Postpartum lumbosacral radiculopathy: a neuraxial anaesthesia complication or an intrinsic obstetric palsy?

Abstract

Postpartum peripheral nerve disorders are an uncommon obstetrical complication, with most cases resulting from intrinsic obstetric palsies. We present the case of a full-term nulliparous pregnant 33-year-old woman with a vacuum-assisted vaginal delivery due to a prolonged second stage of labour and occipitoposterior position of the fetal head. For analgesia, a combined spinal–epidural technique was used. Four hours after delivery, the patient experienced a painless asymmetric motor deficit and hypoesthesia in the lower limbs, followed by sphincter disturbance. Emergent MRI was unremarkable. Electromyography showed signs of a bilateral lumbosacral radiculopathy. The patient experienced a gradual recovery over the following 2 months. Although a definitive aetiological diagnosis could not be confirmed, a lumbosacral polyradiculopathy due to intrinsic obstetric complication was considered. The patient presented several risk factors known to be associated with intrinsic obstetric palsies. Obstetricians and anaesthesiologists have an important role in preventing and diagnosing postpartum peripheral nerve disorders.

Background

Postpartum peripheral nerve disorders are an uncommon obstetrical complication, with an estimated incidence of 1%.¹ These disorders can present with a myriad of symptoms, including back pain, lower limb weakness, sensory deficit or pain, and sphincter disturbance.²

Because a large number of women receive neuraxial anaesthesia–analgesia for labour and delivery, when postpartum lower limbs neurological symptoms emerge, they are often attributed to this invasive technique.

Nevertheless, complications directly attributable to neuraxial anaesthesia are rare,^{3 4} with most cases of neurological injury after delivery occurring due to intrinsic obstetric palsies—compressive injuries related to the mechanics of labour and delivery.⁵

Risk factors for intrinsic obstetric palsies should be known to obstetricians and anaesthesiologists in order to promote potential preventive measures.^{4 6}

With our case report, we intend to present and discuss the potential causes of postpartum peripheral nerve disorders, but also their clinical presentation, diagnostic investigation, risk factors and preventive strategies.

Case presentation

A full-term nulliparous pregnant 33-year-old woman, American Society of Anesthesiologists 2, was admitted to our obstetrics department, in the latent phase of the first stage of labour. She had no relevant medical history and no current medication besides iron and folic acid supplementation.

To provide analgesia for labour and delivery, a combined spinal–epidural technique (27 gauge needle) was performed, with a single puncture in the L3–L4 interspace. At this time, cervical dilation was 3 cm. Skin disinfection was achieved with dyed chlorhexidine diacetate (2%) in 70% isopropyl alcohol. Sufentanil (7.5 μg) was administered in the spinal space and an epidural catheter was left for analgesia top-up doses with ropivacaine 0.2% (10 mL). During this technique, the patient did not experience any neurological symptoms in the lower limbs, namely numbness, tingling, shock-like pain or weakness.

After 24 hours, with full dilation, a vacuum-assisted vaginal delivery was performed due to a prolonged second stage of labour (3.5 hours) and posterior position of the fetal head. Delivery took place in a lithotomy position. After delivery, the obstetrician repaired the vaginal and perineal tears. No immediate complications were registered. The newborn baby girl weighed 3.74 kg, with a 5 min Apgar score of 10 points. After birth, the epidural catheter was removed. The total amount of ropivacaine 0.2% administered to that specified point was 140 mL (during a total of 23 hours).

Four hours after delivery, the patient started reporting tingling and decreased strength in the lower limbs, without pain.

Investigations

At neurological examination, hip flexion/extension was 5/5 on the right, 4+/5 on the left; knee flexion/extension 4/5 on the right, knee flexion 3/5 and knee extension 4/5 on the left; ankle dorsiflexion 5/5 and plantarflexion 4/5 on the right; ankle dorsiflexion 4/5 and plantarflexion 4−/5 on the left. Bilateral patellar and Achilles deep tendon reflexes were absent. There was tactile hypoesthesia of the perineum and lower limbs, more pronounced on the lateral side of the left lower limb. Meningeal signs were absent.

