Introduction and significance
Childbirth is the most common reason for admission to a hospital in the United States.1 Although most parturients expect an uneventful delivery, 9 of every 10 women who deliver in the US experience a complication during pregnancy or at delivery.2 One complication that affects nearly 40,000 women each year, and occurs in roughly 0.3% to 2% of all deliveries, is lower extremity nerve injury.3,4 Nerve palsies are often attributed to anesthesia and neuraxial blockade, when in actuality, these injuries are most often secondary to intrinsic obstetrical causes.
Nerve injury can occur centrally in the brain or spinal cord or in a peripheral nerve. Identifying the patient’s symptoms, and specific deficit, and whether the injury is sensory, motor, or combined, can help distinguish the location of the injury. Managing this complication can be challenging for the clinician as the injury and can have a significant negative impact on a new mother’s postpartum care and discharge to home because ambulation and daily activities may be difficult. Nerve injuries can also pose a significant risk to the newborn, as the caretaker is more prone to falls and may be unable to independently care for the infant. Along with mechanical challenges, there are also emotional concerns. Nerve palsies can be distressing during an already emotional time period for a new mother, as up to 50% to 60% of women experience “baby blues” within the first 2 weeks after childbirth.5,6 Given both the mechanical and emotional challenges after a peripartum nerve injury, maternal support is crucial.
In addition to ensuring appropriate care for the patient, there are also medicolegal implications for the anesthesia provider. Evaluating closed claims from the Comparative Benchmark System between the years 2005 and 2015, 106 (3.7%) were obstetric anesthesiology cases, and 54% of those were related to maternal nerve injury. Of the 58 nerve injury lawsuits, all of the patients had a neuraxial procedure for their delivery.7 Although 50% of nerve injuries typically resolve within 6 to 8 weeks, the remainder can take up to a year to resolve, with some becoming permanent.3,8,9
Peripheral nerve palsies
A majority of peripheral nerve palsies incurred during childbirth are thought to be obstetric in nature, due to either compression or stretch of the nerve.3 Nerve compression likely occurs under the inguinal ligament during prolonged flexion, or by fetal positioning at the pelvic rim, and injury patterns differ depending on the specific nerves compressed. Patients with neuraxial analgesia may be more prone to developing peripartum peripheral nerve injuries because they may have masked nociceptive warning signs of nerve compression during positioning and the second stage of labor and are less likely to change positioning throughout their labor course.9
The incidence of peripartum peripheral nerve injuries varies among sources, but ranges between 0.3% and 2%.3,4,10 The most common purely sensory deficit is due to a lateral femoral cutaneous palsy, which leads to decreased sensation of the lateral thigh. Motor deficits such as weakness of hip flexion and knee extension are most commonly due to femoral nerve injury secondary to compression under the inguinal ligament. The most common nerve palsies, and the presumed mechanism of injury, and the sensory and motor deficits seen on physical examination are listed in Table 1.
Table 1 -
Common nerves injured during labor, proposed mechanism and location of injury, and observed deficit.
||Proposed mechanism and location of injury
|Lateral femoral cutaneous nerve
||Compression under the inguinal ligament, prolonged hip flexion, obesity (increased pressure at hips)
||Sensory: decreased on anterolateral thigh
||Compression under the inguinal ligament, prolonged hip flexion, abduction, and external rotation; retraction during cesarean delivery
||Sensory: decreased on the anterior thigh and the medial calf Motor: weak hip flexion, weak knee extension
|Lumbosacral plexus and sciatic nerve
||Fetal compression due to position, compression against pelvic rim, forceps-assisted vaginal delivery
||Sensory: decreased on posterior thigh Motor: weak quadriceps, weak hip adduction, foot drop, involves multiple levels
||Fetal compression, improper positioning, forceps-assisted vaginal delivery
||Sensory: decreased on medial thigh Motor: weak hip adduction, wide gait
|Common peroneal nerve
||Lower extremity positioning, compression at the fibular head, compression while pushing
||Sensory: decreased on the lateral calf Motor: foot drop
Nerve compression causes a demyelinating injury, which leads to loss of saltatory conduction, and eventually leads to a focal decrease in conduction velocity. Fortunately, the nerve axon usually remains intact, except in cases of severe prolonged compression or in patients with a preexisting neuropathy.11 Because the axon remains intact, the nerves should be able to regenerate and completely recover; however, in the rare instance of axonal injury, regeneration is more limited.
There have been several factors thought to be associated with nerve injury, although not all have been replicated in repeated studies. Nulliparity and prolonged second stage of labor are statistically significant risk factors for developing peripartum lumbosacral spine and lower extremity nerve injuries.3 These findings were confirmed in a prospective observational study where those with a postpartum nerve injury had a prolonged second stage of labor with an average of 94 minutes (13 to 224 min) as compared with a range of 54 to 79 minutes reported in previous studies for a first delivery.12 The longer the descent and expulsion phases, the stronger the compression of the pelvic nerves may be, which makes the nerve more likely to sustain injury.
