Abstract
Neurologic complications of childbirth may be associated with neuraxial analgesia and anesthesia or may result from childbirth itself. Complications of neuraxial anesthesia may be immediate, such as an unexpectedly high block or seizures after unintentional intravenous injection of local anesthetic, or they may be delayed. Immediate complications of neuraxial anesthesia are described in Chapter 23 ; here the discussion is focused on neurologic sequelae.
Although neurologic disorders after childbirth are more likely to have obstetric than anesthetic causes, neuraxial anesthesia is frequently suspected and often blamed. When these injuries occur, a careful history and neurologic examination, together with diagnostic aids such as electromyography, nerve conduction studies, and imaging techniques, can localize the lesion and differentiate obstetric from anesthetic causes. For example, it should be possible to distinguish by simple clinical means between a mononeuropathy, which is likely to have an obstetric cause, and a radiculopathy, which might result from neuraxial blockade. Accurate and prompt diagnosis is essential to increase the likelihood of the best possible outcome.
Keywords
Neurologic complications, Nerve injury, Nerve trauma, Nerve palsy, Neuraxial block complications, Epidural hematoma, Obstetric neurologic injury
Chapter Outline
The Incidence of Neurologic Sequelae, 752
Peripheral Nerve Palsies, 753
Compression of the Lumbosacral Trunk, 755
Obturator Nerve Palsy, 755
Femoral Nerve Palsy, 755
Meralgia Paresthetica, 756
Sciatic Nerve Palsy, 757
Peroneal Nerve Palsy, 757
Compression as a Risk Factor for Peripheral Neuropathy, 757
Postpartum Bladder Dysfunction, 757
Central Nervous System Lesions, 758
Neurologic Sequelae of Dural Puncture, 758
Trauma to Nerve Roots and the Spinal Cord, 758
Space-Occupying Lesions of the Vertebral Canal, 761
Infection, 762
Vascular Disorders, 767
Chemical Injury, 767
Vulnerable Patients, 769
Risk Management and Follow-Up, 770
Diagnosis of Possible Neurologic Injury, 771
Neurologic complications of childbirth may be associated with neuraxial analgesia and anesthesia or may result from childbirth itself. Complications of neuraxial anesthesia may be immediate, such as an unexpectedly high block or seizures after unintentional intravenous injection of local anesthetic, or they may be delayed. Immediate complications of neuraxial anesthesia are described in Chapter 23 ; here the discussion is focused on neurologic sequelae.
Although neurologic disorders after childbirth are more likely to have obstetric than anesthetic causes, neuraxial anesthesia is frequently suspected and often blamed. For example, Tubridy and Redmond described seven women referred with neurologic symptoms after childbirth, all of which had been attributed to epidural analgesia. The women suffered from brachial neuritis, peroneal neuropathy, femoral neuropathy, neck strain, and leg symptoms for which there was no obvious physical cause. In such circumstances, a careful history and neurologic examination, together with diagnostic aids such as electromyography, nerve conduction studies, and imaging techniques, can localize the lesion and differentiate obstetric from anesthetic causes. For example, it should be possible to distinguish by simple clinical means between a mononeuropathy, which is likely to have an obstetric cause, and a radiculopathy, which might result from neuraxial blockade. Accurate and prompt diagnosis is essential to increase the likelihood of the best possible outcome.
The Incidence of Neurologic Sequelae
Patients frequently ask obstetricians and anesthesia providers about the incidence of complications of neuraxial anesthesia. However, even if accurate data were available, the question has no true answer. The incidence of neurologic complications varies widely according to local practice and the skill and training of the practitioners. Some older surveys are based on accurate local records, but the data relate to a time when obstetric and anesthetic practices, equipment, and drugs were radically different. The incidence of serious complications is now too low to be estimated accurately on a local basis. Nonetheless, anesthesia providers have a duty to inform patients of the complications associated with a proposed procedure and are expected to give some estimate of the level of risk.
