|Year : 2016 | Volume
| Issue : 1 | Page : 3-10
Neurological complications in obstetric regional anesthetic practice
Alastair Duncan1, Santosh Patel2
1 Specialty Trainee, North West Deanery, Manchester, United Kingdom
2 Consultant Anaesthetist, Royal Oldham Hospital and Honorary Senior Lecturer, Manchester Medical School, Faculty of Medical and Human Sciences, Manchester, United Kingdom
|Date of Web Publication||22-Apr-2016|
Dr. Alastair Duncan
Department of Anaesthesia, Royal Oldham Hospital, Rochdale Road, Oldham, Manchester, OL1 2JH
Source of Support: None, Conflict of Interest: None
Each year in the United Kingdom, nearly one-third of women giving birth will receive a central neuraxial block (CNB). The majority of postpartum neurological complications are secondary to intrinsic obstetric palsies. Despite this, neurological injury can occur following obstetric regional anesthesia. Any postpartum neurological deficit identified by the patient, anesthetist, midwife, or obstetrician should be investigated thoroughly. Prompt recognition and appropriate management of neurological complications is of the utmost importance in reducing the risk of permanent impairment. Anesthetists must recognize and coordinate the appropriate initial management for the complications associated with CNB in order to prevent permanent neurological damage.
Keywords: Assessment, management, neuraxial anesthesia, neurological complications, postpartum neuropathies
|How to cite this article:|
Duncan A, Patel S. Neurological complications in obstetric regional anesthetic practice. J Obstet Anaesth Crit Care 2016;6:3-10
|How to cite this URL:|
Duncan A, Patel S. Neurological complications in obstetric regional anesthetic practice. J Obstet Anaesth Crit Care [serial online] 2016 [cited 2020 Nov 29];6:3-10. Available from: https://www.joacc.com/text.asp?2016/6/1/3/181055
| Introduction|| |
Each year in the United Kingdom, nearly one-third of women giving birth will receive a central neuraxial block (CNB).  Life-changing neurological complications following CNB are rare. Prompt recognition and appropriate management are of the utmost importance in reducing the risk of permanent neurological impairment.
It is important to emphasize that normal labor accounts for the majority of postpartum neuropathies.  Nerve compression by the fetus in the pelvis, unnatural patient positioning, and instrumental deliveries can all result in neurological pathologies. Despite this fact, anesthetists involved in the care of obstetric patients are not completely absolved of responsibility. Although rare, neurological complications following regional anesthesia can occur.
Postdural puncture headache is a well-recognized and extensively researched neurological complication associated with CNB. The incidence, pathophysiology, clinical features, and management have been extremely well documented and will not be discussed further in this article.
| Incidence|| |
Neurological pathology following delivery may occur in up to 1 in 100 women.  Nonanesthetic causes account for the majority of postpartum neuropathies. Most of these are mild and resolve spontaneously within a period of days to weeks. Occasionally, symptoms may be more prolonged.
Neurological injury resulting from anesthetic intervention is usually transient in nature, resolving within 1 year.  The reported incidence of temporary neurological deficit is 1 in 3900.  The UK's National Anesthesia Audit Project 3 reported the incidence of permanent harm following obstetric CNB as between 1 in 80,000 and 1 in 320,425. 
Despite their rarity, permanent neurological injuries in the obstetric population are catastrophic both for the mother and her family, and the healthcare professionals involved in her care.
| Pathophysiology|| |
To understand nerve injury, an appreciation of neural anatomy must be established. Individual nerve fibers are surrounded by an endoneurium - a layer of connective tissue that organizes axons into fascicles. A second connective tissue layer, the perineurium, surrounds these nerve bundles. The epineurium - the outermost layer of connective tissue - encases the entirety of the nerve. The nerve's dual blood supply consists of an intertwined intrinsic and extrinsic circulation. 