A history of a neurological condition, like preexisting back injury, is also associated with nerve injury. Patients with a preexisting back injury are more likely to assume positions they may otherwise avoid due to discomfort, which may aggravate an existing nerve impingement or compression. Other risk factors for nerve injury include gestational age greater than or equal to 41 weeks, neuraxial placement after 5 cm of cervical dilation, repeated neuraxial procedures, forceps delivery, short stature, and newborn weight ≥3.5 kg.13
In addition to nerve compression and stretch, nerve compromise may also occur from hypotension, which reduces nerve perfusion and may lead to ischemia.14 Nerve tissue requires an uninterrupted blood supply from its capillary network, which may provide some implication of hypotension, especially when nerve injury occurs under general anesthesia.15 Nerve ischemia and decreased perineural blood flow may explain why some peripheral nerve injuries do not fit the classic compression or stretch mechanism. For example, lateral femoral cutaneous nerve injuries are most often caused by compression under the inguinal ligament. However, in a study evaluating 24 women with lateral femoral cutaneous nerve injuries, 4 of these patients had a scheduled cesarean delivery and were never placed in the lithotomy position; thus, the injury was not caused by compression. In addition, all 22 of the femoral nerve injuries identified also demonstrated iliopsoas weakness. The iliopsoas muscle is innervated by the iliacus nerve, which branches off of the femoral nerve proximal to the inguinal ligament, meaning that it is not compressed during lithotomy positioning. This suggests that nerve hypoperfusion, rather than stretch or compression alone, may play a role in nerve injury.3
Fortunately, peripartum peripheral nerve injuries tend to be self-limited and resolve within a few weeks of delivery. A study of 13 patients with postpartum lower limb sensorimotor deficits found that 64% made rapid full recovery, and a minority showed marked improvement at 6 weeks but had some minor persistent symptoms, with a mean recovery time 5±2.5 weeks.16 In another prospective study, among the 26 women with nerve injuries for whom follow-up was completed, the median time to recover was 18 days, but 3 women continued to have a neurological deficit 1 year after delivery. A Kaplan-Meier curve depicting time to recovery from this study is shown in Figure 1.12
Potential safeguards to be considered to minimize peripheral nerve compression include being mindful of patient positioning, avoiding prolonged periods of time in the lithotomy position, placing the hip wedge under the bony pelvis instead of under the buttock, and using lower concentration local anesthetics to allow for minimal motor blockade.17 If a peripheral nerve injury occurs, maternal evaluation and support before discharge are crucial. These patients should be evaluated by physical therapy and possibly physiatry if available. If there is a significant motor impairment, they should be discharged with an assistive device or an orthotic if needed for foot drop, and close follow-up with physical therapy and their obstetrician. Electromyography should also be considered if the diagnosis is not clear based on history and physical examination.
In addition to mechanical concerns, the parturients’ emotional state should be monitored very closely, as an injury of this sort can be very distressing. Gabapentin as a treatment for neuropathic pain can also be considered, as women prescribed gabapentin have less pain and increased maternal satisfaction.18,19 Gabapentin has not been shown to have any effects on the neonate if administered in utero or through breast milk exposure, although these studies have been small.20 Despite its benefits, patients may avoid gabapentin because of its side-effect profile, some which can be quite distressing and dangerous in a new parent, including increased fatigue and dizziness. More studies evaluating women taking gabapentin for their peripheral nerve palsies postpartum are needed.
Central neuraxial system injuries
Central nervous system (CNS) lesions can often be distinguished from peripheral nerve injuries based on the pattern of dysfunction. Central injuries are more likely to be bilateral, have weakness from the injury site distally, are associated with autonomic dysfunction, and may have upper motor neuron signs like spasticity and brisk reflexes.17 As opposed to peripheral nerve injuries, which are primarily believed to be intrinsic obstetric palsies, CNS injuries are more likely to be related to neuraxial anesthesia. Lesions to the CNS can be complex but are fortunately incredibly rare, and include traumatic injury to the nerves or blood vessels, infection, or ischemia.
