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Bilateral Sciatic Neuropathies as a Complication of Positioning During Neuraxial Anesthesia for Cesarean Delivery: A Case Report

Reel, Bradley A. MD*; Odedokun, Tolulope A. MD; Simmons, Daniel B. MD; Hong, Linda MD*

doi: 10.1213/XAA.0000000000001026
Case Reports

Neurologic complications following neuraxial anesthesia for cesarean delivery are rare. We present a 33-year-old parturient who developed prolonged lower extremity weakness following a single-shot subarachnoid block for cesarean delivery. After neurologic evaluation, she was diagnosed with bilateral sciatic neuropathies due to prolonged positioning for the anesthetic. We review the incidence of nerve injury associated with neuraxial anesthesia and risk factors for developing peripheral nerve injury in this context. We offer a solution to prevent this complication from occurring.

From the Departments of *Anesthesia

Gynecology and Obstetrics

Neurology, Brooke Army Medical Center, San Antonio, Texas.

Accepted for publication March 18, 2019.

Funding: None.

The authors declare no conflicts of interest.

The views expressed are those of the authors and do not reflect the official views or policy of the Department of Defense or its components.

Address correspondence to Bradley A. Reel, MD, Department of Anesthesia, Brooke Army Medical Center, 3551 Roger Brooke Dr, San Antonio, TX 78234. Address e-mail to

Sciatic nerve injuries make up only 1% of perioperative nerve injuries. Bilateral sciatic nerve injuries in the postoperative setting are rare.1,2 We present a case of bilateral compressive sciatic neuropathies related to patient positioning during a subarachnoid block for cesarean delivery. There are no prior reports of this complication in the literature. A written Health Insurance Portability and Accountability Act authorization to use/disclose existing protected health information was obtained from the patient.

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A 33-year-old woman with class B diabetes mellitus and obesity (body mass index, 43) presented for an elective repeat cesarean delivery and bilateral tubal ligation. She had no baseline neurologic deficits. Her anesthetic plan was a combined spinal-epidural anesthetic. Epidural placement was difficult, and multiple attempts were unsuccessful. Ultimately, the plan was changed to a single-injection subarachnoid block. Bupivacaine (1.6 mL of 0.75%) and fentanyl (25 mg) were injected without complication. Total time sitting upright for neuraxial anesthesia was approximately 45 minutes. Her feet were not supported during this time. However, she was allowed to position herself for comfort between attempts. She denied paresthesia or weakness while sitting for the procedure. She received no sedatives or analgesics during the neuraxial procedure. The remainder of the surgery was uncomplicated and without hypotension or excessive blood loss. Her positioning during the cesarean delivery was supine with a 1-L normal saline bag placed under the right hip for lateral uterine displacement. She was not placed in a lithotomy position at any time during her hospital course. Total surgical time was 58 minutes, with supine positioning just over 1 hour.

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On postoperative day (POD) 1, the patient noted weakness of the lower legs and numbness on the lateral aspect of the legs below the knee. These symptoms were exacerbated by sitting upright with her legs hanging over the edge of a chair. Neurologic examination on POD 1 demonstrated 1 of 5 strength in ankle dorsiflexion bilaterally and 2 of 5 strength in both ankle plantar flexion and ankle eversion bilaterally. Knee flexion was weak on the left. The Achilles reflexes were absent bilaterally. She had decreased light touch below the knee (left more than right), and pinprick in this region was dysesthetic. She denied back pain and fever. Her vital signs and laboratory values were unremarkable. When the weakness did not improve by POD 2, further evaluation was pursued.

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Magnetic resonance imaging (MRI) of the lumbar spine obtained on POD 2 was unremarkable. The patient experienced mild improvement in strength and sensation during her hospitalization but continued to have disabling weakness in her left lower extremity. Of note, her symptoms were exacerbated when placed in chair or a seated position in the bed. She was seen by inpatient physical therapy (PT) on POD 3; they recommended a temporary wheelchair, ankle-foot orthosis boots due to foot drop, and continued PT. She was discharged on POD 4 with home PT. She was contacted numerous times and reported continued mild improvement but not resolution of her symptoms. She continued to report exacerbation of her symptoms when her legs were in a dependent position. On POD 25, she was seen in the obstetrics clinic. By this time, she was able to ambulate for a short distance without assistance. Her neurologic examination showed 5 of 5 strength in proximal muscle groups in both lower extremities, 4 of 5 strength with dorsiflexion and plantar flexion on the right, 3 of 5 strength with plantar flexion on left, and 2 of 5 strength with dorsiflexion on left. She was subsequently scheduled for nerve conduction studies (NCSs) and electromyography (EMG) due to persistent symptoms. Examination on POD 40, coinciding with NCS and EMG, demonstrated 2 of 5 strength on left ankle dorsiflexion and toe extension; 4 of 5 left ankle plantar flexion, toe flexion, and knee flexion; and 4 of 5 right ankle dorsiflexion, toe extension, and knee flexion. NCS and EMG confirmed the diagnosis of bilateral sciatic neuropathies, left worse than right. Notable findings included an absent left sural sensory response and denervation potentials in the left gastrocnemius, tibialis anterior, and biceps femoris, while the tensor fascia lata, vastus medialis, and lumbar paraspinals were normal. By POD 56, her strength had normalized bilaterally and the numbness had resolved in the right leg. She continued to have persistent paresthesias in the left lower leg, but this eventually resolved as well.

