Abstract
Postpartum neuropathies are common, including femoral neuropathy, peroneal neuropathy, lumbosacral trunk plexopathy, and lateral femoral cutaneous neuropathy. Sciatic mononeuropathy in the peripartum period is rare. Postpartum sciatic neuropathy (PSN) in the setting of cesarean section has been reported before. We present a case series of 2 sciatic mononeuropathies after vaginal delivery.
Case 1 is a 25-year-old woman who presented with a left foot drop after normal vaginal delivery after being in labor for 3 hours. Case 2 is a 24-year-old woman who presented with a right foot drop after normal vaginal delivery and being in labor for 31 hours. Both cases noted foot drops in the immediate postpartum period. Neurologic examinations revealed flail foot, 4/5 hamstring muscle strength on MRC scale and intact hip abduction. They had paresthesia on the posterolateral aspect of the leg, dorsal and plantar aspect of the foot with absent ankle reflex. MRI did not show evidence of spinal cord, nerve root or plexus involvement. Electrodiagnostic studies revealed evidence of sciatic mononeuropathy proximal to the short head of biceps femoris. They were discharged home with an ankle brace and therapy. At 3 months follow up, they had complete resolution of weakness.
There have been a few reported cases of PSN secondary to cesarean section. Sciatic involvement after vaginal delivery is extremely rare. We report 2 cases of PSN after vaginal delivery to highlight that sciatic mononeuropathy can occur not only after cesarean section, but also after uncomplicated vaginal delivery and should raise awareness of this risk to clinicians.
Keywords: mononeuropathies, neuromuscular diseases, nerve compression syndromes, neuromuscular diseases, radiculopathy, neuromuscular diseases, neuromuscular disease, clinical specialty, EMG/NCV, techniques
Introduction
Postpartum neuropathies of the lower extremities have long been recognized as a potential complication that can occur in the setting of multiple perinatal risk factors. Some of these risk factors include: fetal macrosomia, short maternal stature, nulliparity, instrumental delivery, neuraxial anesthesia, prolonged second stage of labor, blood pressure fluctuations, diabetes, pre-existing neuropathies and prolonged positioning. Although any nerve is potentially at a risk for injury, some of the most common lower extremity neuropathies associated with childbirth include: lateral femoral cutaneous nerve, femoral nerve, peroneal (fibular) nerve, lumbosacral plexus, and obturator nerve. Sciatic nerve injuries can occur postpartum but are extremely rare. The sciatic nerve is unique where the 2 nerves, the peroneal and tibial nerves are encased together. In addition to ankle dorsiflexor and plantar flexor weakness, these patients develop weakness of ankle invertors and evertors along with hamstrings weakness. Sensory loss involves the lateral calf and both dorsal and plantar aspects of the foot. Further, the Achilles reflex can be affected. There have been a few cases of postpartum sciatic neuropathy (PSN) secondary to a caesarian section that have been reported before.1,2 The involvement of sciatic nerve in the setting of a vaginal delivery is extremely rare. 3 We report 2 cases of PSN secondary to uncomplicated vaginal delivery.
