factors for consideration include severity of femoral neuropathy, surgical risk, size of hematoma, hemodynamic stability, degree of axonal loss on electrophysiology (based on side-to-side comparison of femoral motor compound muscle action potential), and etiology, with very severe weakness and progression of weakness most frequently advocated for as indications for surgical drainage (59; 38).

Special considerations

Pregnancy

Femoral neuropathy has been estimated to complicate 2.8 of 100,000 vaginal deliveries using lithotomy positioning, based on the frequency of neurologic consultations (77). Twenty-five percent of these cases are bilateral. Prospective studies including more mild cases of femoral neuropathy suggest the incidence is closer to 1% (82). The femoral nerve may be injured via multiple mechanisms, typically via compression under the inguinal ligament. Maintenance of the lithotomy position through the prolonged second stage of labor is an important risk factor, but instrument-assisted delivery and excessive weight gain may also influence risk (54). Injuries to the lateral femoral cutaneous nerve (which is not a branch of the femoral nerve) are the most common postpartum neuropathy.

Anesthesia

Surgical positioning has been implicated in the cause of post-surgical femoral neuropathy, specifically lithotomy positioning and hyperlordotic positioning (77; 02; 26; 04). To prevent compression of the femoral nerve at the inguinal ligament during lithotomy, it is recommended that extreme hip flexion (not hyperflexed more than 80 or 90 degrees) and external rotation be avoided, and prolonged lithotomy positioning discouraged (02; 09).