Obstetric Surveys
The reported incidence of neurologic deficits in obstetric patients varies widely depending on the source and the complications that are being measured. Many surveys have attempted to assess the incidence of neurologic complications of neuraxial anesthesia, but these surveys share common limitations, including low response rates, lack of control groups who did not receive neuraxial anesthesia, and inaccurate diagnosis ( Box 31.1 ). Moreover, bias is created when more attention is paid to patients who received neuraxial blockade than to those who did not. Some of the more relevant surveys are listed in Table 31.1 . Although each survey is distinct in its population, measurements, and reporting, some generalizations can be made. Most of the neurologic complications in these reports were transient, most occurred in patients who labored, and only a very small minority were attributable to neuraxial anesthesia. Peripheral nerve damage was more common than central cord or plexus damage.
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Poor response rate
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Positive reporting bias
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Absence of controls without neuraxial anesthesia
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Greater attention given to those who received neuraxial anesthesia
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Inadequate investigation and lack of accurate diagnosis
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Variable skill and care of obstetric and anesthetic providers
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Older surveys relate to outdated obstetric and anesthetic practices
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Lack of statistical power to assess incidence of rare disorders
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Inaccurate counting of numerator and denominator
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Likelihood of missing cases that arise after hospital discharge
| Study | Type of Study | Population | Number of Neurologic Deficits (Risk Ratio) |
|---|---|---|---|
| Ong et al., 1987 | Medical record review of all patients, interview of those receiving anesthesia in one center (1975–1983) | 23,827 deliveries | 45, all transient (1/530) |
| 12,964 inhalational or no analgesia | 5 (1/2593) | ||
| 9403 epidural procedures | 34 (1/277) | ||
| 1460 general anesthetics and other | 6 (1/243) | ||
| Scott and Hibbard, 1990 | Retrospective multicenter review (1982–1986), no control group | 505,000 epidural procedures |
|
| MacArthur et al., 1992 | Questionnaire sent in 1987 to mothers delivering in one center (1978–1985) | 11,701 women (39%) who responded | Tingling/paresthesias |
| 4766 epidural procedures | 143 upper limb, 23 lower limb | ||
| 6935 no epidural procedures | 150 upper limb, 3 lower limb | ||
| Palot et al., 1994 | Questionnaire listing possible complications sent to hospitals with obstetric beds (1988–1993), no control group | 288,351 epidural procedures |
|
| Scott and Tunstall, 1995 | Prospective multicenter review (1990–1991), no control group |
|
|
| 14,856 spinal procedures | 8 (1/1857) | ||
| Holdcroft et al., 1995 | Regional community and hospital-based trawl (1991–1992) | 48,066 deliveries | 10 new neurologic complications (1/4807) |
| 34,430 no neuraxial block | 1 foot drop, 1 cervical nerve lesion (1/17,215) | ||
| 13,007 epidural procedures | 1 paresthesia of nerve root distribution (1/13,007) (Disorders unrelated to anesthesia: 2 cranial nerve palsies, 1 hypotensive cord damage; 5 peripheral nerve lesions) | ||
| 629 spinal procedures | 0 | ||
| Paech et al., 1998 | Prospective local audit (1989–1994), no control group | 10,995 epidural procedures | 1 traumatic “mononeuropathy” (1/10,995) |
| Holloway et al., 2000 | Retrospective multicenter trawl, elastic time frame, no control group | 29,698 spinal procedures | 4 unrelated to anesthesia (3 meralgia paresthetica, 1 peroneal neuropathy), 10 ?root damage, 1 conus damage, 22 uncertain (overall incidence ?1/986) |
| 12,254 CSE procedures | 5 unrelated to anesthesia (1 femoral neuropathy, 2 foot drop, 2 paresthesia), 6 root damage, 1 meningitis, 1 conus damage, 6 uncertain (overall incidence ?1/901) | ||