Cases
Case 1 is a 25-year-old multiparous parturient who developed a left foot drop following 3 hours of labor and a normal vaginal delivery. She received epidural anesthesia and noted foot drops in the immediate postpartum period following delivery of a 7.3 pounds healthy female neonate. Neurologic examination revealed a flail foot, 4/5 hamstring strength on MRC scale and intact hip abduction on the left side. This was associated with paresthesias on the posterolateral aspect of the leg, dorsal and plantar aspect of the foot with absent ankle reflex on left side. MRI of lumbar spine did not show evidence of spinal cord, nerve root or plexus or sciatic nerve involvement or enhancement. The patient was discharged home with supportive care including ankle brace and physical therapy. Electrodiagnostic studies after a month, revealed evidence of a left sciatic mononeuropathy proximal to the short head of biceps femoris. The lumbar paraspinals, hip flexors, extensors, abductors, adductors and internal rotators were found to be normal on needle examination (Tables 1, 2 and 3). At 3 months follow up, she had complete resolution of weakness and paresthesias. Case 2 is a 24-year-old primiparous parturient who developed a right foot drop following 31 hours of labor and a normal vaginal delivery that required vacuum device to assist with delivery. She received epidural anesthesia and noted foot drops in the immediate postpartum period following delivery of a 7.8 pounds healthy male neonate. Neurologic examination revealed a flail foot, 4/5 hamstring strength on MRC scale and intact hip abduction on the right side. This was associated with paresthesias on the posterolateral aspect of the leg, dorsal and plantar aspect of the foot with absent ankle reflex on right side. MRI lumbar spine did not show evidence of spinal cord, nerve root or plexus or sciatic nerve involvement or enhancement. She was discharged home with supportive care including ankle brace and physical therapy. Electrodiagnostic studies after a month, revealed evidence of a right sciatic mononeuropathy proximal to the short head of biceps femoris. The lumbar paraspinals, hip flexors, extensors, abductors, adductors and internal rotators were found to be normal on needle examination (Tables 1, 2 and 4). At 3 months follow up, she had residual paresthesias involving the dorsum of the foot. Both cases were previously healthy without evidence of short stature, gestational diabetes, or peripheral nerve entrapments. There was no evidence of blood pressure fluctuations during labor and delivery. Both cases endorsed frequent repositioning during labor.
Table 1.
MNC: Motor Nerve Conduction, L: Left, R: Right, ms: Milliseconds, mV: Millivolts, m/s: Meters Per Seconds, EDB: Extensor Digitorum Brevis, AH: Abductor Hallucis, BOLD: Affected Side.
MNC | CASE 1 | CASE 2 | |||||
---|---|---|---|---|---|---|---|
Nerve / Sites | Muscle | Latency ms |
Amplitude mV |
Velocity m/s |
Latency ms |
Amplitude mV |
Velocity m/s |
L Peroneal | |||||||
Ankle | EDB | 3.70 | 2.5 | 4.43 | 3.2 | ||
Fibular head | EDB | 10.57 | 2.2 | 42 | 10.05 | 3.1 | 50 |
Popliteal fossa | EDB | 12.03 | 2.2 | 55 | 11.46 | 3.5 | 57 |
R Peroneal | |||||||
Ankle | EDB | 3.23 | 7.7 | 5.05 | 3.9 | ||
Fibular head | EDB | 9.22 | 7.1 | 48 | 11.41 | 4.1 | 42 |
Popliteal fossa | EDB | 10.94 | 7.9 | 47 | 14.06 | 4.1 | 42 |
L Tibial | |||||||
Ankle | AH | 3.33 | 8.6 | 3.49 | 13.9 | ||
Popliteal fossa | AH | 11.88 | 5.9 | 41 | 11.77 | 10.8 | 47 |
R Tibial | |||||||
Ankle | AH | 3.59 | 12.1 | 4.11 | 10.4 | ||
Popliteal fossa | AH | 10.89 | 8.0 | 43 | 13.18 | 9.2 | 43 |
Table 2.
SNC: Sensory Nerve Conduction, L: Left, R: Right, ms: Milliseconds, µV: Microvolts, m/s: Meters Per Seconds, NR: Not Recordable, BOLD: Affected Side.
SNC | CASE 1 | CASE 2 | |||||||
---|---|---|---|---|---|---|---|---|---|
Nerve / Sites | Rec. Site | Onset Lat ms |
Peak Lat ms |
NP Amp µV |
Velocity m/s |
Onset Lat ms |
Peak Lat ms |
NP Amp µV |
Velocity m/s |
L Sural | |||||||||
Calf | Ankle | 2.29 | 3.02 | 8.9 | 61 | 2.40 | 3.23 | 15.0 | 58 |
R Sural | |||||||||
Calf | Ankle | 2.60 | 3.33 | 21.3 | 54 | 3.13 | 3.91 | 10.0 | 45 |
L Superficial peroneal | |||||||||
Lateral leg | Ankle | NR | NR | NR | NR | 1.88 | 2.50 | 20.5 | 53 |
R Superficial peroneal | |||||||||
Lateral leg | Ankle | 1.88 | 2.40 | 17.5 | 75 | 2.14 | 2.92 | 32.0 | 47 |
Table 3.
