Neurologic Complications of Regional Anesthesia in Obstetrics: A Current Review

 

Introduction

 

For both parturients and anesthesiologists the most feared complication of regional anesthesia is a neurologic deficit. Fortunately, neurologic deficits are very rare, especially in obstetric patients. Most neurological injuries are due to obstetrical, not anesthetic causes. A focused history, physical examination, and laboratory tests are needed to ensure proper diagnosis and treatment. The obstetric and anesthetic causes of neurological deficits will be reviewed.

History/physical examination/laboratory tests

 

A proper history should focus on the exact onset, location, and radiation of symptoms. Was there pain during needle insertion or injection of local anesthetic? Was there a period of full recovery or was the anesthetic block prolonged? Do the symptoms follow a dermatomal or peripheral nerve pattern? Items to inquire about specifically related to OB include: leg position (especially during second stage of labor), duration and degree of hyperflexion of the hips, length of second stage and the use of forceps.

On physical exam, a detailed neurologic assessment must be performed. Careful mapping of symptoms and findings may reveal a pattern consistent with nerve injury involving a single dermatome or peripheral nerve. Areas to check include: sensory and motor tone of the paraspinous muscles (innervated by posterior rami of the nerve root), tenderness to deep palpation of the spinous processes (transmits pressure to epidural space, suggestive of intrapinal mass), sacroiliac joint tenderness or localized areas of erythema or purulence. Detailed documentation in the chart is very important for good patient care and may serve in your future defense.1

Peripheral nerve injuries may occur. The common peroneal nerve is prone to compression at the fibular head during positioning in stirrups. Symptoms include lateral calf paresthesia, dorsal sensory loss between the 1st and 2nd toes, along with foot drop and inversion. Pressure on the lateral femoral cutaneous nerve as it passes under the inguinal ligament produces numbness along the lateral aspect of the thigh. This usually recovers spontaneously within 6 weeks. The femoral nerve may be compressed by the inguinal ligament during flexion of the hip. Symptoms include quadriceps weakness and hyperalgesia in the thigh and calf. The lumbosacral trunk may be injured within the pelvis by the fetal head (especially with forceps or occiput postero-lateral position). Symptoms may be unilateral (75%) or bilateral (25%) and may affect the quadriceps, hip adduction and cause foot drop.2,3

The preliminary differential diagnosis will suggest which tests are needed. If fever accompanies back pain or headache, a white blood cell count and CSF evaluation (septic meningitis) are needed. If symptoms are isolated to a single nerve root, CT or MRI will be helpful. History of a recent regional anesthetic does not prove causation. An occult herniated disc may become symptomatic after positioning and pushing during delivery. Any bilateral symptoms or deficits warrant a CT or MRI scan to determine compression by an intraspinal mass (e.g. blood or abscess). CT scan is superior to MRI for detection of intracranial blood, especially subarachnoid hemorrhage, and for defining cortical bone structure. MRI is superior for intracranial and intraspinal soft tissue lesions. Gadolinium enhanced MRI increases detection of neoplastic and inflammatory lesions (e.g. abscess).4

Electrophysiologic testing may also be helpful. EMG can help document the time and location of injury. After denervation, muscle fibers begin to discharge spontaneously, but changes are not seen until 2-3 weeks after injury. Thus, an abnormal EMG obtained within the first week following a regional anesthetic is useful for determining preexisting disease. If an interval change occurs 4-6 weeks later, then the injury occurred around the time of delivery. Injury at the level of the nerve root should affect both the anterior and the posterior rami. If the paraspinous area (supplied by the posterior ramus) is not affected, then the level of nerve injury is distal to the nerve root and not caused by central neuraxial anesthesia. Nerve conduction-velocity studies can provide immediate information about both motor and sensory nerves. Lesions proximal to the dorsal root ganglia do not affect the sensory potential and thus help to distinguish radicular from peripheral nerve disease. Somatosensory evoked potentials (SSEPs) monitor the dorsal column of the spinal cord and are a key, objective test of sensory function. SSEPs are sensitive to spinal cord damage produced by compression, mechanical distraction and ischemia. Motor evoked potentials (MEPs) measure the descending motor pathways in the anterior spinal cord. A magnetic field is used to stimulate the motor cortex with responses measured in the peripheral muscles. Although not widely available, MEPs are a superb, objective test to assess motor pathways.5

Obstetric related neurological deficits

 

Neurologic injury related to labor and delivery occurs more commonly than anesthetic related deficits. Parturients who do not receive regional or general anesthesia may experience compression nerve injury, or rarely, an ischemic spinal cord injury. The incidence of permanent neurological deficits is as high as 1/ 2,100 (1.6-4.8/10,000).2,6,7 Past obstetric practice allowed protracted labor and the frequent use of forceps, which contributed to lumbosacral plexus injury. The fetal head may also compress and injure the lumbosacral plexus as it crosses the ala of the sacrum or the posterior brim of the pelvis. This injury is more common in nulliparous women with platypelloid pelvises, large babies, cephalopelvic disproportion, vertex presentation and forceps delivery.2,3 Compressive nerve injuries of this type may involve multiple root levels and appear as injuries to the femoral or obturator nerves with sensory impairment in the 4th and 5th lumbar dermatomes.