| Dar et al., 2002 | Prospective local audit of immediate symptoms (1998–1999) | 1376 vaginal deliveries without anesthesia (random sample of 21 examined + 1 complaint) | 4 peripheral neuropathy, 1 foot drop, 2 vague (1/3) |
| 2615 regional blocks (all followed up) | 21 had neurologic symptoms | ||
| 1782 vaginal deliveries | 7 peripheral neuropathies, 1 foot drop, 3 vague (1/162) | ||
| 833 cesarean deliveries | 8 numb areas, 2 vague (1/83) | ||
| Auroy et al., 2002 | Prospective multicenter survey, no control group | 29,732 epidural procedures | 0 |
| 5640 spinal procedures | 2 “peripheral neuropathy” | ||
| Moen et al., 2004 | National postal survey and search of administrative files (1990–1999), no control group | 205,000 epidural procedures | 1 epidural hematoma (HELLP), 1 epidural abscess, 2 cord damage, 2 intracranial subdural hematoma, 1 abducent nerve palsy (1/29,286) |
| 50,000 spinal procedures | 1 spinal hematoma (HELLP), 1 cord damage (1/25,000) | ||
| Wong et al., 2003 | Prospective 1-year survey (1997–1998) at a single institution | 5603 laboring patients (72% with neuraxial blocks) and 454 nonlaboring patients | 66 nerve injuries (63 in laboring, 3 in nonlaboring). Lateral femoral cutaneous nerve (24) and femoral nerve (22) injuries most common |
| Cook et al., 2009 | National audit of major complications of neuraxial blockade over 1 year (unstated), obstetric and nonobstetric, no control group | 329,425 obstetric procedures | 1 epidural abscess, 2 nerve injury, 1 unknown |
| 161,550 epidural procedures |
| ||
| 133,525 spinal procedures | Possible harm per 100,000 (95% CI), 1.5 (1–5.4) | ||
| 25,350 CSE procedures | Possible harm per 100,000 (95% CI), 3.9 (1–22) | ||
| D’Angelo et al., 2014 | Prospective multicenter survey (2004–2009) |
|
|
One of these reports from Leeds in the United Kingdom involved 3991 women who delivered in one center in a 1-year period. Twenty-one women presenting with symptoms after neuraxial blockade were matched with 21 asymptomatic control patients who had also received neuraxial blockade and 21 additional women who had not. Only one woman who had not had a neuraxial block had symptoms, and she was found to have foot drop after a vacuum extraction. Typical peripheral neuropathies occurred among those who delivered vaginally; sacral numbness was most commonly detected after cesarean delivery. All changes were transient, and none could be attributed to neuraxial anesthesia. Similar neurologic deficits were detected among the randomly selected, asymptomatic 21 control patients who had not undergone an anesthetic intervention. In contrast, negligible deficits could be detected among the 21 asymptomatic control women who had undergone an anesthetic intervention. These results demonstrate that minor neurologic deficits are to be found postpartum quite frequently if sought, but only those who have had anesthetic intervention are likely to complain or be questioned.
A prospective survey among 6057 women who delivered in one year in Chicago corroborates the findings of the Leeds study. The incidence of lower limb nerve injuries was approximately 1% (24 lateral femoral cutaneous nerve, 22 femoral nerve, 3 peroneal nerve, 3 lumbosacral plexus, 2 sciatic nerve, 3 obturator nerve, and 5 radicular injuries). Significant risk factors identified by logistic regression analysis included nulliparity and a prolonged second stage of labor but not neuraxial anesthesia.
A UK national audit of neuraxial blocks, without controls, published in 2009, found that the risk for major complications was 6- to 14-fold higher for perioperative than for obstetric procedures. Among the obstetric patients, the risk was highest for combined spinal-epidural (CSE), intermediate for spinal, and lowest for epidural procedures. Finally, the Serious Complication Repository (SCORE) project sponsored by the Society for Obstetric Anesthesia and Perinatology collected data from 30 institutions and more than 250,000 neuraxial blocks in the United States over a 5-year period (2004 to 2009); the incidence of anesthesia-related nerve injury for obstetric patients was approximately 1 in 35,000 deliveries. Four cases of epidural abscess/meningitis and a single case of epidural hematoma were reported.