Nerve damage can result from a variety of mechanisms including compression, stretching, ischemia, chemical toxins, and penetrating injuries.  Nerve injuries are commonly classified using one of the two internationally recognized systems. Seddon described three types of nerve injury - neuropraxia, axonotmesis, and neurotmesis - based on the severity of tissue injury and prognosis.  The more recent description by Sunderland offers greater detail and expands upon Seddon's classification [Table 1]. 
| Nonanaesthetic Causes of Postpartum Neuropathies|| |
The majority of postpartum neuropathies may be explained by the position of the fetus in the pelvis, positioning of the mother to assist delivery and instrumental deliveries [Table 2].
| Anaesthetic Causes of Postpartum Neuropathies|| |
Direct trauma to the nerve remains the most common cause of postpartum neuropathy associated with CNBs. Vertebral canal hematomas (VCH) and epidural abscesses are far less common but have more potential to cause catastrophic neurological impairment. Infective organisms and other neurotoxic agents can be introduced during CNB [Table 3].
| Clinical Features of Nonanaesthetic Causes of Postpartum Neuropathies|| |
Causes of postpartum neuropathies resulting from compression of the lumbosacral trunk can be difficult to differentiate. Compressive neuropathies may be caused by direct pressure exerted by the fetal head, excessive hip flexion in the lithotomy position, or instrumental delivery. Determining which individual nerves have been affected allows the team to construct differential diagnoses and identify the potential causes [Table 4].
|Table 4: Postpartum neuropathies resulting from compression of the nerve|
Click here to view
Prolonged and severe periods of hypotension compromise the arterial blood supply to the spinal cord, but thresholds for either cannot be defined.  Neurological modalities supplied by the single anterior spinal artery are most vulnerable to vascular compromise. The anterior spinal artery syndrome can present such as loss of pain and temperature sensation, areflexia, and complete motor paralysis below the level of the lesion. Fine touch, proprioception, and vibration sensation are preserved through the intact dorsal columns, which are supplied by two posterior spinal arteries. 
Fifteen percent of the population have a dual arterial supply to the conus medullaris, originating from the thoracic aorta and internal iliac arteries. , In those without a dual arterial supply, a clinical syndrome similar to cauda equina could arise if the fetal head were to obstruct the internal iliac arteries.
| Clinical Features of Anaesthetic Causes of Postpartum Neuropathies|| |
Traumatic nerve injuries associated with CNBs commonly occur at the nerve root close to the site of instrumentation. Needles, catheters, and injectate can damage the spinal cord or conus medullaris directly.
Research using a porcine model demonstrated a correlation between larger needle gauge and increasing the severity of peripheral nerve damage following intentional nerve injury. The clinical significance of these findings is still to be determined, but a smaller diameter needle may be advisable to reduce the risk of nerve injury. 
The first symptoms may become apparent during insertion of the needle. The majority of cases related to traumatic nerve injury have been associated with paresthesia on insertion.  Of note, transient paresthesia is not uncommon when inserting epidural catheters, and this does not appear to be associated with permanent neurological injury. 
Pain, paresthesia, and muscular weakness in the distribution of the nerve may be evident immediately after the effects of the CNB have regressed.  In the obstetric population, the risk of permanent neurological impairment following CNB is extremely low. The majority of patients experiencing traumatic nerve injury recover fully. ,
Vertebral canal hematoma
Both technically challenging CNBs and those breach a vessel wall with either the needle or catheter, are recognized risk factors for the development of VCH. , The risk is increased in the presence of anticoagulants or antiplatelets and has been quoted to be as high as 1:1800 in the nonobstetric population. 
The incidence of breaching a vessel wall during CNB with an epidural catheter has been quoted as 1%; however, the incidence may be higher as blood may not be present in the needle or catheter in all circumstances.  Patients without coagulation abnormalities who have a bloody tap do not appear to be at an increased risk of developing VCH.
The popularity of CNB in obstetrics is increasing, as is the use of anticoagulants for obese parturients. Guidance addressing regional anesthesia for patients with abnormalities in coagulation was published by a collaborative working party in 2013.  The guideline details the timings at which performing CNB and administering doses of anticoagulation after CNB are considered safe.
The clinical features of an acute VCH include sudden onset back pain, often radicular in character, with motor and sensory deficits below the level of the spinal cord compression. 
It can be difficult to differentiate pathological from expected motor and sensory deficits in the period immediately after CNB. Nonetheless, pathological deficits will outlast the expected duration of CNB. The severity and duration of neurological deficits increase with time.
Epidural infection and abscess formation results from hematogenous bacterial seeding of the epidural space. Guidelines published by the Association of Anesthetists of Great Britain and Ireland in 2014 described the optimum aseptic technique for CNB in order to minimize the risk of contamination and infection. Emphasis was placed on scrupulous hand washing, barrier precautions, and the use of chlorhexidine in alcohol for skin asepsis. 