The spinal cord in the majority of adults tapers at L1 to L2 and forms the conus medullaris. Distally, the spinal nerves continue to branch out diagonally, forming the cauda equina. Injury to these areas can present differently. Conus medullaris syndrome presents with bilateral motor and sensory loss, saddle anesthesia, and loss of bowel and bladder function, but usually does not present with radicular pain. Cauda equina syndrome typically presents more gradually, is unilateral, causes radicular pain, and also eventually leads to loss of bowel or bladder function. The major blood supply to the spinal cord at this level includes the anterior median longitudinal arterial trunk and the bilateral posterior spinal arteries. Injury to the conus medullaris is most commonly due to direct needle trauma as seen with multiple case reports with imaging showing the site of damage.21
Insertion of epidural catheters or spinal needles can lead to injury either by ensnaring a root, causing intravascular trauma, or via direct irritation to the nerve root, often signified to the patient as a paresthesia sensation that radiates down a unilateral leg. No published studies have shown that paresthesias are a sensitive or specific marker for nerve injury; however, this is an area of ongoing investigation.22 Common practice is to proceed if the paresthesia is mild and transient, but the needle should be removed and redirected if persistent. Although it would seem that direct nerve injury would be more common with an intrathecal catheter versus an epidural catheter, a retrospective review of 761 intrathecal catheters over a 12-year time period did not find any neurological complications, excluding postdural puncture headache sequelae.23
For labor analgesia and anesthesia, neuraxial placement is usually attempted at either the L3 to L4 or L4 to L5 interspaces. However, anesthesia providers are not always able to reliably predict the interspace level. This phenomenon was demonstrated in a study in which anesthesiology providers placed radiopaque markers on the backs of 100 patients undergoing magnetic resonance imaging and estimated the level of placement.24 These markers were then compared with the actual level seen on imaging. The correct level was only identified 29% of the time, and often, the anesthesiology providers believed themselves to be marking lower than the actual space. Approximately 50% of the time, the anesthetists were 1 level off, and ∼12% of the time, they were off by 2 levels (Fig. 2). Imaging also revealed that the spinal cord terminated below L1 in 19% of patients.24 This signifies that the risk of direct trauma is an unfortunate but real possibility, especially if the provider is inserting the needle higher than intended and performing a spinal or a combined spinal-epidural technique. It is important to keep in mind that the advancement of a spinal needle should be stopped as soon as entering the subarachnoid space to help avoid the risk of direct needle trauma. In addition, patients with spinal cord pathology may be at even higher risk of causing trauma. For example, patients with spina bifida occulta, neural tube defects, and tethered cords are often not offered neuraxial anesthesia for concern of leading to catastrophic trauma such as direct spinal cord injury. It is noteworthy that if a patient underwent a spinal cord detethering procedure, updated imaging is still advised before initiating neuraxial anesthesia as studies show ∼2.7% of cords may retether.25
Beyond direct spinal cord or nerve trauma, providers must consider compressive trauma from neuraxial hematomas. Fortunately, epidural hematomas are incredibly rare, and occur at a rate of 1 in 183,383 procedures in the general population.26 A review of 166 case reports of all patients (not just parturients) with neuraxial blocks and spinal hematomas from 1994 to 2015 found that there were 3 predominant risk factor categories: patient-related factors such as hemostatic and spinal disorders, procedure-related factors such as complicated block placement, and drug-related risks due to antihemostatic drug use.27 These risk factors do not seem to be as significant in the obstetric population, as a systematic review from 1952 to 2016 revealed no cases of obstetric spinal-epidural hematoma in pregnant women receiving thromboprophylaxis; however, the total number of patients is unknown, preventing quantitative risk assessment.28 In addition, low-dose aspirin (81 mg) and nonsteroidal anti-inflammatory drugs do not appear to be associated with an increase in the risk of neuraxial hematoma.29
Keeping epidural hematomas on the differential diagnosis for lower extremity weakness even in patients not on thromboprophylaxis is critically important. The diagnosis of an epidural hematoma can be complex because the blood can accumulate during labor while still anesthetized, and a motor blockade may be undetected or remote from placement or removal of the catheter. Rapid recognition and treatment is essential for recovery. Ideally, decompression should occur within 12 hours of the start of symptoms for the best surgical outcome, but reports have shown positive outcomes even when performed within 24 hours.27 Fortunately, there have been several case reports where patients have had positive outcomes even when the hematoma collected late including an epidural hematoma that accumulated 9 days after removal of the labor epidural catheter, despite laboratory values being normal. The case described a patient who presented with acute back pain, sensory deficit, and ascending weakness. The team quickly ordered a magnetic resonance imaging, surgical depression was performed within 4 hours of symptom onset, and the patient gained full recovery of her motor function.30 A more recent case report described a patient who underwent an uncomplicated cesarean delivery for twin pregnancy under combined spinal-epidural. The patient was started on dalteparin with the catheter in place, and was removed on postoperative day 3, 12 hours after last dalteparin administration. More than 70 hours after removal of the epidural catheter, the patient described low back pain with radiation, urinary retention, and eventually a lower limb motor deficit several hours later. She eventually underwent a decompression laminectomy, and gained partial recovery of her deficits.31