Several conclusions can be drawn from these surveys. Despite an increased cesarean delivery rate in the past several decades, obstetric palsies still occur, and the reported frequency of neurologic sequelae depends on how hard one seeks them. The risk for transient mild deficits after childbirth may be quite high. A true figure for anesthetic complications cannot be calculated, even from thorough surveys, because (1) the diagnosis is rarely accurate and (2) definitions, severity, and duration are often ill defined. Table 31.1 demonstrates a variation in the incidence of neurologic sequelae from 1 in 3 for mild symptoms with no neuraxial block to 1 in 200,000 for spinal hematoma.
Other Surveys
Modern surveys of neurologic complications of spinal and epidural anesthesia among nonobstetric populations may yield more reliable results but still lack sensitivity to detect all potential problems and are commonly conducted in relatively elderly and sick populations. Auroy et al., Moen et al., Cook et al., and Pitkanen et al. surveyed mixed populations and found a lower incidence of serious sequelae in obstetric than in nonobstetric patients. It is therefore invalid to extrapolate findings from one population to the other. The reported risk for neurologic problems varies greatly with the patient population, local practice and skill, completeness of detection, and inclusion criteria. Hence, it is difficult to put any firm figure on the risk for neurologic complications after neuraxial anesthesia in obstetric patients.
Peripehral Nerve Palsies
Postpartum nerve injury is often assumed to be caused by neuraxial anesthesia, but peripheral nerve palsies, which generally have obstetric causes, are much more common than anesthesia-related injury, with a reported incidence between 0.6 and 92 per 10,000. They may arise from compression in the pelvis by the fetal head, or from more distal compression, the signs of which may be overlooked in the presence of neuraxial anesthesia. Proposed risk factors for postpartum neuropathies include a prolonged second stage of labor, difficult instrumental delivery, nulliparity, and prolonged use of the lithotomy position.
Reference to the distribution of spinal dermatomes and peripheral nerve sensory innervation demonstrates the distinction between peripheral and central lesions ( Fig. 31.1 ). Central lesions are most often bilateral, create weakness or paralysis from the site of the lesion distally, are often associated with autonomic dysfunction, and may be associated with upper motor neuron signs such as spasticity, brisk reflexes, and bowel and bladder dysfunction. In contrast, peripheral nerve lesions are typically unilateral, with weakness or paralysis limited to a single muscle or muscle group that the peripheral nerve innervates. Peripheral injuries create sensory deficits in the distribution of the specific nerve, while central lesions typically involve multiple dermatomes with a defined sensory level. Spinal nerve root lesions are also manifested by weakness that involves several lower extremity joints and movements ( Fig. 31.2 ). Obstetric peripheral nerve injuries include compression of the lumbosacral trunk and palsies of the obturator, femoral, lateral femoral cutaneous, sciatic, and peroneal nerves.
Compression of the Lumbosacral Trunk
Compression of the lumbosacral trunk by the fetal head at the pelvic brim ( Fig. 31.3 ) preferentially affects the more medial fibers that make up the peroneal rather than the tibial nerve. In addition to weakness that predominantly affects ankle dorsiflexion (foot drop), compression of the lumbosacral trunk produces sensory disturbance mainly involving the L5 dermatome (see Fig. 31.1 ). This palsy most often results from cephalopelvic disproportion and is therefore typically seen after prolonged labor and difficult vaginal delivery.
Obturator Nerve Palsy
The obturator nerve is susceptible to compressive injury as it crosses the brim of the pelvis and within the obturator canal (see Fig. 31.3 ). The mother may complain of pain when the damage occurs, followed by weakness of hip adduction and internal rotation, with sensory disturbance over the medial thigh (see Fig. 31.1 ). She may have an abnormal gait secondary to weakness of thigh adduction. Cases are reported after both labor and cesarean delivery ; three of 66 new nerve injuries detected in a prospective study by Wong et al. were obturator nerve injuries. The most likely cause of obturator nerve palsy is compression of the nerve between the pelvis and fetal head or forceps applied to the fetal head.
