Postpartum Neuropathy

Abstract

Neurologic complications in the obstetric population are rare and mostare intrinsic obstetric palsies. Intrinsic obstetric palsies have long been recognized. However, with the widespread introduction ofneuraxial anesthetic and analgesic techniques, there is an increased concern that neurologic complications are due to the anesthetic procedure. Fortunately, the intrinsic obstetric palsies are transient. However, serious neurologic complications due to anesthesia, albeit rare, can occur. The present manuscript reviews the literature on intrinsic obstetric palsies and neurologic complications of anesthesia in pregnancy. Intrinsic obstetric palsies. The incidence of these palsies varies, according to study methodology, from 0.6 to almost 100 per 10.000 deliveries (1). The best two studies, with individual patient follow up, report the highest incidence (2,3). Neuraxial anesthetic techniques might indirectly influence the incidence because patients are less mobile, feel less prodromes and have longer second stages. Dar et al. reported 23 women with a palsy out of 3991 parturients (incidence 5.8/1000) (2). However, they also recruited 8 asymptomatic women which had a palsy, always after vaginal delivery. Wong et al. prospectively evaluated 6048 women who had delivered (3). Fifty six women (0.92 %) had a confirmed obstetric palsy. Especially nulliparous women and those with a prolonged second stage of labor were at increased risk. Most intrinsic palsies are lateral femoral cutaneous nerve and femoral nerve injuries. All other neve lesions are less common (3). The mechanism of injury is secondary to compression, traction and ischemia during the process of childbirth. During labor and delivery, the fetal head may compress the lumbosacral trunk, or compress blood vessels supplying the trunk, conus medullaris or cauda equina. Hematoma may cause nerve compression. Iat-rogenic compression (e.g., by forceps) or traction of nerves (e.g., the lateral femoral cutaneous nerve at the inguinal ligament or secondary to traction during abdominal delivery with retractors) may occur. Positions assumed during labor and delivery may contribute to nerve injury. For example, there is increased traction on the femoral nerve when the thighs are flexed and externally rotated, a common pushing position. Common peroneal neuropathy has been attributed to pressure from the parturient's hand as she supported her flexed thighs and legs and to squatting during childbirth or due to compression by leg supports. Fortunately, symptoms usually resolve spontaneously. Wong et al. noted that it may take up to a year, but all patients had full recovery. However in most patients within 6 months symptoms have resolved (3). The median recovery duration was 6-8 weeks. Evaluation of postpartum complaints of lower extremity numbness, weakness, and pain should occur as soon as possible in order to eliminate rare life-or limb threatening pathophysiology as the cause of symptoms. Evaluation in the postpartum period may be complicated by common obstetric co-morbidities. Fever, urinary retention and incontinence, and anal sphincter dysfunction are common after childbirth. Differential diagnosis of central versus peripheral nerve root injury is aided by examination of the paraspinous muscles. The paraspinous muscles and skin over the lower back are innervated by nerves of the posterior rami. Injury at the nerve root level affects both the posterior and anterior rami of the nerve root. Therefore, intact paraspinous muscles and sensation of the lower back suggests a more distal injury. Central lesions are more often accompanied by back pain. Immediate magnetic resonance imaging is the current gold standard to rule out central lesions. Electromyography (EMG) may aid in determining the site of injury and degree of axonal loss, and thus the prognosis for recovery,48 however, an EMG only measures large nerve fiber changes and may take as long as 3 weeks after injury to show changes. There is little benefit to an EMG in women with stable peripheral neuropathies other than determining prognosis. Early EMG changes indicate pre-existing injury. Direct neurologic complications of neuraxial anesthesia techniques. Fortunately serious neurologic complications following neuraxial anesthesia are rare. The true incidence is however difficult to ascertain. In the obstetric population several studies have been trying to estimate the true incidence. Auroy et al. in France reported a prospective evaluation of 103,750 regional anesthetics performed ofwhich almost 71,000 were spinal or epidural procedures (4). Thirty neurologic complications were reported in these central neuraxial blocks, but most were in non-obstetric patients. In the largest group, 35,000 obstetric patients only 2 peripheral nerve injuries were reported. Moen et al. reported neurological complications over a 10 year period in Sweden (5). Almost 1.800.000 million central neuraxial blocks were performed, 200.000 were in obstetric patients. The risk for developing a neurologic injury is 1 in 25.000 for spinal anesthesia and 1 in 3600 for epidural anesthesia. However in obstetric patients this is only 1 in 25000. Spinal hematoma occurred in 1 in 200000 obstetric patients, while it occurred much more frequent in non-obstetric patients. Ruppen et al. reported on a meta-analysis of trials looking at the incidence of complications following epidural anesthesia in obstetric patients (6). The incidence of epidural hematoma was 1 in 168.000, epidural infection 1 in 145.000 and persistent neurologic injury 1 in 237.000. Conus damage due to spinal needle puncture can occur if the spinal needle is inserted at a level higher the L3 (7). In a small group of patients the conus ends lower then the L1 vertebral body. Moreover, anesthetists are notoriously bad in identifying the correct interspace using only anatomical landmarks. Conclusions: Neurologic deficit postpartum is usually an instrinsic obstetric palsy. However, serious anesthesia related problems can occur. So prompt evaluation is necessary. Conus damage must be prevented using the correct interspace and stopping injection whenever paresthesia or pain occur.