Femoral nerve injury decreases sensation over the anterior thigh and medial calf and impairs quadriceps strength, hip flexion and patellar reflex. Proximal lesions at the level of the lumbosacral plexus also may decrease hip flexion due to iliopsoas weakness.

The obturator nerve can be compressed against the lateral pelvic wall or during its course in the obturator canal. This results in decreased sensation over the medial thigh, weakness of the hip adductors and decreased ability to internally rotate.

Ischemic injury may also produce neurologic deficits. The spinal cord may become ischemic during periods of hypotension or by compression of its blood supply. The anterior part of the lower spinal cord is supplied by either the artery of Adamkiewicz (85%) or a branch of the iliac artery (15%).8 The feeder vessels from the iliac artery may be compressed as they cross the lumbosacral trunk. The artery of Adamkiewicz supplies the anterior 2/3rds of the spinal cord and injury results in the loss of motor function (anterior horn), as well as pain and temperature (spinothalamic tract). This is known as anterior spinal artery syndrome. The dorsal column, which carries vibration and joint sensation, is supplied by the vertebral arteries and are therefore spared. Arteriovenous malformation within the spinal cord may also rarely cause paraplegia. The mechanism of injury is increased spinal venous pressure, which predisposes to arterial stasis during periods of moderate hypotension or compression.

Anesthesia related neurologic deficits

 

Serious neurological complications related to regional anesthesia are fortunately very rare. Neurological complications may be due to direct nerve trauma, severe hypotension, cardiac arrest, equipment problems, adverse drug effect, administration of the wrong drug and wrong site of administration.

Direct trauma to nervous tissue may occur at the level of the spinal cord, nerve root, or peripheral nerve. Two thirds of anesthesia related neurological complications are associated with either paresthesia (direct nerve trauma) or pain during injection (intraneuronal location).9 Epidural needle insertion is most likely to contact a nerve root.

Spinal needles may touch nerve roots, or directly injure the spinal cord. If the patient reports localized pain with insertion of an epidural or spinal needle or catheter, stop immediately! Transient paresthesia with threading an epidural catheter is common. Anatomic variation may alter landmarks and place nervous tissue at risk for injury. The spinal cord usually terminates at the 1st lumbar vertebrae (60%) but may go as low as the L2-3 space (10%). In addition, the superior iliac crest is usually at the L4 spinous process or L4-5 interspace (79%), however, it may be as high as the L3-4 interspace (4%).10

Auroy et al. prospectively monitored neurologic complications in more than 103,000 regional anesthetics.9 All deficits were present within 48 hours after anesthesia. Most (29/34) were transient, with recovery occurring between 2 days and 3 months. Spinal anesthesia was significantly more likely to result in both neurologic injury (5.9 vs. 2/10,000) and radiculopathy (4.7 vs. 1.7/10,000), compared to epidural anesthesia. All radiculopathies resolved except one (spinal). Of the patients who developed deficits without paresthesia, 12/13 occurred following spinal anesthesia, most with lidocaine 5%. In this series only one patient (who was elderly and experienced prolonged hypotension) became paraplegic.9

Scott et al monitored 505,000 epidural blocks in parturients, finding only 38 single root neuropathies (0.75/10,000). All deficits resolved by 3 months except for one.11 In a similar study involving 123,000 regional anesthetics in parturients, 46 cases of single nerve root neuropathy were reported (3.7/10,000), with complete recovery in all patients by 3 months.12

Cardiac arrest occurred significantly more commonly following spinal anesthesia compared to epidural (6.4 vs. 1/10,000). While fatal cardiac arrest occurred in elderly patients undergoing hip arthroplasty (5/6), most recovered without sequelae (25).9 In obstetric patients, there were 3 cardiac arrests in 505,000 epidurals (0.06/10,000). Two patients recovered without sequelae and one had brain damage after severe hypotension following a `top-up'.12 Intravascular administration of bupivacaine will result in cardiac arrest. Bupivacaine binds avidly to the sodium channel in a `fast in - slow out' manner. Thus, cardiac resuscitation is extremely difficult and often requires cardio-pulmonary bypass until the bupivacaine dissociates from the sodium channel and is metabolized. Bretylium has been suggested for resuscitation during bupivacaine-induced cardiac arrest.

Epidural catheters may rarely break or shear. Catheters are never to be withdrawn through the needle. If part of a catheter is left in a patient, the patient should be informed. However, no surgery or attempts to retrieve the catheter are warranted unless there are persistent neurologic symptoms.

The epidural space is remarkably tolerant to chemical contamination. However, the subarachnoid space is not. Drugs that have been accidentally injected into the epidural space without sequelae include thiopental, magnesium and TPN. Only undiluted KCL produced permanent paraplegia following epidural administration.