Femoral Nerve Palsy
The femoral nerve does not enter the true pelvis and is therefore not vulnerable to compression by the fetal head but rather is vulnerable to stretch injury as it passes beneath the inguinal ligament. The femoral nerve may be injured proximal to or at the inguinal ligament. Proximal injuries are associated with weakness of hip flexion, whereas more distal injuries spare the motor supply to the iliopsoas muscle. The patient with a femoral neuropathy may walk satisfactorily on a level surface but may be unable to climb stairs; the patellar reflex is diminished or absent. Although the incidence of femoral nerve palsy has decreased as a result of changes in obstetric management (e.g., fewer deliveries with prolonged second stage), it is still one of the most common obstetric nerve injuries. Approximately one-third of the postpartum palsies detected by Wong et al. were femoral nerve palsies. Dar et al. detected five cases in their small population, although the symptoms were transient. Damage may result from prolonged flexion, abduction, and external rotation of the hips during the second stage of labor and also during procedures conducted in an excessive lithotomy position. The hips should therefore never remain continuously flexed during the second stage of labor.
Meralgia Paresthetica
Meralgia paresthetica is a neuropathy of the lateral femoral cutaneous nerve, a purely sensory nerve also known as the lateral cutaneous nerve of the thigh. First described more than 100 years ago, meralgia paresthetica is commonly encountered in pregnancy and childbirth. It is the most common nerve injury of pregnancy. The palsy may arise both during pregnancy, typically at about 30 weeks’ gestation, and intrapartum, in association with increasing intra-abdominal pressure. The distribution is unlike that of a nerve root lesion (see Fig. 31.1 ), yet the disturbance is commonly misattributed to neuraxial blockade. Meralgia paresthetica manifests as numbness, tingling, burning, or other paresthesias affecting the anterolateral aspect of the thigh. The most likely cause is entrapment of the nerve as it passes around the anterior superior iliac spine beneath or through the inguinal ligament, where its vulnerability is increased by a gravid uterus or by retractors used during pelvic surgery. The compressive effect of edema may also contribute. The condition can be expected to resolve after childbirth.
Sciatic Nerve Palsy
Sciatic nerve palsy arises from compression of the nerve, usually in the buttock. It is not commonly mentioned in surveys or generally recognized as a complication of childbirth, possibly because it is mistaken for a lesion of the lumbosacral trunk. It gives rise to loss of sensation below the knee with sparing of the medial leg, and loss of movement below the knee. Posterior cutaneous nerve and gluteal function are preserved, implying damage distal to the lumbosacral plexus, where the gluteal nerves branch off the sciatic nerve ( Fig. 31.4 ). Three cases out of 66 new nerve injuries were detected by Wong et al. It has occurred during childbirth with neuraxial blockade, either from sitting in one position too long or from a hip wedge misplaced during cesarean delivery. It has also been reported after iliac artery balloon placement for cesarean delivery in a woman with placenta percreta.
Peroneal Nerve Palsy
The common peroneal nerve is vulnerable to compression as it passes around the head of the fibula below the knee. It is also susceptible to damage while it still forms part of the sciatic nerve as it leaves the pelvis. When the peroneal nerve is damaged at the knee, there is sensory impairment on the anterolateral calf and the dorsum of the foot. Foot drop may be profound, with steppage gait and weak ankle eversion, but plantar flexion and inversion at the ankle are preserved. Peroneal nerve palsy may be caused by prolonged squatting, sometimes popular in “natural childbirth,” by excessive knee flexion for any reason, by compression of the lateral side of the knee against any hard object, even the patient’s hand, and by prolonged use of the lithotomy position. The incidence of peroneal nerve palsy is lower than that of lateral femoral cutaneous and femoral nerve palsy.
Compression as a Risk Factor for Peripheral Neuropathy
During pregnancy, nerve compression caused by edema may be a factor in the genesis of several peripheral neuropathies, such as carpal tunnel syndrome, Bell’s palsy, and meralgia paresthetica. Neuraxial blockade may indirectly contribute to compression injuries because it may decrease the ability of a woman to perceive that her legs are in a position that contributes to compression-induced neuropathy. Practices that providers should observe to lessen the risk for compression-induced neuropathy are listed in Box 31.2 .
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Be mindful of patient positioning that could contribute to nerve compression, particularly with neuraxial blockade.