The possibility of an epidural haematoma as a complication of neuraxial analgesia with subsequent cauda equine syndrome was considered and an emergent lumbosacral MRI was taken. MRI results showed no bleeding complication, no discal pathology or other signs of degenerative changes in the lumbar spine, and no changes in the distribution and signal of the cauda equina nerve roots and spinal cord (figure 1).

Figure 1.

Lumbosacral MRI—sagital view, T2—showing no lumbar spine, cauda equina nerve roots or terminal spinal cord changes.

In the subsequent days, the patient suffered clinical deterioration with increased weakness and urinary and faecal sphincter disturbance. At this moment, examination revealed a more severe motor disturbance in the left L5 and S1 myotomes. Electromyography performed 10 days after symptom onset showed reduced compound muscle action potential (CMAP) on left fibular and tibial nerves, with F-wave latency on the left tibial nerve. H-reflex was bilateral absent. No signs of active denervation were documented. A follow-up electromyography showed a bilateral lumbosacral radiculopathy, from L3 to S1, more severe in the left L5 and S1 nerve roots. At this time, there were signs of active denervation and frank reinnervation.

Although a definitive aetiological diagnosis could not be confirmed, a lumbosacral polyradiculopathy/cauda equine syndrome due to intrinsic obstetric complication was considered.

Outcome and follow-up

After the initiation of motor rehabilitation, in the following weeks, the patient experienced total motor recovery. Saddle paraesthesia and urinary sphincter persisted for 2 months.

Discussion

Although postpartum peripheral nerve disorders are rare,¹ they can result in long-term morbidity.

When these neurological complications occur, and because women may receive neuraxial anaesthesia–analgesia for labour and delivery, anaesthesiologists are usually the first to be consulted. Indeed, although neurological complications can occur after central neural blocks, they are extremely rare.⁷ This seems to be particular true in the obstetric field, when comparing with other populations.^{7 8} Clinicians should not forget that neurological deficits are much more frequent secondary to labour and delivery process.⁹ More rarely, pregnancy and puerperium-related medical diseases or patients’ premorbid conditions can also be implicated.

Neurological complications associated with neuraxial anaesthesia–analgesia can be divided into traumatic, chemical, infectious and haemorrhagic.^{5 10}

Traumatic injuries can exceptionally occur due to direct spinal cord injury or at the nerve roots near the place of the needle insertion. In traumatic injuries, it would be expected that patients report immediate symptoms, which was not the case. Neuraxial anaesthesia–analgesia should be discontinued in any patient who experiences persistent neurological symptoms since local anaesthetics may mask the recognition of signs and symptoms of nerve injuries.

Chemical injuries (arachnoiditis) due to direct neurotoxicity were classically described in patients submitted to continuous spinal anaesthesia,^{11 12} particularly with hyperbaric 5% lidocaine.¹³ In our case, ropivacaine was used, which shows less potential of neurotoxicity,¹⁴ and was not administered in the subarachnoid space. Also, our technique with single puncture using a 27 gauge needle makes the flux of ropivacaine to the subarachnoid space unlikely.¹⁵ Chemical injuries can also result from traces of chlorhexidine containing skin preparations being transmitted into the subarachnoid space. Some cases of arachnoiditis can cause progressive inflammation and fibrosis (adhesive arachnoiditis), resulting in progressive and permanent loss of spinal cord functions. In these cases, pain and meningeal signs are usually present, and lumbosacral MRI shows thickening and clumping of cauda equina nerve roots.¹⁶

Infectious complications can also rarely result from neuraxial anaesthesia, and are largely prevented with procedures performed under strict aseptic conditions. In infectious meningitis, clinical presentation include fever, headache and meningeal signs.¹⁷

Epidural haematomas are rare, but serious complications of neuraxial anaesthesia. Because early diagnosis and surgical decompression are fundamental to achieve better outcomes,¹⁸ every patient with suspected bleeding complication must undertake emergent lumbosacral imaging.