In contrast to VCH, the symptoms associated with an epidural abscess are more insidious in nature, which can lead to delays in diagnosis.  Patients may describe fever, malaise, headache, back pain (that may be radicular in nature), and neurological deficits in the hours to days following CNB. 
The examination may reveal tenderness to palpation over the site of an epidural abscess and pain on movement, particularly flexion of the lumbar spine. Motor weakness and bladder and bowel dysfunction may precede paraplegia as the abscess expands.
Cauda equina syndrome
The cauda equina is a bundle of lumbosacral spinal nerves and nerve roots originating from the conus medullaris of the spinal cord. They provide motor innervation to the lower limbs, urethral and anal sphincters, and sensory innervation to the perineal dermatomes and lower limbs. 
Cauda equina syndrome results from any lesion that compresses the cauda equina nerve roots, including VCH and epidural abscess. The clinical features relate to those described under the relevant headings.
Bacterial meningitis is a rare complication of CNB that can occur when the dura is breached, and an infectious agent is introduced to the cerebrospinal fluid (CSF) via contaminated equipment. Hematogenous bacterial seeding is another method by which a patient with bacteremia can develop bacterial meningitis following CNB.
The symptoms associated with meningitis usually develop 24-48 h after CNB.  Meningism is the triad of nuchal rigidity (neck stiffness), photophobia and headache. It is commonly associated with fever and back pain may be present. Symptoms of severe, advanced meningitis include altered mental status, vomiting, and seizures. Kernig's sign (extension of the knee with the hip flexed at 90° causing pain and restriction beyond 135°) and Brudzinski's neck sign (passive flexion of the neck causes flexion of both legs and hips) may be positive.
Aseptic meningitis produces symptoms similar to those witnessed in bacterial meningitis; however, no organism is isolated when CSF is cultured. , It tends to occur within 24 h of CNB and is generally self-limiting in nature.
Chronic adhesive arachnoiditis (CAA) is an extremely rare but debilitating condition. It is hypothesized that an irritant results in inflammation of the arachnoid and intrathecal elements. Collagen formation between nerve roots and pia arachnoid develops during resolution of the inflammation. This encapsulates the nerve roots, compromising their vascular supply and resulting in atrophy.  It has received much attention in the public eye over the past 10-15 years. Despite this interest, the debate remains over whether it constitutes a single disease entity.
CAA is best described as clinically significant nonspecific inflammation of the arachnoid and intrathecal elements. A complex clinical picture with varied symptomatology may present months or years after the original insult. The back pain increased by activity, with or without bilateral leg pain, is typical, but a range of neurological abnormalities has been reported making the diagnosis challenging. 
Transient neurological syndrome
Transient neurological syndrome (TNS) or transient radicular irritation is a syndrome of pain and dysesthesia in the buttocks, thighs or calves after spinal anesthesia.  It is self-limiting and resolves within 72 h in most cases. Lidocaine has been implicated in the majority of cases, but bupivacaine has also been found to cause a mild TNS with subtle clinical features. 
| Evaluation and Management|| |
Before performing any CNB, a detailed anesthetic history should be taken. This should detail any preexisting neurological deficits and elicit potential risk factors for the development of neurological complications following the intervention. Particular significance is placed upon preexisting coagulopathies, localized skin infection overlying the site of insertion and signs of systemic sepsis. General anesthesia should be considered and discussed with the patient if contraindications to CNB are proven.
Dilemmas regarding whether or not to perform CNB on a patient with chorioamnionitis are relatively common in obstetric anesthesia. A case series of over 500 patients with chorioamnionitis who received CNB reported no subsequent epidural or spinal infection.  Despite these results, the decision to perform CNB on a patient with chorioamnionitis should be made on an individual risk-benefit basis having discussed the potential risks with the patient.
Any postpartum neurological deficit identified by the patient, anesthetist, midwife, or obstetrician should be investigated thoroughly. Taking a history, performing a neurological examination, requesting diagnostic investigations, and initiating appropriate management in a multidisciplinary setting should minimize the risk of permanent neurological injury.
