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Neurologic Injury in the Surgical Treatment of Idiopathic Scoliosis: Guidelines for Assessment and Management

Dr. Guille or a member of his immediate family serves as a board member, owner, officer, or committee member of The Pediatric Orthopaedic Society of North America, the Scoliosis Research Society, and the Eastern Orthopaedic Association; is affiliated with the publication Orthopedics; and is a member of a speakers’ bureau or has made paid presentations on behalf of and is a paid consultant or an employee of Medtronic Sofamor Danek. Dr. Samdani or a member of his immediate family is a member of a speakers’ bureau or has made paid presentations on behalf of DePuy, Stryker, and Spinevision; serves as a paid consultant to DePuy and Spinevision; and has received research or institutional support from DePuy. Dr. Betz or a member of his immediate family has received royalties from DePuy, Osteotech, Medtronic Sofamor Danek, Synthes, Spinevision, and Osteotech; serves as a paid consultant to or is an employee of DePuy, Medtronic Sofamor Danek, Osteotech, Spinevision, Synthes, Orthovita, NuVasive, Omrix, Spinemedica, and Orthocon; has received research or institutional support from DePuy and Synthes; and has stock or stock options held in Orthocon and Spinemedica. None of the following authors or a member of their immediate families has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Pahys, Dr. D’Andrea, and Dr. Beck.

Dr. Pahys is Chief Resident, Albert Einstein Medical Center, Philadelphia, PA. Dr. Guille is Co-Director, Division of Spinal Disorders, and Director of Pediatric Orthopaedic Surgery, Brandywine Institute of Orthopaedics, Pottstown, PA. Dr. D’Andrea is Co-Director, Division of Spinal Disorders, Brandywine Institute of Orthopaedics. Dr. Samdani is Director of Spinal Surgery, Shriners Hospital for Children, Philadelphia. Dr. Beck is Spine Surgeon, Teton Orthopaedics, Jackson Hole, WY. Dr. Betz is Chief of Staff and Medical Director, Spinal Cord Injury Unit, Shriners Hospital for Children, Philadelphia.

Reprint requests: Dr. Guille, Brandywine Institute of Orthopaedics, Suite 611, 600 Creekside Drive, Pottstown, PA 19464.

	Abstract

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
Iatrogenic spinal cord injury resulting from surgical treatment of spinal deformity is a relatively uncommon but devastating complication. Publications on the prevalence of spinal cord injury following surgery are numerous, but no definitive review with clinically pertinent treatment guidelines exists. Methods to reduce the risk of neurologic complications with scoliosis surgery include adequate patient evaluation and preoperative planning, intraoperative preparation, intraoperative neuromonitoring, and postoperative management. Treatment algorithms may be useful in the clinical setting to manage intraoperative or postoperative neurologic injury.

Spinal fusion has been the mainstay of surgical treatment in patients with adolescent idiopathic scoliosis for nearly a century.1 Posterior spinal fusion has progressed from the use of casts to induce and hold corrections, to the Harrington rod system, to multihook systems, to the more recent advent of segmental pedicle rod-and-screw fixation in an effort to provide a more powerful means of three-dimensional curve correction.2 Instrumented anterior spinal fusion has also evolved since its introduction in 1969,3 offering the potential benefits of sparing distal fusion levels. Accordingly, corrective maneuvers that once consisted of pure distraction and compression now include translation and derotation.

The strength and corrective power of modern instrumentation has dramatically improved, with a decreased rate of pseudarthrosis.4 With advances in surgical techniques and instrumentation, correction of larger deformities is becoming more common. However, the rate of neurologic complications remains relatively unchanged.5-7 Segmental fixation allows for improved curve correction, but the increased number of anchor points may increase the risk of neurologic injury.

	Prevalence of Iatrogenic Spinal Cord Injury

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
The reported prevalence of spinal cord injury (SCI) following scoliosis surgery varies from 0.3% to 1.4%.5-7 MacEwen et al5 first evaluated this complication in a report for the Scoliosis Research Society (SRS) after the popularization of the use of instrumentation to correct scoliosis. In this initial study, the reported prevalence of neurologic complication was 0.72% for all diagnoses. Of the 74 patients identified, 55% were reported to have complete paraplegia postoperatively, and 45% to have an incomplete injury when partial motor and/or sensory function was present in either or both lower extremities following surgery. Of these patients, 49% had idiopathic scoliosis, 28% had congenital scoliosis, 9% had paralytic scoliosis, and 14% had scoliotic curves resulting from various conditions such as neurofibromatosis, neuroblastoma, and syringomyelia.

