Neurologic complications after lumbar spine surgery may be broadly classified by the mechanism of injury and by the time period during which they occur. The causes of injury are generally either indirect or direct, with the latter including laceration, compression, traction, and avulsion injuries to the neural elements. Such direct causes are most commonly the result of a technical mishap by the surgeon. Indirect injuries are due to the disruption of the blood supply to the spinal cord and nerve roots or to the gradual compression of the neural elements, as by correction of deformity or by a postoperative hematoma. This type of injury is usually the result of ischemia or the disruption of axoplasmic flow, which provides neural nutrition. Its causes are more difficult to define and are often inexplicable.
Neurologic injuries categorized by the time period during which the insult occurs may be intraoperative, early postoperative (1 to 14 days), or delayed postoperative (after 14 days) events. Intraoperative events are generally related to complications arising from anesthesia, patient positioning, surgical technique, or procedure-specific risks. Early in the postoperative period and up to 2 weeks after surgery, neurologic injuries are most commonly secondary to direct compression of the neural elements. This is often caused by the mass effect of postoperative hematoma, pseudomeningoceles, and epidural abscesses. After partial diskectomy, retained fragments or recurrent herniations may also cause neurologic symptoms in this time period. After 14 days from surgery, recurrent disk herniation should be considered more likely, although this may occur earlier as well.
To both minimize and prevent potential neurologic complications that may occur in association with lumbar spine surgery, the surgeon must thoroughly understand the relevant anatomy and must do meticulous preoperative planning. Additionally, a thorough understanding of the etiology of the complications can decrease their incidence. When complications do occur, rapid recognition and appropriate treatment can minimize their effect.
Knowledge of the relevant anatomy is essential to minimizing direct neural injuries. The spinal cord terminates as the conus medullaris at the level of the inferior border of L1 and the superior border of L2. Spinal cord tissue is much less tolerant of traction and compression than the nerve roots are. Even minimal manipulation of the cord may cause profound neurologic consequences. Focal injury to the conus medullaris can cause injury to the function of the lower sacral roots and result in disturbances in bowel, bladder, or sexual function with or without other obvious neurologic deficits in the lower extremities.
The spinal nerve roots, while more tolerant of mechanical deformation than the spinal cord, are less tolerant than the peripheral nerves. The intradural nerve rootlets are covered by only a thin membranous root sheath, which is permeable to cerebral spinal fluid for nutrition.1 In contrast, peripheral nerves are protected by an epineurium and a perineurium. This, in addition to a more developed connective tissue layer, makes peripheral nerves much less susceptible to injury than the intrathecal nerve rootlets.
The results of experimental studies in dogs suggest that when the thecal sac is compressed acutely to 45% of its normal area (i.e., to approximately 75 of the normal 170 mm2), significant nerve-root compression occurs, with measurable changes in both motor and sensory function.2 The motor nerve roots recover more quickly than the sensory roots after the pressure is released; thus, transient compression is more likely to affect the sensory roots. The critical value of 75 mm2 can be used for the radiologic diagnosis of central spinal stenosis. Reducing the cross-sectional area of the thecal sac to approximately 65 mm2 generates a pressure level of about 50 mm Hg in the cauda equina. Measurable changes in spinal nerveroot conduction generally occur between 50 and 75 mm Hg.3 The effects of compression are related not only to the duration of compression and the pressure itself but also to the rate of onset.4 In the acute injury setting, rapid application of compression to the nerve roots causes more pronounced tissue changes than slow application. The application of pressure over multiple spinal levels and the combination of compression with systemic hypotension can lower these threshold injury levels.
The pedicle is a constant anatomic landmark that can be used to locate the exiting nerve root and thus minimize the likelihood of inadvertent injury to it. If the anatomy is aberrant, the one constant is the relationship of the pedicle to the nerve root, which lies along the inferomedial edge of the pedicle. In cases with poor visualization of the nerve root, resection of bone until the pedicle is visible will aid in the identification of the exiting nerve root.