Epidural hematoma is another feared, but rarely seen complication of regional anesthesia (1/150,000-250,000) in healthy patients.13 Most epidural hematomas following regional anesthesia occurred in patients with hemostatic abnormalities, particularly those on anticoagulants. Low molecular weight heparins have been responsible for over 35 epidural hematomas following regional anesthesia and should be considered a strong relative contraindication. The symptoms of epidural hematoma are bilateral leg weakness, urinary incontinence and loss of rectal sphincter tone. These severe neurologic deficits may be preceded by sharp pain in the back or legs with progression over a few hours. Prolonged motor paralysis without regression of block should raise suspicion. Stat CT or MRI is indicated. Symptomatic epidural hematoma must be decompressed surgically within 6 hours for the best chance of full recovery.

Epidural abscess is rare, accounting for 0.2-1.2/10,000 tertiary hospital admissions. Epidural abscess is usually due to infection in the body seeding the epidural space. In one review, epidural anesthesia was associated with only in 1 in 39 epidural abscesses.14 while epidural anesthesia was unrelated to 35 abscesses in another review. Symptoms of epidural abscess usually develop a few days to a few weeks after delivery. In a series of over 500,000 epidurals, only one patient (diabetic) developed an abscess, albeit 11 months after delivery.11 Symptoms include fever, malaise, and headache and back pain at the level of the infection. Pain will be found on deep palpation over the site. White blood cell count will be elevated. Progression of symptoms to nerve root pain usually takes 1-3 days. Neurologic deficits will progress as the spinal cord is compressed including: lower extremity pain, weakness, bowel and bladder dysfunction and paraplegia. Surgical treatment is necessary.

Conclusion

 

In summary, neurologic complications due to regional anesthesia are very rare in obstetric patients. Although it is more likely that neurologic complaints are due to factors associated with labor and delivery (1.6-4.8/10,000), it is imperative to explore the possible deficits related to regional anesthetic techniques (0-1.2/10,000). A careful history, physical exam, laboratory testing and use of imaging techniques will help to ensure an accurate diagnosis and good outcome.

Dr. Mark Zakowski will present more details of this topic at the SOAP annual meeting in a refresher course lecture. For more details on this topic including tables and figures, refer to Obstetric Anesthesia, Norris ed, Chapter 39 "Postoperative Complications Associated with Regional Anesthesia in the Parturient" by Dr. Zakowski.

References

 

  1. Zakowski MI. Postoperative complications associated with regional anesthesia in the parturient. In Obstetric Anesthesia, 2nd ed. Ed Norris M, Lippincott Williams & Wilkins, Philadelphia, 1999.
  2. Cole JT. Maternal obstetric paralysis. Am J Obstet Gynecol 1946:52:372-86.
  3. Graham JG. Neurological complications of pregnancy and anaesthesia. Clin Obstet Gynecol 1982:9:333-50
  4. Chan S et al. CT and MRI. In Rowland LP ed, Merritt's textbook of neurology, Baltimore, Williams & Witkins, 1995:59-66.
  5. Lange DJ Trojaborg W. Electromyography and nerve conduction studies in neuromuscular disease. In Rowland LP, Ed. Merritt's textbook of neurology, Baltimore, Williams & Witkins, 1995:77.
  6. Tilleman AJB. Traumatic neuritis in the puerperium. Am J Obstet Gynecol 1935:29:660-6
  7. Holdcroft A et al. Neurological complications associated with pregnancy. Br J Anaesth 1995:75:522
  8. Lazorthes G et al. La vascularization de la moelle epiniere (etude anatomique et physiologique) Rev Neurol 1962:106:535-57
  9. Auroy Y Narchi P, Messiah A, et al Serious complications related to regional anesthesia: results of a prospective survey in France. Anesthesthesiology 1997:87:479-86
  10. Render CA. The reproducibility of the iliac crest as marker of lumbar spine level. Anaesthesia 1996:51:1070
  11. Scott DB Hibbard BM. Serious non-fatal complications associated with extradural block in obstetric practice. Br J Anaesth 1990:64:537-41.
  12. Scott DB Tunstall ME Serious complications associated with epidural/spinal blockade in obsterics: a two-year prospective study. Int J Obstet Aanesth 1995:4:133-9.
  13. Horlocker TT Regional anesthesia and analgesia in the patient receiving thromboprophylaxis. [editorial] Reg Anesth 1996:21:503-7.
  14. Baker AS et al. Spinal epidural abscess. N Engl J Med 1975:293:463.

Mark Zakowski, MD
Director of Obstetric Anesthesia
Cedars-Sinai Medical Center
Los Angeles, CA

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  • Baker AS et al. Spinal epidural abscess. N Engl J Med 1975:293:463.
  • Mark Zakowski, MD
    Director of Obstetric Anesthesia
    Cedars-Sinai Medical Center
    Los Angeles, CA