Winter6 reanalyzed data from 1993 and reported a marked decline in neurologic complications following surgery to correct spinal deformity. The SRS data from that year demonstrated no complete injuries and a 0.3% prevalence of incomplete neurologic injuries in 2,031 procedures for kyphosis and scoliosis. The most recent data available from the SRS, in 2006, identified 31 postoperative neurologic deficits in 6,334 cases performed for adolescent idiopathic scoliosis from 2001 through 2003 (0.5%), none of which was a complete neurologic injury.7 Full neurologic recovery was recorded in 61% of patients, and partial or no neurologic recovery from the initial injury was reported in 39%. This study was limited by compliance, with data submission <100%; thus, it may represent only a subset of cases performed by SRS members. However, the report remains one of the largest series of surgical complications in patients treated for adolescent idiopathic scoliosis.7

Although the reported occurrence of iatrogenic neurologic injury is low, the risk is still considerable because the complication could be a life-changing event. Thus, extensive documentation and preoperative discussions with the patient and family regarding the potential neurologic complications are paramount.

	Mechanisms of Neurologic Injury

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
There are several causes of iatrogenic neurologic deficit resulting from correction of spinal deformity. Intraoperative SCI may result from direct cord trauma stemming from placement of wires, hooks, or pedicle screws, as well as an expanding postoperative epidural hematoma. Distraction or compression of the spinal cord following corrective maneuvers for the curve may lead to neurologic deficit secondary to either distraction of the neural elements or excessive tension on the local vasculature, leading to decreased blood flow and cord ischemia. Spinal cord ischemia may also result from prolonged extreme hypotension (mean arterial pressure <55 mm Hg), hypoxia secondary to decreased hemoglobin level, or vascular compromise after ligation of the segmental vessels in an anterior procedure.6

	Patient Evaluation and Preoperative Planning

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
A complete patient history and physical examination are essential to a thorough preoperative workup. A patient with a history of congenital kyphosis, neurofibromatosis, or skeletal dysplasia is at a considerably increased risk of iatrogenic neurologic complications.5 Meticulous examination of the motor, sensory, and reflex function as well as gait assessment is critical in screening patients for potential intraspinal and brain stem anomalies such as Arnold-Chiari malformation, tethered cord, and syringomyelia. Any abnormality or asymmetry in the motor or sensory examination is cause for concern, as are reports of paresthesias, bowel/bladder dysfunction, or excessive neck/back pain.8 Absence or asymmetry of abdominal reflexes has been reported to be suggestive of syringomyelia.9 Brain stem and intraspinal anomalies have been reported in 37%10 of patients with congenital scoliosis and in 21.7%11 of those with infantile/juvenile scoliosis.

Definitive guidelines for acquiring a preoperative MRI scan have yet to be established. Patients with infantile or juvenile idiopathic scoliosis, or with congenital anomalies, should undergo a screening MRI scan, given the prevalence of intraspinal anomalies (21.7% to 37%).10,11 In contrast, routine preoperative MRI evaluation is likely unnecessary in the patient with adolescent idiopathic scoliosis because the prevalence of intraspinal anomalies is very low (2% to 4%).12 However, MRI should be considered in any patient with presumed adolescent idiopathic scoliosis who exhibits any of the following: atypical curve pattern (eg, apex left thoracic curve), apical thoracic kyphosis, rapidly progressing curvature, excessive headaches, atypical back pain, and/or abnormal neurologic examination.12,13

	Intraoperative Preparation

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
Careful intraoperative preparation is mandatory for a successful procedure. Before induction, the surgeon should discuss with the anesthesia and neuromonitoring teams details regarding the patient, the intended procedure, and the surgical time frame. Two large-bore 18-gauge peripheral intravenous lines are recommended; central venous access is normally only necessary when adequate peripheral access is unobtainable. An arterial line may be used to closely monitor mean arterial blood pressure. Somatosensory-evoked potential (SSEP) and motor-evoked potential (MEP) leads are placed and checked before the patient is turned into the prone position. The upper extremities are padded and positioned to avoid injury to the brachial plexus.

To facilitate endotracheal intubation, anesthesia is typically induced with intravenous propofol and a single dose of a nondepolarizing neuromuscular relaxant (eg, rocuronium, vecuronium). The patient is maintained on a continuous intravenous infusion of sufentanil citrate and/or propofol. This combination allows for excellent sedation throughout the procedure without interfering with neuromonitoring recordings.14-17

Maintaining adequate blood pressure is essential for spinal cord perfusion. However, a balance should be maintained to minimize intraoperative blood loss and transfusions. With a mean arterial blood pressure of <55 mm Hg, increased risk of spinal cord ischemia has been reported.14,18 Mild hypotensive anesthesia is used in an effort to control blood loss. The mean arterial blood pressure is maintained at 65 to 70 mm Hg during exposure and placement of instrumentation.15 Approximately 30 minutes before performing corrective maneuvers, the surgeon should notify the anesthesiologist to gradually elevate the mean arterial blood pressure to >70 mm Hg to maintain cord perfusion during spinal manipulation and correction.