During anterior lumbar surgery, the hypogastric nerve plexus and sympathetic chain are at risk of injury. The aorta, the vena cava, and collateral vessels are prevertebral and in close proximity to the hypogastric nerve plexus. This nerve plexus is approximately 6 to 8 cm in length along the surface of the aorta and extends from the cephalad aspect of L4 (as the superior hypogastric plexus) to the first sacral vertebra. As the plexus enters the pelvis, it divides into right and left divisions, which course distally and join the inferior hypogastric plexus. These fibers innervate the seminal vesicles and vas deferens in the male; injury to these structures can lead to retrograde ejaculation. Injury to the hypogastric plexus in approaches to the L5-S1 disk space is minimized by blunt dissection directly on the anterior surface of the disk. Sweeping the prevertebral tissues and hypogastric nerve plexus laterally, rather than dissecting through these structures, decreases the risk of injury to the nerve fibers. The use of bipolar cautery and limited exposure also helps to minimize the risk of injury. The exposure of upper lumbar segments is not associated with as high a risk for retrograde ejaculation as the exposure of L5-S1, because the sympathetic fibers involved lie on the anterior aortic wall. Injury to the sympathetic chain, which lies along the anterior border of the psoas muscle, can manifest as patient complaints of contralateral foot coldness. In fact, vasodilatation secondary to this injury causes increased warmth in the ipsilateral foot.
Failure to recognize variations in normal anatomy on preoperative studies may predispose to injury (e.g., asymptomatic spina bifida). Such a finding may necessitate a particularly careful dissection or alteration in surgical approach. Similar caution is necessary after prior laminectomies or with widened interlaminar spaces. It is good practice to review all preoperative radiographs just prior to surgery, with special attention to the variant anatomy in each individual case.
In other situations, such as in patients with high-grade lumbar or cervical stenosis, preoperative consideration of patient positioning may help avoid unexpected injury. For example, patients with cervical stenosis should be carefully transferred to the prone position with their heads in a neutral or slightly flexed position, or awake positioning should be used. In severe cases, consideration should also be given to fiberoptic intubation. In patients with high-grade lumbar spinal stenosis, use of large Kerrison rongeurs should be avoided in favor of the motorized diamond burr. Under these conditions, placement of cottonoid pledgets within a tightly narrowed epidural space should be avoided.
Prior to surgery, patients should be instructed to discontinue the use of anti-inflammatory medications (for 2 to 3 days) and aspirin (for 2 to 10 days) to minimize intraoperative and postoperative blood loss. Patients should also be questioned about complementary or alternative medications, such as gingko and cayenne, which can have effects on clotting.
Complications Related to Induction of Anesthesia and Patient Positioning
The risk of intraoperative neurologic injuries begins with the induction of anesthesia and positioning of the patient for surgery. The incidence of significant neurologic injury, including complete paralysis, secondary to spinal or epidural anesthesia has been reported to be approximately 0.02%.5 Injuries related to these types of anesthesia are usually secondary to direct mechanisms. These include laceration by inadvertent needle placement and compression of the neural elements secondary to postinjection hematoma. Paralysis can occur in patients with low-lying spinal cords who undergo routine epidural or intrathecal injections of anesthetic agents. Peripheral nerve injury secondary to the placement of intravenous and arterial lines, although uncommon, can also occur.
Peripheral nerve injuries after lumbar spine surgery more typically occur secondary to malpositioning or improper padding of the patient. In posterior lumbar surgery, the patient is usually placed in a prone position on rolls or on a four-poster padded frame (e.g., Relton frame) or Andrews-type table. After positioning, it is important to ensure that the abdomen hangs free, so as to minimize intraoperative blood loss. Regardless of the type of frame used, well-padded support is necessary, with care taken to avoid excessive pressure on the chest wall and pelvis. Extra foam padding of the posts aids in distributing pressure uniformly to the patient’s skin and helps to avoid skin blisters and burns. Every patient should be positioned and padded as would be appropriate for a much longer duration of surgery than projected. Direct compressive or traction injuries of upper- and lower-extremity nerves can occur. In particular, excessive pressure or stretch at the brachial plexus or femoral nerve can lead to upper- and lower-extremity nerve palsies, respectively. In the upper extremity, the ulnar and anterior interosseous nerves are particularly susceptible to external pressure, as are the peroneal and lateral femoral cutaneous nerves of the lower limbs.