EMG: Electromyography, L: Left, IA: Insertional Activity, Fib: Fibrillation Potentials, PSW: Positive Sharp Waves, Fasc: Fasciculation Potentials, MUAP: Motor Unit Action Potential, Amp: Amplitude, Dur: Duration, PPP: Polyphasic Potentials, N: Normal.
EMG Summary Table | CASE 1 | |||||||
---|---|---|---|---|---|---|---|---|
Spontaneous | MUAP | Recruitment | ||||||
Muscle | IA | Fib | PSW | Fasc | Amp | Dur. | PPP | Pattern |
L. Tibialis anterior | 2+ | 2+ | 1+ | None | N | N | 2+ | Reduced |
L. Gastrocnemius (Medial head) | 2+ | 2+ | 2+ | None | N | N | 1+ | Reduced |
L. Peroneus longus | 2+ | 2+ | 2+ | None | N | N | 2+ | Reduced |
L. Tibialis posterior | 2+ | 2+ | 1+ | None | N | N | None | Reduced |
L. Vastus medialis | N | None | None | None | N | N | None | N |
L. Biceps femoris (short head) | 2+ | 2+ | 2+ | None | N | N | 2+ | Reduced |
L. Biceps femoris (long head) | N | None | None | None | N | N | None | N |
L. Gluteus medius | N | None | None | None | N | N | None | N |
L. Gluteus maximus | N | None | None | None | N | N | None | N |
L. L5 paraspinal | N | None | None | None | N | N | None | N |
Table 4.
EMG: Electromyography, R: Right, IA: Insertional Activity, Fib: Fibrillation Potentials, PSW: Positive Sharp Waves, Fasc: Fasciculation Potentials, MUAP: Motor Unit Action Potential, Amp: Amplitude, Dur: Duration, PPP: Polyphasic Potentials, N: Normal.
EMG Summary Table | CASE 2 | |||||||
---|---|---|---|---|---|---|---|---|
Spontaneous | MUAP | Recruitment | ||||||
Muscle | IA | Fib | PSW | Fasc | Amp | Dur. | PPP | Pattern |
R. Tibialis anterior | 2+ | 2+ | None | None | N | N | None | Reduced |
R. Gastrocnemius (Medial head) | 2+ | None | 2+ | None | N | N | None | Reduced |
R. Peroneus longus | 2+ | 2+ | 2+ | None | N | N | None | Reduced |
R. Tibialis posterior | 2+ | 2+ | 1+ | None | N | N | None | Reduced |
R. Vastus medialis | N | None | None | None | N | N | None | N |
R. Biceps femoris (short head) | 2+ | 2+ | 2+ | None | N | N | None | Severely reduced |
R. Biceps femoris (long head) | N | None | None | None | N | N | None | N |
R. Gluteus medius | N | None | None | None | N | N | None | N |
R. Gluteus maximus | N | None | None | None | N | N | None | N |
R. L5 paraspinal | N | None | None | None | N | N | None | N |
Discussion
Postpartum obstetric neuropathies occur in approximately 1% of deliveries. 4 In contrast, complications related to neuraxial anesthesia are extremely rare. However, neuraxial anesthesia in addition to perinatal risk factors, increases the risk of an obstetric neuropathy due to the lack of sensation in lower extremities.4,5 Absence of sensation can prevent women from sensing alterations in their limbs resulting in lesser likelihood of adjusting their position. Neuraxial anesthesia also prolongs the second stage of labor thereby increasing the risk of nerve injury. A study evaluating lower extremity neuropathy associated with lithotomy positions in surgical patients found that the frequency of neuropathy increased just after 2 hours of lithotomy positioning. 6 Women with neuraxial anesthesia change positions less often during labor and push more frequently while in the lithotomy position predisposing them to lower extremity neuropathy. 7
Although several types of neuropathies of the lower extremity can occur postpartum, the occurrence of PSN is relatively rare. 8 One retrospective review found the incidence of PSN to be 2 in 6046 births. 4 PSNs have been frequently reported in less developed countries where IM injections in the gluteal region are used for pain control during labor and delivery. 9 So far, a handful of cases of PSN have been reported after caesarean section;1,2,10 however, a case of PSN after an uncomplicated vaginal delivery has not been reported to date. We report a case series of PSN after uncomplicated vaginal delivery in the absence of perinatal risk factors. Case 1 was a multiparous woman without evidence of gestational diabetes which is in contrast to previously reported PSN after vaginal delivery which was associated with several perinatal risk factors. 