First described by Winckel in 1878, postpartum femoral neuropathy after vaginal delivery is now rare [1-4]. Byrnes , in 1913, described an incidence of 1.7%-4.7%. Although the current incidence is not known, only a few isolated cases have been reported in recent years. The declining incidence of femoral neuropathy may reflect the decreased duration of labor and increased cesarean delivery with modern obstetric practice.
A healthy 27-yr-old primigravida, at 42 wk gestation, 150-cm, 70-kg, with an uncomplicated prenatal course, was admitted in labor. Labor was complicated by a prolonged active phase. At a cervical dilation of 8 cm, 100% effacement, and -1 station, an uneventful combined spinal/epidural anesthetic was administered using intrathecal sufentanil (10 micro gram) and isobaric bupivacaine (2.5 mg), followed by an epidural infusion of bupivacaine 0.125% with fentanyl 2 micro gram/mL at 10 mL/h when the cervix was 10 cm dilated. The second stage of labor continued for 3.5 h. An assisted vacuum extraction over a midline episiotomy delivered a healthy, 4200-g baby boy with Apgar scores of 8 and 9 at 1 and 5 min.
The postpartum course was complicated by bilateral weakness and numbness in both knees, with a tendency to "buckle" (not able to stand straight up) and inability to support weight. Neurologic examination showed an absent left knee jerk and an attenuated right knee jerk. All other deep tendon reflexes were normal. There was decreased sensation to pinprick and cold in an oval pattern centered at the knees and extending 10 cm above and below. No other sensory deficit was noted. Mild weakness of both quadriceps was found. The iliopsoas, thigh adductors, and all other muscle groups were normal bilaterally. No bowel or bladder dysfunction was reported. The remaining neurologic examination was normal. A neurology consultation was obtained.
Because of the bilateral nature of the deficit, a lumbosacral spine magnetic resonance image was performed to rule out an epidural hematoma. The neurologist confirmed the findings consistent with bilateral femoral neuropathy. Nerve conduction studies were considered inconclusive at this stage and therefore not performed.
The patient was discharged on Day 4 postpartum with home physical therapy. Full recovery required 10 wk.
In the presence of bilateral neurologic deficit, especially when an epidural or spinal anesthetic has been used, one should rule out the rare etiologies directly related to the neuraxial block, some of which may require immediate surgical intervention for full recovery. These include spinal cord ischemia, direct trauma to a spinal nerve or the spinal cord, chemical contamination of the local anesthetic solution, toxicity of the local anesthetic, or space-occupying lesion (such as a hematoma or abscess). Causes unrelated to the neuraxial block include preexisting neurologic disease, neurologic injury due to malpositioning, and overstretching of the limbs or retractors used during operative procedures. After proper history, the patient must be thoroughly examined and investigated to establish the exact cause of the neurologic deficit. A neurology consultation is useful to confirm the correct diagnosis for medicolegal implications.
Postpartum femoral neuropathy is now a rare occurrence. Vargo et al.  reported an incidence of postpartum peripheral nerve injury of 1/13,000 deliveries and recounted the incidence of postpartum femoral neuropathy as reported by several authors such as Ernst in 1900 (30/800 deliveries), Meyer in 1901 (17/1000 deliveries), and Hauch in 1906 (32/680 deliveries) and recounted the incidence of postpartum "foot drop" as reported by Beattie in 1933 (3/8000 deliveries), Tillman in 1935 (9/18,000 deliveries), and Cole in 1946 (7/45,000 deliveries). The decrease in incidence of postpartum femoral neuropathy is coincidental with the increase in cesarean deliveries and the shorter duration of the second stage of labor.
Postpartum femoral neuropathies have been described primarily in primigravidas, usually after a difficult delivery (cephalopelvic disproportion or dystocia). Approximately 25% of cases are bilateral. They are usually self-limited, with spontaneous resolution within weeks to months [2,3,5-8].
The femoral nerve originates from the posterior divisions of L2-4 spinal nerves. It travels within the psoas muscle where it gives branches to innervate the latter. It emerges from the lower third of the lateral border of the psoas, approximately 4 cm above the inguinal ligament. It courses in the groove between the psoas muscle anteriorly and the iliacus muscle posteriorly. It leaves the pelvis, passes beneath the inguinal ligament, and gives sensory branches to the anterior thigh and medial leg, and motor branches to the quadriceps and sartorius [9-12].
There are two postulated mechanisms of postpartum femoral neuropathy. The most commonly recognized is pressure-induced ischemia. With vaginal delivery, hyperflexion, abduction, and external rotation of the thighs into the exaggerated lithotomy posture forces the femoral nerve against the inguinal ligament and may cause nerve damage [9,10,12]. With this mechanism of femoral nerve compression, the iliopsoas should be normal. If the iliopsoas is involved, the most likely mechanism is stretch-induced ischemia at the level of the iliopsoas groove where the nerve is covered by a tight iliac fascia and can be compressed. A low-lying fetal head may compress and damage the femoral nerve . Femoral neuropathy has also been associated with diabetes mellitus (especially in the presence of macrosomic babies causing cephalopelvic disproportion), hemorrhagic disorders, anticoagulant therapy, abdominal or pelvic surgery, appendiceal abscess, trauma, iliac artery aneurysm, inguinal adenopathy, self-retaining retractors during surgery, and cesarean section .
When femoral neuropathy occurs, weakness of the quadriceps (knee extension) or psoas (hip flexion) can result in difficulty with rising from a chair or climbing stairs, and can make the knee buckle. Knee jerk is typically depressed or absent. Sensory deficit over the anterior medial thigh is minimal. It may be difficult to differentiate this clinical presentation from lumbosacral plexopathy (unilateral foot drop, adductor or quadriceps weakness, and sensory deficit over the anteromedial aspect of the thigh and leg).
Diagnosis of postpartum femoral neuropathy is mainly by history and physical examination. Nerve conduction and electromyographic studies remain normal for 1 to 3 wk after injury, and therefore are not helpful in the initial diagnosis .
In the patient presented here, the most likely mechanism of injury was femoral nerve compression at the inguinal ligament (with absence of iliopsoas involvement). The predisposing factor was probably the long second stage of labor.
The prognosis is excellent, with spontaneous resolution in 1 to 6 mo. However, the patient may require physical therapy, bracing, and use of assistive devices.
We wish to thank Lisa Bellner, MD, from Rehabilitation Medicine, New Haven, CT, for her advice on the manuscript.
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