In patients with coexistent cervical and lumbar stenosis, careful positioning of the head in neutral or slight flexion is mandatory to avoid cervical myelopathy or spinal cord injury, either while transferring the patient prone or during final positioning. A Mayfield three-point head holder provides very reliable positioning for long-duration surgical procedures and for high-risk patients. This avoids pressure on the face and in particular on the eyes. Ophthalmic injuries have been reported secondary to excessive pressure on the eyes, resulting in permanent blindness in rare instances.6
Direct and Indirect Surgical Injuries
Direct and indirect injuries related to surgical technique make up the majority of intraoperative neurologic complications. Three factors appear to predispose to iatrogenic injuries: the relative inexperience of the surgeon, failure to follow meticulous surgical technique, and a history of prior surgical procedures on the patient. In patients with undisturbed anatomy, the frequency of injury should be very rare. If injuries are occurring relatively more frequently, it is mandatory that the surgeon reevaluate the surgical techniques employed (Table 1).
Most neurologic injuries from direct trauma are related to either trauma by surgical instruments or placement of pedicle screws or hooks. Several principles should be observed to minimize risks. Appropriately sized rongeurs down to 1 mm with a small foot-plate should be available. When removing bone or soft tissue, one must always check to see that the dura has been dissected free (especially in patients with rheumatoid arthritis) and that adequate space is available for the Kerrison foot-plate. If scarring or adhesions are present, careful dissection with angled curettes or dural elevators is required. If the area is too narrow, bone must be removed from above with either motorized burrs or osteotomes before rongeurs can be safely used. Protection of the dura with cottonoid pledgets should be avoided in these conditions. Use of magnification, such as with loupes or an operating microscope, can be helpful in difficult situations. In general, Kerrison rongeurs should be directed parallel to the exiting nerve root to avoid transection. Motorized burrs are passed from medial to lateral to avoid dural damage. Diamondtipped burrs with copious saline irrigation can be used safely close to the dura with a lower risk of laceration.
During diskectomy, the exiting nerve root must be mobilized medially to expose the herniation. In large herniations, it may not be possible to completely mobilize the root without excessive traction. If that is the case, the disk should be removed before complete mobilization. Before incising the disk anulus, one should always make sure that the exiting root has been mobilized and protected. Meticulous hemostasis is important to avoid mistaking a nerve root for a disk fragment. The smallest pituitary rongeurs should be used to remove the disk, and they should be opened only after they have been inserted in the disk space.
Occasionally, the suction tip can become nicked by another instrument, such as the burr. The sharp edge created can cause a dural or nerve root laceration. For this reason, the suction tip should be checked and discarded if damaged.
Other laceration injuries may occur with the use of osteotomes during medial facetectomies and during aggressive bone removal with the rongeur. Tearing or ripping of the ligamentum flavum should be avoided. Particular care is needed when removing the bone fragments of the medial facet, because the capsule of the facet is often adherent to the ligamentum flavum or the dura itself. Any movement of the dura while bone is being removed, either during facetectomy or when a Kerrison rongeur is being used, should alert the surgeon that such an attachment may be present. Use of a Penfield or Woodson probe can help loosen any attachments to the dura. Performing bone removal while leaving the ligamentum flavum intact may also serve as an added measure of protection to the thecal sac.
Compression or contusion of the nerve roots or cauda equina is another potential type of neurologic injury related to surgical technique. Excessive thecal sac retraction, especially prior to adequate decompression of the spinal canal in patients with lumbar stenosis, can cause ischemic injuries. As noted previously, compression of the thecal sac to less than 45% of its crosssectional area can cause changes in motor and sensory root conduction. Poorly visualized nerve roots are often subject to such unrecognized compression. Bertrand described the “battered-root” syndrome, in which new-onset numbness after laminectomy or laminotomy strongly suggests intraoperative root injury.5 Excessive compression with cottonoid pledgets, gel foam, or malpositioned fat grafts has also been reported as a source of intraoperative neurologic compromise.7
The incidence of nerve-root avulsion injuries has been reported to be approximately 0.4%5 Forceful retraction of a nerve root, especially within a stenotic foramen, can be an inadvertent cause of a nerve-root avulsion. This can also occur during aggressive bone removal. The incidence of conjoined nerve roots in the lumbar spine has been reported to be between 2% and 14%,5 and probably is more common than is generally acknowledged. Failure to recognize a conjoined nerve root can result in excessive compression, laceration, or avulsion. Adequately visualizing the nerve-root sleeve and working laterally relative to the nerve root will help to minimize the incidence of this complication. In many instances, when the nerve root cannot be identified or mobilized, it is better to remove more bone until the pedicle is exposed than to place undue traction on the neural elements.