3 In case 2, the patient was in a supine lithotomy position for prolonged duration during delivery, without any dystocia. Hence, the mechanism of sciatic nerve injury could be the unrecognized prolonged nerve entrapment due to the inappropriate lithotomy position under a sensory block. Other possible theories for this phenomenon include lower plexus involvement such as entrapment at the sciatic notch or the pyriformis muscle or at the ischium. 11 Prolonged compression can lead to nerve ischemia causing axonal damage in addition to compressive demyelination. Interrogating the role of blood pressure, studies on animal models demonstrated that generalized hypoperfusion states can lead to segmental decreased microcirculation in nerve segments (“watershed zone”) causing maximal nerve damage. 12 In summary, this case highlights that PSN can occur not only after cesarean section delivery, but also after an uncomplicated vaginal delivery and should raise awareness of this risk to clinicians.
Sciatic nerve injury can cause a wide array of symptoms, from minor sensory changes to disabling paralysis of the muscles of the ankle and foot. When assessing a woman with postpartum leg weakness, a careful neurologic examination is crucial and should include a detailed history and examination of muscle strength, reflexes, and the distribution of sensory loss. The presence of hamstring weakness in addition to foot drop should alert the clinicians regarding a possibility of sciatic neuropathy. On the contrary, cauda equina or epidural trauma is frequently associated with bowel, and bladder abnormalities. Lumbosacral radiculopathies are typically characterized by radicular pain and lumbosacral plexopathies involve hip abductors, and hip extensors in addition to foot drop. Diagnosis of peripheral nerve injuries can often be made at the bedside through a comprehensive neurological assessment. However, the recovery depends primarily on the nerve pathology. Most compressive neuropathies (peroneal neuropathy, lumbosacral plexopathy) are demyelinating where the patients improve in a matter of days to weeks. If symptoms persist beyond 3 weeks, axonal damage needs to be ruled out. Electromyography procedure can be helpful not only in identifying the nerve pathology (axonal vs demyelination) but also aid in localization and prognosis. If the examination reveals any evidence of spinal cord, conus, or cauda equina injury, imaging with MRI is recommended on an urgent basis. If spinal epidural hematoma or abscess is present, immediate surgical decompression may be indicated. From a clinical standpoint, postpartum neuropathies involving the foot muscles tend to have a better prognosis compared to those involving proximal limb muscles due to involvement of isolated nerves in distal limb compared to major nerves in the proximal limbs. A study by Yoo et al reported the utility of segmental fractional anisotrophy analysis in evaluating proximal compressive neuropathy. 13 Following placement of neuraxial anesthesia and during delivery, it is imperative that maternal positioning be considered and reassessed throughout the labor course. Additionally, nerve injury can result from an extended period of low pressure as well as a short interval of high pressure. 14
Physical therapy is the mainstay of treatment in PSN. In our experience, recovery occurs in a two-step process. In the first stage, relatively rapid improvement occurs over days to weeks from remyelination of demyelinated fibers. This is followed by relative stabilization and a much slower recovery over several months to years from axonal regrowth and reinnervation. Therapy is aimed at expediting recovery and preventing progression of muscle weakness. Although most peroneal neuropathies benefit from the use of ankle foot orthotic brace, sciatic neuropathies frequently require knee stabilizing braces. Local analgesics such as a lidocaine patch or pain medications may be required in some cases. Postpartum medications for neuropathic pain such as tricyclics or gabapentin may be used in certain cases.
Teaching Points
• This case report highlights that, PSN can occur after uncomplicated vaginal delivery in the absence of perinatal risk factors.
• Differential diagnosis for postpartum foot drop includes: peroneal neuropathy vs lumbosacral plexopathy vs sciatic neuropathy.