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Avoid prolonged use of the lithotomy position; regularly reduce hip flexion and abduction.
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Avoid prolonged positioning that may cause compression of the sciatic or peroneal nerve.
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Place the hip wedge under the bony pelvis rather than the buttock.
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Use low-dose local anesthetic/opioid combinations during labor to allow maximum mobility.
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Encourage the parturient to change position regularly.
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Ensure that those caring for women receiving low-dose local anesthetic/opioid combinations understand that numbness or weakness may be signs of nerve compression; such symptoms should prompt an immediate change of position.
Postpartum Bladder Dysfunction
There are several mechanisms by which bladder function may be disturbed postpartum ( Fig. 31.5 ). In theory, neuraxial blockade (1) may provoke the need for bladder catheterization with increased risk for infection, (2) may allow bladder distention to go undetected, and (3) on very rare occasions, may be associated with cauda equina syndrome (see later discussion). However, several postpartum studies of bladder function have found no association with neuraxial analgesia or only a weak correlation between epidural analgesia and an increased residual volume immediately postpartum. In contrast, a prolonged second stage of labor, instrumental delivery, and perineal damage have been identified as significant factors for postpartum bladder dysfunction. No association has been found between epidural analgesia and stress incontinence or urinary frequency.
Central Nervous System Lesions
Lesions of the central nervous system (CNS) after childbirth have complex causes ( Fig. 31.6 ), and may be classified as traumatic (to nervous tissue, meninges, or blood vessels), infectious, ischemic, or chemical (to nervous tissue or meninges). Anesthesia providers should bear in mind that even central lesions may have causes other than neuraxial block, for example a prolapsed intervertebral disc. Apart from sequelae of dural puncture, serious iatrogenic complications related to neuraxial analgesia and anesthesia are remarkably rare.
Neurologic Sequelae of Dural Puncture
The subject of post–dural puncture headache is discussed in detail in Chapter 30 . Other neurologic sequelae of dural puncture include meningitis (see later discussion), cranial nerve palsies, and subdural hematoma. These often present as headache but are distinct from disorders that should be included in the differential diagnosis for postpartum headache, including tension/stress and migraine headaches, cortical vein and venous sinus thrombosis, preeclampsia, hypertensive encephalopathy, intracerebral or subarachnoid hemorrhage, internal carotid artery dissection, and posterior reversible encephalopathy syndrome. It can be difficult to distinguish post–dural puncture headache from other serious causes of headache because signs and symptoms overlap.
Cranial Nerve Palsy
Major loss of cerebrospinal fluid (CSF), usually following unintentional dural puncture with a large-bore needle, may cause a number of cranial nerve palsies; those affecting cranial nerves VI, VII, and VIII are the most frequently reported. Because of its long course within the cranium, the abducens nerve (VI) is the most vulnerable. All cranial nerve palsies require prompt PDPH treatment (e.g., epidural blood patch), but even after the blood patch recovery may be delayed. In the case of cranial nerve VIII dysfunction, tinnitus may not resolve. Trigeminal nerve dysfunction is usually a transient effect of high neuraxial blockade, but trigeminal and facial nerve palsies have also been reported in relation to post–dural puncture headache and subdural hematoma.
Cranial Subdural Hematoma
More seriously, reduced CSF pressure may cause rupture of bridge meningeal veins and result in cranial subdural hematoma, a rare but potentially fatal condition. Palot et al. identified one case in 288,351 obstetric epidural procedures. In 2000, Loo et al. identified eight cases in their systematic review of published cases of neurologic complications in obstetric regional anesthesia. Although commonly believed to result only from dural puncture with a large-bore needle or a cutting spinal needle, subdural hematoma requiring craniotomy has been reported after puncture with a small-gauge, pencil-point spinal needle and after an unintentional dural puncture that had been appropriately treated with an epidural blood patch. A thorough review of 56 cases of subdural hematoma in obstetric patients who received neuraxial blocks (34 epidural, 20 spinal, 2 CSE) published in 2016 showed that predisposing risk factors such as coagulation disorders, aneurysms or arteriovenous malformations, or head trauma were present in only a minority of patients. Persistent headache was present in more than 80% of cases, and focal neurologic signs were present in nearly 70%. Whenever headache persists after treatment with an epidural blood patch (particularly if the headache is accompanied by altered consciousness, seizures, or other focal neurologic findings), magnetic resonance imaging (MRI) is warranted to exclude subdural hematoma, which may be fatal without urgent surgery.