The frequency of dural tears as a complication of lumbar surgery can be reduced through meticulous technique. Although identification of a dural tear is typically made after the sudden leak of spinal fluid, identification of dural tears that have not yet disrupted the arachnoid layer is also important. Most tears can be repaired primarily with 5–0 or 6–0 suture with a running stitch. Care must be taken to avoid incorporating any neural elements into the closure. After closure, a Valsalva maneuver aids in the identification of a persistent or residual leak. In these cases, reinforcement of the repair is possible with muscle or fat grafts sutured over the repair to the dura. The use of fibrin glue, which is derived from equal volumes of thrombin and cryoprecipitate, may add to the reinforcement of tenuous repairs. Larger defects in the dura may require patch grafting with a segment of fascia from the paravertebral muscles. Once the repair has been made, a watertight closure without wound drains is required for the overlying fascia, subcutaneous tissue, and skin. Postoperatively, patients are typically kept supine for several days to reduce the hydrostatic pressure on the dural repair.
Persistent or residual dural leaks at the time of initial repair may be treated by the percutaneous placement of a subarachnoid drain immediately after the procedure. The placement of a subarachnoid drain above the dural tear allows diversion of spinal fluid and a decrease in hydrostatic pressure at the repair site. Patients should be kept supine after surgery for as long as 5 days, and prophylactic antibiotic coverage should be maintained. Continuous drainage at a rate of 10 to 15 mL/hr is recommended. In addition, close monitoring of spinal fluid levels of protein, glucose, and cell count is important until the drain is discontinued. Daily Gram stains and cultures of the collected spinal fluid should also be obtained.
Complications Due to Changes in Spinal Alignment
Neurologic complications sometimes occur without an obvious intraoperative cause. These indirect injuries are usually the result of disruption of the vascular perfusion of the spinal cord or nerve roots. More commonly associated with scoliosis surgery, cord ischemia can occur secondary to application of excessive distraction forces to a relatively rigid spinal deformity. It can also occur secondary to excessive hypotension. Any change in neurologic monitoring signals during these maneuvers should alert the surgeon to possible neurologic injury. The degree of correction of the spinal deformity should be lessened or completely released, and a return to baseline of the evoked potentials should occur before further reduction is attempted. In some instances, the removal of the posterior instrumentation is indicated. Ischemic events involving the spinal cord and neural elements are estimated to occur in approximately 1 of every 3,000 surgical procedures for scoliosis.5
Another procedure with high risk for neural deficit is reduction of spondylolisthesis. Decompression of the neural foramina (especially at L5) before instrumentation and avoidance of nerve-root compression from manual downward pressure during the process of drilling, tapping, and insertion of pedicle screws or the placement of rods reduces the risk of neurologic injury. However, root injury is probably secondary to effective lengthening of the root associated with deformity reduction or to release of reduction or resection of the sacral dome (sacral shortening).
Injuries Due to Instrumentation
The risk of neural injury secondary to aberrant pedicle-screw placement has been reported.5 A number of principles should be adhered to in order to minimize that risk. The proper starting point should be identified by using osseous landmarks or, in cases of severe deformity, by directly palpating the pedicle through a laminotomy. Once the pedicle has been probed, it should be checked for inadvertent perforations. After tapping, the hole should be checked again for perforations. Radiography or fluoroscopy should be used to evaluate the placement of screws and the overall alignment after insertion of hardware. Intraoperative pediclescrew stimulation with electromyography is commonly used to ensure proper pedicle-screw placement.8 Stimulation of the pedicle screw that results in nerve-root conductivity below a certain threshold stimulation can be indicative of screw breakout or pedicle fracture. Reorientation or redrilling of the screw hole is warranted. Fractures of the pedicle secondary to screw misplacement can also cause direct nerve-root impingement by the fragment of bone.