• Peroneal neuropathy typically occurs due to compression of common peroneal nerve at the fibular head causing weakness of ankle dorsiflexion (deep peroneal) and ankle eversion (superficial peroneal).
• Lumbosacral plexopathy typically occurs due to compression of lumbosacral trunk at pelvic rim causing weakness of knee flexion (sciatic), hip abduction, extension, and internal rotation (gluteal nerves) in addition to peroneal and tibial group of muscles.
• Sciatic neuropathy which is rare can be characterized by weakness of knee flexion (sciatic) in addition to peroneal and tibial muscle groups.
Footnotes
Author’s Note: Poster presentation: American Association of Neuromuscular & Electrodiagnostic Medicine Annual meeting in September 2022.
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.
Informed consent: We have obtained written consents for the cases reported in the manuscript.
ORCID iD
Bhavesh Trikamji https://orcid.org/0000-0002-4814-2118
References
- 1.Roy S, Levine AB, Herbison GJ, Jacobs SR. Intraoperative positioning during cesarean as a cause of sciatic neuropathy. Obstet Gynecol. 2002;99(4):652. [DOI] [PubMed] [Google Scholar]
- 2.Postaci A, Karabeyoglu I, Erdogan G, Turan O, Dikmen B. A case of sciatic neuropathy after caesarean section under spinal anaesthesia. Int J Obstet Anesth. 2006;15(4):317. [DOI] [PubMed] [Google Scholar]
- 3.Kim SH, Kim IH, Lee SY. Sciatic neuropathy after normal vaginal delivery: A case report. J Clin Neurosci. 2020;72:480-482. [DOI] [PubMed] [Google Scholar]
- 4.Wong CA. Neurologic deficits and labor analgesia. Reg Anesth Pain Med. 2004;29(4):341. [DOI] [PubMed] [Google Scholar]
- 5.Massey EW, Guidon AC. Peripheral neuropathies in pregnancy. Continuum (Minneap Minn). 2014;20(1):100. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Bsteh G, Wanschitz JV, Gruber H, Seppi K, Löscher WN. Prognosis and prognostic factors in non-traumatic acute-onset compressive mononeuropathies--radial and peroneal mononeuropathies. Eur J Neurol. 2013;20(6):981. [DOI] [PubMed] [Google Scholar]
- 7.Wong CA. Nerve injuries after neuraxial anaesthesia and their medicolegal implications. Best Pract Res Clin Obstet Gynaecol. 2010;24(3):367. [DOI] [PubMed] [Google Scholar]
- 8.Birnbach DJ, Hernandez M, van Zundert AA. Neurologic complications of neuraxial analgesia for labor. Curr Opin Anaesthesiol. 2005;18:513. [DOI] [PubMed] [Google Scholar]
- 9.Kim HJ, Park SH. Sciatic nerve injection injury. J Int Med Res. 2014;42(4):887. [DOI] [PubMed] [Google Scholar]
- 10.Silva M, Mallinson C, Reynolds F. Sciatic nerve palsy following childbirth. Anaesthesia. 1996;51:1144. [DOI] [PubMed] [Google Scholar]
- 11.Saw JL, Hale J, Madhavan A, Ringler MD, Toledano M, Naddaf E. Ischiofemoral impingement syndrome provoked by labor: An unusual case of complete sciatic mononeuropathy. Neuroradiol J. 2022;36:116-118. 19714009221109895. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Kelly CJ, Augustine C, Rooney BP, Bouchier-Hayes DJ. An investigation of the pathophysiology of ischaemic neuropathy. Eur J Vasc Surg. 1991;5:535. [DOI] [PubMed] [Google Scholar]
- 13.Yoo Y, Kim SJ, Oh J. Postpartum sciatic neuropathy: segmental fractional anisotropy analysis to disclose neurapraxia. Neurology. 2016;87(9):954. [DOI] [PubMed] [Google Scholar]
- 14.Radawski MM, Strakowski JA, Johnson EW. Acute common peroneal neuropathy due to hand positioning in normal labor and delivery. Obstet Gynecol. 2011;118(2 Pt 2):421-423. [DOI] [PubMed] [Google Scholar]