The pre-anesthetic and obstetric histories may help identify the etiology of postpartum neuropathies. Specific features from the history must be ascertained in order to help create the differential diagnosis [Table 5].
|Table 5: Historical features that can assist in the diagnosis of neurological complications|
Click here to view
Sensory and/or motor palsy without pain is suggestive of intrinsic obstetric palsy. Nerve injury associated with anesthetic interventions are commonly accompanied by back pain. Worsening neurological symptoms or those that present after a symptom-free period should be reviewed immediately.
A full neurological examination, including assessment of the cranial nerves and signs of concurrent sepsis, is essential. Mapping of the patient's symptoms may reveal a pattern consistent with a peripheral nerve injury.
Examination of the back should be undertaken. Skin changes around the site of needle insertion should be noted. Sensation and motor tone of the paraspinous muscles, which are innervated by the posterior rami, may give an indication as to whether the nerve root has been injured, or the damage is distal to this point. Tenderness to palpation of the spinous processes should alert the anesthetist to the potential of a vertebral canal space-occupying lesion.
Routine laboratory investigations including a full blood count, blood cultures and coagulation screen should be performed if the diagnosis of an epidural abscess, meningitis and VCH is suspected. More invasive investigations such as lumbar puncture and CSF analysis are helpful in suspected cases of meningitis.
Magnetic resonance imaging (MRI) with or without gadolinium contrast may reveal swelling of the spinal cord and areas of inflammation. MRI is the gold standard investigation for suspected space-occupying lesions. 
Electrophysiological investigations can differentiate between central and peripheral nerve injury, identify the muscles affected and give a likely prognosis of neural recovery. They can also produce a temporal estimate as to the timing of the injury, which is of particular note with regards to litigation. Therefore, assessment within 72 h of neurological deficit is important to demonstrate preexisting pathologies as new electrophysiological changes take the time to evolve.
Prompt recognition and treatment of limb or life-threatening pathologies remains the crux of managing neurological complications following obstetric regional anesthesia. If space-occupying lesions and meningitis can be excluded confidently, an alternative diagnosis, its prognosis and treatments must be explored. This commonly involves reassurance for self-limiting symptoms, referral to a physiotherapist for common intrinsic obstetric palsies and discussion with a neurologist for more complex neurological complications [Figure 1].
| Prognosis of Nerve Injuries Unrelated to Anesthetic Intervention|| |
Intrinsic obstetric neuropathies nearly always resolve spontaneously within 2 months.  Conservative management including minimizing periods of standing, avoiding positions that could exacerbate the nerve injury (e.g., excessive hip flexion) and simple oral analgesics may aid recovery. 
The long-term outcome of ischemic neuropathies is difficult to classify and can vary from paraplegia to mild motor weakness. Prognosis depends on the degree of the initial neurological deficit and evidence of improvement within the first 24 h. 
| Prognosis of Nerve Injuries Related to Anesthetic Intervention|| |
Neurological injury resulting from direct trauma by a regional anesthetic needle or catheter is usually transient in nature, resolving within 1 year.  Rarely, symptoms may persist indefinitely.
Recovery following VCH or epidural abscess is directly related to the time interval from onset of the space-occupying lesion to surgical decompression. An interval >8 h is associated with a high-risk of permanent neurological injury. 
If the appropriate antibiotics are commenced early, the prognosis of bacterial meningitis is generally positive. Despite this, any delay in recognition or administration of the appropriate antibiotics increases the morbidity and mortality risk. 
Aseptic meningitis follows a relatively benign course with symptoms resolving spontaneously without any specific treatment. 
Chronic adhesive arachnoiditis
Evidence regarding CAA following obstetric regional anesthesia is limited. There have been case reports of CAA developing after injection of chlorhexidine, which is used for asepsis, into the epidural and intrathecal spaces.  The current guidelines recommend the use of 0.5% chlorhexidine in alcohol for CNB asepsis. This provides the safest compromise between risk of infection and neurotoxicity. Preventing contamination of chlorhexidine and CNB equipment is key in minimizing the risk of neurotoxicity.
The spectrum of symptoms and delayed onset makes diagnosis difficult with a prediction of prognosis even more so.  Some patients' symptoms appear to a plateau, whereas there is another group of patients who develop a progressive deterioration that can result in loss of function in the affected limbs.