Patients noted to have postoperative neurologic deficits or leg pain after the placement of instrumentation should be evaluated with computed tomography (CT). This is preferable to magnetic resonance (MR) imaging because it accurately demonstrates screw placement. Questionable screw placement in the clinical setting of new-onset leg pain or neurologic deficit is best managed by reoperation to remove or replace the device and to ensure adequate neural foraminal decompression (Fig. 1).
Posterior interbody grafts, or cages, used during posterior-lumbar interbody fusions potentially can dislodge and impinge on the nerve roots or cauda equina, causing serious neurologic sequelae. The incidence of this complication is in the range of 0.3% to 2.4%.9 Another problem with such procedures is the wide exposure required for graft insertion, with resultant traction injury or development of instability.
Anterior interbody devices carry similar risks with regard to incorrect placement and dislodgment. With the placement of anterior interbody fusion devices, injury to the hypogastric plexus secondary to the traumatic exposure can result in retrograde ejaculation in men. The incidence of injury to the plexus has been reported to be in the range of 1% to 5% with the use of these devices, especially when utilizing a laparoscopic approach.10 The risk of such an injury after open anterior lumbar fusion surgery has been reported to be 0.42%.11 Additionally, malplacement of anterior interbody devices themselves or expulsion of disk material posteriorly into the spinal canal can cause neurologic compromise, with an incidence of 2% to 4%.10
Bone Graft-Related Neurologic Injury
The site from which bone graft is harvested is often the origin of postoperative pain. Kurz et al12 noted a 15% incidence of pain in the first 3 postoperative months. Frymoyer et al13 noted this problem in up to 37% of patients as long as 14 years after surgery. In many instances, the postoperative pain was part of a general pain syndrome. Persistent pain was more common in patients in whom the grafts had been taken from the same side as their preoperative sciatica.
Donor-site pain can also be specifically related to peripheral nerve injury. This may be secondary to involvement of the lateral femoral cutaneous nerve (meralgia paresthetica) during harvesting of anterior iliac crest bone. Nerve symptoms may result from entrapment secondary to scar formation, hematoma, or laceration. The variant anatomy of this nerve as it crosses the anterior ilium mandates careful dissection. The incidence of this complication is reportedly between 1% and 14%.14 Beginning the incision at a point 3 cm posterior to the anterior superior iliac spine lessens the chance of this complication.
When taking a bone graft from the posterior iliac crest, one should be aware of the location of the superior cluneal nerves and the sciatic nerve.12 The risks associated with bone-graft harvesting from this area can be significant. The incision should be parallel to the midline, as the incidence of superior cluneal nerve injuries increases with extension of the incision more than 8 cm lateral to the posterior superior iliac spine. The superior cluneal nerves are cutaneous branches of the proximal three lumbar nerves and supply sensation to a large portion of the buttock after piercing the lumbodorsal fascia. Although there is a large degree of cross-innervation, numbness or painful neuromas may develop after laceration. Palpation of the sciatic notch may aid the surgeon in establishing landmarks for taking the graft and avoiding injury to the sciatic nerve or superior gluteal artery. The direction of use of the osteotome or gouge should always be cephalad and tangential to the notch.
Complications in the Early Postoperative Period
A careful neurologic assessment when the patient awakens from surgery provides an index examination to distinguish a deficit that may have occurred intraoperatively from one that occurs in the early postoperative period. Anatomic correlation of the neurologic deficit noted on examination with intraoperative events often facilitates early diagnosis. This is often more valuable than attempts at postoperative imaging with CT, MR imaging, or plain radiography. Evaluation of perineal sensation and sphincter tone is also essential, particularly after high lumbar surgery when the possibility of spinal cord injury exists. The development of neurologic symptoms in a patient who awakened from lumbar surgery neurologically intact should alert the surgeon to the possibility of the development of new neural element compression. The importance of an early accurate baseline examination cannot be overemphasized, as diagnostic imaging of the neural elements with MR imaging or CT can be difficult to interpret in the early postoperative period.