Identifying who is at the highest risk of developing an epidural hematoma is important. Thrombocytopenia is a condition that has often been an indication for an anesthesiologist to refuse administration of neuraxial analgesia in a laboring patient. The Multicenter Perioperative Outcomes Group retrospectively reviewed the risk of spinal and epidural hematomas after neuraxial techniques in thrombocytopenic parturients. They found a total of 573 parturients with a platelet count of <100,000 mm3 who had been subjected to neuraxial techniques. No cases of epidural hematoma requiring surgical decompression were observed despite significant thrombocytopenia, with quite a few cases with platelet levels <70,000 mm3 (Fig. 3).32 The distribution of thrombocytopenic patients receiving a neuraxial blockade is shown in Figure 3. Based on the confidence intervals from this review combined with data from previous studies identified in the systemic review, the authors found the risk of epidural hematoma for a platelet count of 0 to 49,000 mm3 to be 11%, for a platelet count of 50,000 to 69,000 mm3 to be 3%, and for a platelet count of 70,000 to 100,000 mm3 to be 0.2%.32 The Society for Obstetric Anesthesia and Perinatology consensus statement released in early 2021 concluded that the risk of an epidural hematoma with a platelet count >70,000 mm3 is very low in the obstetric patient, and within the appropriate clinical context, it is safe to proceed with a neuraxial procedure.33
Platelet counts may also be affected by anticoagulation, especially in the setting of starting heparin, which can cause heparin-induced thrombocytopenia. Considering the increased initiative to administer appropriate venous thromboembolism antepartum in admitted patients and postpartum, especially within obstetrics, it is important to time anticoagulation appropriately with placement and removal of neuraxial blockade. Parturients may be prescribed heparin or low–molecular-weight heparin (LMWH) during their third trimester of pregnancy. Society for Obstetric Anesthesia and Perinatology guidelines recommend that providers wait 4 to 6 hours after low-dose unfractionated heparin (UFH) (5000 U bid or tid) before performing a neuraxial procedure, and >24 hours and normal coagulation status (activated partial thromboplastin time within normal range or anti-factor Xa undetectable) after high-dose subcutaneous UFH (>10,000 U bid).34 Providers should wait 12 hours after the last dose of low-dose LMWH, typically enoxaparin 40 mg once daily, and wait 24 hours after high-dose LMWH (enoxaparin 1 mg/kg bid) before performing a neuraxial procedure.34 After delivery, UFH thromboprophylaxis should not start until 1 hour after placement and 1 hour after removal of the epidural catheter. Low-dose LMWH can be restarted 12 hours after the neuraxial procedure and 4 hours after removal of the catheter. For higher dose LMWH, providers should consider waiting >24 hours after the procedure and 4 hours after catheter removal before restarting.34
Other rare complications caused by neuraxial placement can be infection manifested as epidural abscesses or meningitis, which occurs in about 1 in 168,391 neuraxial procedures.26 Risk factors for epidural abscess include prolonged catheterization, poor aseptic technique, multiple attempts, polyurethane occlusive dressing, and immunocompromised state. Infection source is likely from the patients’ skin or body fluids in the bed, tracking along the catheter entry point. Before washing hands and putting on gloves, all jewelry (eg, rings, watches, etc.) should be removed. Higher microbial counts have been noted in health care workers who do not routinely remove these items before handwashing.35 Meningitis is similar to epidural abscess in that the anesthesiologist’s sterility practice can have a direct influence on its development. Specific risk factors include the anesthesia provider not wearing a mask, and manual removal of the placenta.17 One of the early case study reports described 4 cases of iatrogenic meningitis after spinal anesthesia occurring over a 4-year period. All cases involved the same anesthesiologist, who had a history of recurrent pharyngitis and did not wear a mask during the procedure.36 It is now required by the Center for Disease Control for all proceduralists to wear surgical masks during neuraxial procedures.
Meningitis can be challenging to diagnose, as it can often be confounded with a postdural puncture headache. An observational study of the closed claims analysis in the United States and The Netherlands from 2007 to 2017 found 14 cases of meningitis (not all obstetrical patients), but in 4 of the 14 meningitis cases, the patients’ headache was mistakenly confused for postdural puncture headache, and all 4 of these patients were treated with an epidural blood patch. Patients in this study showed full recovery in 40% of events after being adequately treated with antibiotics.37
Peripartum neurological complications are complex and can have a significant negative impact on a parturients’ postpartum course and discharge. Peripheral nerve palsies are most commonly due to intrinsic obstetric palsies, but continued research needs to be carried out to determine anesthetic factors that may contribute to these injuries. CNS injuries are most commonly related to anesthetic factors and highlight the importance of safe needle practices, diligent attention to coagulation abnormalities and anticoagulant medications, and sterility.
Conflict of interest disclosure
The authors declare they have nothing to disclose.
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