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Nerve injury occurs due to direct pressure on, stretching of, or vascular injury to neural tissue. Prolonged labor or hypotension may increase the risk of nerve injury. In the parturient, compression of the lumbosacral trunk may occur as the fetus descends during labor and the head crosses the ala of the sacrum. Neurologic injuries related to fetal descent are more common than those related to anesthetic procedures, with serious complications occurring at a rate of 2 to 5 per 10,000 in the laboring patient without a neuraxial block.3 In contrast, permanent injury from spinal hematoma or epidural abscess after neuraxial block occurs at a rate of approximately 1 of 150,000.3 Most neurologic injuries associated with childbirth or neuraxial block are transient and resolve within 1 year. The most common mechanism of nerve injury during neuraxial anesthesia is direct trauma.4 Other causes of nerve injury in the parturient include incorrect leg positioning in stirrups, difficult forceps applications during an operative vaginal delivery, or labor and delivery with abnormal fetal presentation. The peroneal, saphenous, and lateral femoral cutaneous nerves can be injured in an improperly placed lithotomy position. Femoral and obturator neuropathies have also been reported after prolonged labor.5 Compressive nerve injury associated with upright positioning during neuraxial anesthesia, as occurred in this case, has not been previously reported.

Sciatic neuropathy in the context of childbirth is uncommon. The sciatic nerve is derived from the lumbosacral trunk (L4-L5 roots) and the ventral rami of the sacral plexus (primarily S1-S3 roots). It exits the pelvis through the greater sciatic foramen and descends to supply motor fibers to the hamstring muscles in the thigh and all muscles below the knee; it also supplies the sensation to the lateral lower leg and the dorsal and plantar surfaces of the foot. Injury to the sciatic nerve most frequently occurs in the trauma patient and as a complication of hip surgery.6

Silva et al7 reported 2 cases of right-sided postpartum sciatic neuropathy. One patient received epidural analgesia for vaginal delivery but ultimately required cesarean delivery for failure of labor to progress. The other had epidural anesthesia for an elective cesarean delivery. The mechanisms were presumed to be prolonged sitting in the context of a dense block during labor for the patient who attempted vaginal delivery and prolonged left uterine displacement positioning with injury to the right sciatic nerve caused by the device used to maintain the positioning in the other patient. The latter case was possibly complicated by the presence of hypotension.7 Subsequently, 3 cases of left-sided postpartum sciatic neuropathies were reported that were attributed to intraoperative positioning during cesarean delivery. In each case, the patient was placed in the left lateral tilt position with a wedge under the right hip. The resulting pressure on the left buttock was thought to cause focal compression of the sciatic nerve; none of these cases were associated with hypotension.2,8,9

Our patient had bilateral postpartum sciatic neuropathies, of which there are no prior reports in the literature. As in previous cases, our patient was positioned with a left lateral tilt intraoperatively. We cannot exclude the possibility that our patient’s sciatic neuropathies were due to intraoperative positioning, especially because she did not have symptoms during the neuraxial procedure. However, we suspect that the patient’s injury likely occurred while she was seated upright with her legs hanging off the edge of the table during placement of the neuraxial block. This mechanism explains the bilateral involvement and is further supported by the patient’s immediate recurrence or exacerbation of symptoms when placed in a sitting position. The lack of symptoms during the neuraxial procedure does not degrade the argument that this is the culprit for her injury because paresthesias are not a sensitive indicator for nerve injury.10 Additional evidence supporting this mechanism includes a negative MRI, absence of labor before cesarean delivery, no lithotomy positioning, no clear stretch injury, no hypotension, and no excessive blood loss. The impact of gestational diabetes on her risk for nerve injury is uncertain. There is minimal literature discussing gestational diabetes as a risk factor for peripartum nerve injury. Also, her diabetes mellitus was well controlled. This complication may have been prevented if her feet had supported with a stool during the procedure. Although the patient was able to make herself comfortable between attempts, she was limited in her positioning due to the need to maintain sterility. This case reinforces the importance of careful positioning during placement of neuraxial anesthesia as well as the need for early involvement of neurology consultants in obstetric patients with peripartum neurologic symptoms.

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Name: Bradley A. Reel, MD.

Contribution: This author helped care for the patient, and prepare, write, and edit the manuscript.

Name: Tolulope A. Odedokun, MD.

Contribution: This author helped care for the patient, and prepare, write, and edit the manuscript.

Name: Daniel B. Simmons, MD.

Contribution: This author helped care for the patient, and prepare, write, and edit the manuscript.

Name: Linda Hong, MD.

Contribution: This author helped care for the patient, and prepare, write, and edit the manuscript.

This manuscript was handled by: BobbieJean Sweitzer, MD, FACP.

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10. Barrington MJ, Brull R, Reina MA, Hadzic A; New York School of Regional Anesthesia Website. Complications and prevention of neurologic injury with peripheral nerve blocks. Accessed February 3, 2019.
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