Neurologic deficits that develop in the early postoperative period (1 to 14 days) usually occur secondary to retained disk fragments after diskectomy, postoperative hematoma, pseudomeningocele, herniation of a fat graft, or (rarely) an epidural abscess. Acute spondylolisthesis secondary to iatrogenic instability may also present with a new neurologic deficit. This is more likely to occur in the late postoperative period; when it does occur in the early postoperative period, it is more likely to occur after aggressive lateral decompressions with violation of the pars or facet joints. Plain radiography and CT may be helpful in the evaluation of this problem.
Recurrent Disk Herniation
After diskectomy for disk herniation, the incidence of neural compression by a retained or missed fragment of disk is approximately 0.2%.15 The patient typically awakens from surgery and reports unrelieved symptoms of radiculopathy. Because early postoperative imaging is difficult to interpret, reexploration based on the clinical examination findings and symptoms may be indicated to ensure the removal of any remaining disk fragment. Of course, more than one fragment may be causing residual compression. At the time of the index procedure, suspicion that a fragment of disk may have been missed should be raised by the presence of friable disk material or multiple fragments.
The development of a postoperative epidural hematoma may be associated with excessive or poorly controlled intraoperative bleeding. Patients often have few complaints initially, but significant increasing back pain subsequently develops. This may progress to unremitting leg pain or even cauda equina syndrome in severe cases. Patients with increasing back or leg pain require careful monitoring. A complete neurologic assessment is mandatory, including a rectal examination and a check for perianal pin-prick sensation. If neurologic deterioration occurs, a spinal imaging study, such as CT-myelography or MR imaging, should be performed. In obvious cases, the patient can be immediately taken to the operating room for evacuation without imaging. The presence of an epidural hematoma is a surgical emergency, requiring decompression.
In the 2- to 4-week period after surgery, epidural abscess (Fig. 2) becomes a potential cause of newonset neurologic deficits, although this is a rare complication. Epidural abscesses, like hematomas, require urgent decompression.
Dural tears that occur during surgery and that are not recognized and repaired or are inadequately repaired can result in the formation of a pseudomeningocele5 (Fig. 3). With the increased number of operations for stenosis being performed, this complication may be more frequent than previously suspected. The incidence of pseudomeningocele formation is estimated to be between 0.07% and 2%.8 The prevalence of incidental durotomy is higher, at approximately 4%.8 Incidental durotomy is the second most common cause of lawsuits after lumbar spine surgery and the most common complication of repeat laminectomy.8
The formation of pseudomeningoceles is more common after lumbar spine surgery than after cervical spine surgery. Although small dural tears can close spontaneously, many continue to leak and form pseudomeningoceles. The use of agents such as Adcon-L may precipitate continued leakage of unrecognized dural lacerations.16 These can be noted as a slowly expanding fluid mass or soft-tissue bulging on physical examination. Patients usually present with a progressively worsening headache. Both the mass and the headache may increase in magnitude on standing. Diagnosis is readily made early by using myelography followed by CT. Magnetic resonance imaging may also be helpful in the diagnosis, but it may be difficult to differ-entiate a pseudomeningocele from a postoperative hematoma with this modality. The onset of neurologic symptoms may present either insidiously or acutely with pain, headache, and sudden neurologic deficit. A neurologic deficit may occur when one or more nerve roots herniate out of the dural tear and become trapped within the pseudomeningocele.
Treatment of pseudomeningoceles includes surgical exploration and repair. Careful dissection is required. Excision of the cyst is not necessary, but opening of the cyst to avoid injury to the trapped roots is usually required before closure and repair.
Neurologic complications after lumbar spine surgery are neither common nor necessarily foreseeable. With the increasing number of lumbar spine operations being performed, the number of patients who will sustain neurologic injury can be expected to increase. Because of the often irreversible and dramatic nature of these injuries, as well as the lack of definitive treatments once they have occurred, it is obviously best to prevent these injuries through use of meticulous operative technique, awareness of risk, and close attention to perioperative details.
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