Transient neurological syndrome
As the name suggests, symptoms associated with a TNS generally resolve within 72 h. Reassurance and simple oral analgesics are usually all, that is, required for symptom control.
| Conclusion|| |
The majority of postpartum neurological complications are secondary to intrinsic obstetric palsies. Despite this, neurological injury can occur following obstetric regional anesthesia. The anesthetists must recognize and coordinate the appropriate initial management for the complications associated with CNB in order to prevent permanent neurological damage.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Loo CC, Dahlgren G, Irestedt L. Neurological complications in obstetric regional anaesthesia. Int J Obstet Anesth 2000;9:99-124.
Wong CA, Scavone BM, Dugan S, Smith JC, Prather H, Ganchiff JN, et al.
Incidence of postpartum lumbosacral spine and lower extremity nerve injuries. Obstet Gynecol 2003;101:279-88.
Wong CA. Neurologic deficits and labor analgesia. Reg Anesth Pain Med 2004;29:341-51.
Ruppen W, Derry S, McQuay H, Moore RA. Incidence of epidural hematoma, infection, and neurologic injury in obstetric patients with epidural analgesia/anesthesia. Anesthesiology 2006;105:394-9.
Cook TM, Counsell D, Wildsmith JA; Royal College of Anaesthetists Third National Audit Project. Major complications of central neuraxial block: Report on the Third National Audit Project of the Royal College of Anaesthetists. Br J Anaesth 2009;102:179-90.
Jeng CL, Torrillo TM, Rosenblatt MA. Complications of peripheral nerve blocks. Br J Anaesth 2010;105 Suppl 1:i97-107.
Robinson LR. traumatic injury to peripheral nerves. Suppl Clin Neurophysiol 2004;57:173-186.
Seddon HJ. Three types of nerve injury. Brain 1943;66:237-88.
Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain 1951;74:491-516.
Scott DB, Hibbard BM. Serious non-fatal complications associated with extradural block in obstetric practice. Br J Anaesth 1990;64:537-41.
Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central neuraxial blockades in Sweden 1990-1999. Anesthesiology 2004;101:950-9.
Reynolds F. Infection as a complication of neuraxial blockade. Int J Obstet Anesth 2005;14:183-8.
Rice I, Wee MY, Thomson K. Obstetric epidurals and chronic adhesive arachnoiditis. Br J Anaesth 2004;92:109-20.
Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: Clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol 2006;63:1113-20.
MacArthur A. Neurological complications of regional obstetric anesthesia. Tech Reg Anesth Pain Manag 2003;7:229-34.
Reynolds F. Neurologic complications of pregnancy and regional anesthesia. In: Chestnut DH, Polley LS, Tsen LC, Wong CA, editors. Obstetric Anesthesia: Principles and Practice. 4 th
ed. Philadelphia, USA: Elsevier Mosby; 2009. p. 701-26.
Steinfeldt T, Nimphius W, Werner T, Vassiliou T, Kill C, Karakas E, et al.
Nerve injury by needle nerve perforation in regional anaesthesia: Does size matter? Br J Anaesth 2010;104:245-53.
Auroy Y, Narchi P, Messiah A, Litt L, Rouvier B, Samii K. Serious complications related to regional anesthesia: Results of a prospective survey in France. Anesthesiology 1997;87:479-86.
Yoshii WY, Rottman RL, Rosenblatt RM. Epidural catheter-induced traumatic radiculopathy in obstetrics. Reg Anesth 2001;92:252-6.
Reynolds F. Damage to the conus medullaris following spinal anaesthesia. Anaesthesia 2001;56:238-47.
Rajakulendran Y, Rahman S, Venkat N. Long-term neurological complication following traumatic damage to the spinal cord with a 25 gauge whitacre spinal needle. Int J Obstet Anesth 1999;8:62-6.
Perlas A. Management of a suspected spinal-epidural hematoma. Tech Reg Anesth Pain Manag 2006;10:62-5.
Horlocker TT. Regional anaesthesia in the patient receiving antithrombotic and antiplatelet therapy. Br J Anaesth 2011;107 Suppl 1:i96-106.
Verniquet AJ. Vessel puncture with epidural catheters. Experience in obstetric patients. Anaesthesia 1980;35:660-2.
Working Party; Association of Anaesthetists of Great Britain & Ireland; Obstetric Anaesthetists′ Association; Regional Anaesthesia UK. Regional anaesthesia and patients with abnormalities of coagulation: The Association of Anaesthetists of Great Britain & Ireland the Obstetric Anaesthetists′ Association Regional Anaesthesia UK. Anaesthesia 2013;68:966-72.
Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia. Anesth Analg 1994;79:1165-77.
Association of Anaesthetists of Great Britain and Ireland, Obstetric Anaesthetists′ Association; Regional Anaesthesia UK; Association of Paediatric Anaesthetists of Great Britain and Ireland, Campbell JP, Plaat F, Checketts MR, et al.
Safety guideline: Skin antisepsis for central neuraxial blockade. Anaesthesia 2014;69:1279-86.
Davis DP, Wold RM, Patel RJ, Tran AJ, Tokhi RN, Chan TC, et al.
The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. J Emerg Med 2004;26:285-91.
Grewal S, Hocking G, Wildsmith JA. Epidural abscesses. Br J Anaesth 2006;96:292-302.
Fraser S, Roberts L, Murphy E. Cauda equina syndrome: A literature review of its definition and clinical presentation. Arch Phys Med Rehabil 2009;90:1964-8.
Baer ET. Post-dural puncture bacterial meningitis. Anesthesiology 2006;105:381-93.
Burke D, Wildsmith JA. Meningitis after spinal anaesthesia. Br J Anaesth 1997;78:635-6.
Burton CV. Lumbosacral arachnoiditis. Spine (Phila Pa 1976) 1978;3: 24-30.
Schneider M, Ettlin T, Kaufmann M, Schumacher P, Urwyler A, Hampl K, et al.
Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesth Analg 1993;76:1154-7.
Tarkkila P, Huhtala J, Tuominen M. Transient radicular irritation after spinal anaesthesia with hyperbaric 5% lignocaine. Br J Anaesth 1995; 74:328-9.
Goodman EJ, DeHorta E, Taguiam JM. Safety of spinal and epidural anesthesia in parturients with chorioamnionitis. Reg Anesth 1996;21:436-41.
Van Diver T, Camann W. Meralgia paresthetica in the parturient. Int J Obstet Anesth 1995;4:109-12.
Cheshire WP, Santos CC, Massey EW, Howard JF Jr. Spinal cord infarction: Etiology and outcome. Neurology 1996;47:321-30.
van de Beek D, Brouwer MC, Thwaites GE, Tunkel AR. Advances in treatment of bacterial meningitis. Lancet 2012;380:1693-702.
Bert AA, Laasberg LH. Aseptic meningitis following spinal anesthesia - A complication of the past? Anesthesiology 1985;62:674-7.
Guyer DW, Wiltse LL, Eskay ML, Guyer BH. The long-range prognosis of arachnoiditis. Spine (Phila Pa 1976) 1989;14:1332-41.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]
|This article has been cited by|
||On Evidence-Based Practice Guideline, Analgesia and Anesthesia in the Intrapartum Period
| ||Barbara A. True,Martha Rider Sleutel |
| ||Journal of Obstetric, Gynecologic & Neonatal Nursing. 2020; |
|[Pubmed] | [DOI]|
||Bilateral Sciatic Neuropathies as a Complication of Positioning During Neuraxial Anesthesia for Cesarean Delivery
| ||Bradley A. Reel,Tolulope A. Odedokun,Daniel B. Simmons,Linda Hong |
| ||A & A Practice. 2019; 13(5): 173 |
|[Pubmed] | [DOI]|
||Lower-limb neurologic deficit after vaginal delivery; a prospective observational study
| ||A. Tournier,A.C. Doremieux,E. Drumez,J. Labreuche,F. Cassim,S. Bartolo,P. Richart,C. Garabedian,D. Subtil |
| ||International Journal of Obstetric Anesthesia. 2019; |
|[Pubmed] | [DOI]|
||Prolonged sensory impairment in the perineal region after painless delivery through lumbar epidural anesthesia
| ||Maiko T Uemura,Takahiro Mezaki,Hiroshi Shibasaki,Ryosuke Takahashi |
| ||Neurology and Clinical Neuroscience. 2018; |
|[Pubmed] | [DOI]|
||Immediate postpartum neurological deficits in the lower extremity: a prospective observational study
| ||A. Richards,T. McLaren,M.J. Paech,E.A. Nathan,E. Beattie,N. McDonnell |
| ||International Journal of Obstetric Anesthesia. 2017; |
|[Pubmed] | [DOI]|