Trauma to Nerve Roots and the Spinal Cord
Insertion of a spinal needle or epidural catheter may be accompanied by paresthesia that is sometimes painful. However, such a paresthesia is neither sensitive nor specific for nerve injury. If a paresthesia is encountered, advancement of the needle or catheter should be halted. It is generally deemed appropriate to then continue spinal or epidural catheter placement after the paresthesia subsides. Continued paresthesias should prompt removal and redirection of the needle. Although a flexible catheter is unlikely to do lasting damage to a nerve root in the epidural space, nerve roots in the subarachnoid space are more vulnerable.
Trauma Associated with Attempted Epidural Catheter Insertion
An epidural catheter may injure nerve roots either because it is inappropriately rigid or because an undue length is advanced and ensnares a root. A catheter seemingly advanced into the epidural space may lodge in an intervertebral foramen or even pass into the paravertebral space. In rare instances, the epidural catheter and the artery of Adamkiewicz share the same foramen. If the epidural catheter is stiff enough to compress the artery within the unyielding foramen, the blood supply to the spinal cord may be impaired. This is a possible cause of anterior spinal artery syndrome. Clinical reports indicate that the condition resolves rapidly and completely if the catheter is withdrawn before permanent damage has occurred.
Injury to the spinal cord may result from attempted identification of the epidural space in the presence of a tethered spinal cord or as a result of unintentional dural puncture at a higher-than-anticipated interspace (see later discussion). Patients with spina bifida occulta may safely undergo both epidural and spinal anesthesia as the spinal cord is rarely tethered in true spina bifida occulta (see Chapter 47 ). However, if there is concern for occult spinal dysmorphism, which is more frequently associated with a tethered cord, it is prudent to obtain a lumbar MRI before initiating a neuraxial procedure. Insertion of an epidural catheter in an anesthetized patient increases the risk for spinal cord damage, and catastrophic injury may occur with injection of fluid into the substance of the spinal cord.
Trauma Associated with Spinal Anesthesia
Insertion of a spinal needle below the level of the spinal cord sometimes causes brief radiating pain or paresthesia, which may be associated with persistent paresthesia in the same dermatomal distribution. Prolonged symptoms involving more than one spinal segment suggest damage to the spinal cord itself. Damage to the terminal portion of the cord (the conus medullaris) without intracord injection has also been reported in healthy conscious parturients receiving spinal or CSE anesthesia using a pencil-point needle. Typically, the patient complains of pain on needle insertion before any fluid is injected, often followed by the normal appearance of CSF from the needle hub, easy injection of the local anesthetic agent, and a normal onset of neural blockade. On recovery, there is unilateral numbness, which is succeeded by pain and paresthesia in the L5 to S1 distribution and foot drop, and in some cases urinary symptoms; sensory symptoms may last for months or years. The MRI appearance is one of a small syrinx or hematoma within the conus on the same side as the pain on insertion and subsequent leg symptoms ( Fig. 31.7 ). In the majority of cases, the anesthesia provider believed the interspace selected was L2–L3. In one patient who subsequently died of other causes, hematomyelia was confirmed at autopsy. After a rash of cases of conus damage in the 1990s, the practice of spinal needle insertion may have been modified by aware providers, but an abnormally long cord may still be damaged with the best of techniques.
Related posts:
Patient Safety and Team Training
Systemic Analgesia: Parenteral and Inhalational Agents
Anesthesia for Cesarean Delivery
Maternal Mortality
Cardiovascular Disease
Practice Guidelines for Obstetric Anesthesia: an Updated Report by the American Society of Anesthesiologists Task Force on Obstetric Anesthesia and the Society for Obstetric Anesthesia and Perinatology
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