	Intraoperative Neuromonitoring

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
The Stagnara wake-up test has been widely used in the intraoperative assessment of neurologic function since its first description in 1973.19 This test involves a temporary reduction in anesthesia, after which the patient is asked to move the upper and lower extremities. The study is limited in that it is entirely reliant on patient compliance and thus cannot be performed in patients who are unable to follow commands because of intellectual and developmental disability, young age, or preoperative weakness.18 The test itself carries risk, including self-extubation, loss of intravenous access, loss of safe patient positioning on the table, air embolism, and postoperative recollection of the event. Furthermore, the wake-up test is a global assessment of spinal cord function and does not provide the surgical team with any precise data with regard to subtle weakness, timing, or location of the neurologic injury.18 Thus, an early neurologic injury presenting only as motor weakness may not be identifiable with the wake-up test because it is not possible to obtain a true motor strength examination in this situation. The wake-up test was historically the benchmark for intraoperative neurologic assessment, and it is still used at some centers in conjunction with advanced neuromonitoring techniques as a means of confirming neurologic status.20

SSEP monitoring was first reported by Nash et al21 in 1977 as a method of intraoperatively monitoring the dorsal spinal column. Intraoperative SSEPs are markedly affected by anesthesia; high concentrations of inhalation agents may cause false reductions in recorded amplitude and increased latencies.20 However, the use of propofol as an anesthetic has been demonstrated to cause a reduced rate of false depression in SSEP signals.22,23 Recent studies have established the ability to achieve dependable SSEP data in 98% of patients without preexisting neurologic disorders.14

More recently, SSEP monitoring has been combined with transcranial MEP (tcMEP) monitoring to increase the sensitivity and specificity for detection of intraoperative neurologic injury. As with SSEP, tcMEP is also influenced by inhalation agents, as well as by marked intraoperative hypotension (mean arterial blood pressure <50 mm Hg) and hyper-/hypothermia.24 Furthermore, most false-positive tcMEP changes occur when the mean systolic blood pressure is too low; in some cases, keeping the mean at >80 mm Hg is necessary to eliminate false-positive results. Theoretically, tcMEP monitoring assesses the anterior motor portion of the spinal cord via cortical stimulation. It has been argued that MEP data are not indicative of a true motor response but rather measure antidromic sensory activity.25 However, it has been shown that tcMEP data reflect neural transmission through corticospinal motor tracts;15,26 these data may show changes in activity earlier than SSEP monitoring does, enabling the surgeon to implement corrective procedures closer to the moment of neurologic injury.15,25-27

As reported by Padberg et al,25 combined MEP and SSEP monitoring enabled prediction of the postoperative neurologic status with 98.6% sensitivity and 100% specificity in 500 patients over a 10-year period. This study established combined MEP and SSEP testing as an improvement in care, obviating the need for routine wake-up tests. The authors used the Stagnara wake-up test only to confirm neurologic injury identified by MEP and SSEP, defined as a 50% decrease in baseline amplitude and a 10% increase in latency. Schwartz et al15 reported 100% sensitivity with tcMEP for identifying true-positive neurologic deficits in 1,121 consecutive patients treated for scoliosis in a large multicenter study. Complications such as seizures, cardiac arrhythmias, scalp burns, headache, tongue lacerations, and nightmares have been described with the use of tcMEP. However, Schwartz et al15 found only two self-limited tongue lacerations secondary to tcMEP in their study.

With anterior spine surgery, the segmental vessels are often ligated for exposure and fusion, which may compromise spinal cord perfusion. Ligation should be performed in the mid portion of the vertebral body. Apel et al28 described temporarily clamping the segmental vessels to assess for any resultant neurologic changes in monitoring prior to formal ligation. Bridwell et al29 reported an increased incidence of paraplegia following segmental vessel ligation with combined anterior-posterior procedures compared with either an anterior- or a posterior-only approach. Bassett et al30 showed no changes in SSEP monitoring with ligation of the segmental vessels in anterior spinal surgery, demonstrating sufficient perimedullary collateral circulation of the spinal cord. In 1996, Winter et al31 reported on 1,197 anterior spinal procedures performed over a 24-year period and found no evidence of paraplegia secondary to segmental vessel ligation. Recently, Tsirikos et al32 demonstrated no neurologic injuries with unilateral segmental vessel ligation in 331 consecutive pediatric patients who underwent anterior spinal surgery for deformity.