As stated above, compressive or stretch nerve injuries related to the mechanics of labour or delivery (intrinsic obstetric palsies) are the most frequent cause of postpartum peripheral nerve disorders. They can result in single nerve (eg, lateral femoral cutaneous, femoral, obturator and pudendal nerves) or multiple nerve root lesion¹⁹ and can be bilateral in up to 25% of cases.

Different risk factors, some of which were present in our case, have been shown to be associated with these complications: nulliparity, maternal short stature, fetal macrosomia, persistent transverse or posterior position of the fetal head, prolonged lithotomy position in labour, prolonged second stage of labour and operative vaginal delivery.^{1 6}

Besides peripheral nerve injuries, prolonged second stage of labour is known to be associated with adverse maternal (eg, postpartum haemorrhage, infection and perineal trauma) and neonatal events (eg, lower Apgar score and neonatal intensive care unit admissions),^{20 21} so its potential risks should be weighed against the disadvantages and risks of an operative vaginal delivery or caesarean birth.²²

Between operative vaginal deliveries, forceps seems to be associated with severe perineal tears, maternal peripheral nerve injuries and neonatal facial trauma,^{1 23 24} while vacuum-assisted is more likely to fail to achieve a vaginal birth, and results in higher rates of neonatal cephalohaematoma.^{23 24} In general, operative vaginal deliveries have lower rates of long-term maternal complications, but higher risk of perineal tears and neonatal traumatic injuries, compared with caesarean birth.

As in other cases, the possibility of a complication of neuraxial anaesthesia–analgesia was initially suspected by the obstetric team.¹⁹ Taking into account the clinical presentation, without pain and any signs of infection, and the absence of relevant MRI findings, there is no direct evidence of an anaesthetic complication in our case. However, because it is always difficult to establish a definite link between symptoms and a potential chemical toxicity of analgesia, at least the contribution of this mechanism cannot be excluded.²⁴

Compared with previous case reports or case series,^{19 25} the presented patient shares some of the abovementioned risk factors of intrinsic obstetric palsy. All received epidural anaesthesia and presented with neurological signs on the first day after delivery.

Only one reported pain and most had a good long-term outcome.

In addition to careful neurological examination and imaging evaluation, the importance of electrophysiological assessment (electromyography) should not be overlooked. It helps in defining the neurogenic basis of symptoms, may localise the responsible lesion and contributed to the definition of its severity.²⁶ Repeating electromyography (after 4 weeks) will help to define the prognosis.²⁶

Obstetric and anaesthetic teams must recognise the mentioned risk factors for intrinsic obstetric injury in order to adopt preventive strategies. These strategies should focus on avoiding positions that could exacerbate nerve injury (prolonged tight flexion or extreme thigh abduction and external rotation), advising women to change limb position during the second stage of labour, using preventive padding, and using low concentration of local anaesthetics during regional anaesthesia.¹⁹

Although the initial symptoms are often major, because prognosis is most often good, new mothers presenting postpartum lower limb nerve injury should be reassured.¹⁹ Consultation with a physiatrist and rehabilitation as necessary should be conducted as soon as appropriate.

Patient’s perspective.

I never thought that something like this could happen. It was very distressing to think that I could never walk again. The first days after delivery were difficult to cope with. I thank all the doctors, nurses and physiotherapists for their work and support.

Learning points.

• Obstetricians and anaesthesiologists have an important role in preventing and diagnosing postpartum peripheral nerve disorders.

• Although rare, complications of neuraxial analgesia should be promptly excluded since an emergent intervention may be necessary.

• Most cases seem to result from intrinsic obstetric injury, but definitive diagnosis may often be difficult.

• Detailed clinical, imaging and electrophysiological assessments are needed to support the diagnosis and to establish prognosis.