The ankle clonus test has been described to assess the lower extremity stretch reflex. Central reflex inhibition prevents rhythmic contraction on the calf muscle upon passive dorsiflexion of the ankle in an otherwise normal, awake patient. Clonus may be elicited as a patient is emerging from general anesthesia because lower motor neuron function returns before the inhibitory action of upper motor neurons. Absence of ankle clonus may indicate SCI, but it may be secondary to a light level of anesthesia insufficient to maintain cortical inhibition. Thus, ankle clonus is not a consistent measure of spinal cord function.14,33

	Intraoperative Neurologic Complications

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
The SSEP/MEP signals must be continuously monitored throughout the procedure, especially during placement of instrumentation and deformity correction. Immediate action is required when damage to the spinal cord or peripheral nerve is suspected at any time during the procedure in response to changes of >50% amplitude and >10% latency in the SSEP/MEP signals.15,25 An algorithm may aid the primary surgeon in determining the causative factor and initiating appropriate treatment (Figure 1).

View larger version (22K): [in this window] [in a new window]   Figure 1 Algorithm for management of intraoperative neurologic injury in the patient with scoliosis. ICU = intensive care unit, MAP = mean arterial blood pressure

Increase Spinal Cord Perfusion
Immediately following identification of neuromonitoring signal changes, the hemodynamic and oxygenation status of the patient should be optimized in an effort to improve perfusion to the spinal cord. The mean arterial blood pressure is elevated to >80 mm Hg, or 20% above baseline values.15 Hemoglobin and blood glucose levels are evaluated and corrected. Patient body temperature should also be monitored and elevated to >36.5°C (97.7°F) to optimize neuromonitoring. These measures have been shown to increase spinal cord perfusion.34

Stagnara Wake-up Test
Changes in neuromonitoring signal suggestive of persistent neurologic deficit may be cause for considering a confirmatory test. Such testing should be used only in a patient who is capable of understanding specific directions; it is unreliable in patients who are very young, have significant cognitive impairment, or have preexisting weakness.18 Prior to induction of anesthesia, the patient should be counseled that he or she will be asked to perform several commands upon waking from anesthesia.

Frequent assessment of the patient’s neuromonitoring status is recommended as instrumentation is placed and corrective maneuvers are performed.15 Doing so allows the surgeon to most reliably pinpoint the possible inciting factor, such as a malpositioned implant and/or tension on the cord caused by corrective maneuvers. Thus, potentially problematic instrumentation can be removed or correction relaxed while waiting for the patient to awaken from anesthesia for the wake-up test.

Release of Correction
The surgeon should give strong consideration to releasing the tension on the spine when all of the aforementioned parameters (eg, mean arterial blood pressure, temperature, hemoglobin level) have been reasonably corrected and there is an absence of expected motor function with the wake-up test. After release of correction, a second wake-up test can be considered when SSEP/MEP signals indicate persistent abnormality. If an improvement in wake-up test and/or neuromonitoring is discovered after release of surgical correction, the surgeon has the option of fusing the spine in situ or attempting a more modest correction.35 When no improvement in neurologic function is elicited after release of tension, all screws and/or hooks should be reassessed. The stability of the spine also should be evaluated. When removal of instrumentation would compromise the stability of the spinal column, such as after vertebral body resection, the surgeon may be forced to maintain the existing instrumentation and fuse the spine under the least amount of tension.18 If osteotomies were performed, the canal should be assessed for fragments of bone, gel foam, or bone wax, which may cause cord compression.

Pedicle screw position should be critically examined in light of a monitoring change. The position of each screw can be reassessed using one measure or a combination of several. High stimulation thresholds of each fixation point, as indicated by triggered electromyography, theoretically indicate intracortical screw position secondary to increased resistance to current flow through cortical bone.36 Any pedicle screw with a markedly lower electromyography threshold (<60%) in relation to the rest of the construct should be reassessed because this may indicate a possible pedicle wall breach.37 Screw position can also be evaluated with the use of intraoperative fluoroscopy. A pedicle screw tip located past the midline of the vertebral body on PA radiographs is suggestive of a medial pedicle breach.38

In the presence of any or all of these signs, the screw may be removed to reassess the tract with direct palpation. A small laminotomy may also be performed to evaluate the integrity of the medial pedicle cortex with or without screw removal. Early removal of instrumentation may increase the possibility of neurologic improvement, provided the spine will not be significantly destabilized with removal of instrumentation.5,35

The ability to obtain adequate postoperative imaging studies is one potential advantage of removal of instrumentation. The quality of CT and MRI scans is superior when no instrumentation is present to create artifact. Even titanium constructs can produce artifact on CT or MRI scans. An MRI scan may be done in the presence of titanium instrumentation; otherwise, a CT scan can be ordered. If the instrumentation is retained and standard CT or MRI scanning is inconclusive, a CT myelogram can be performed. If an abnormality (eg, screw malposition, hematoma) is identified, immediate return to the operating room is indicated for decompression and/or removal of instrumentation within 3 hours of the initial injury.5 If sufficient imaging can be performed and there is no identifiable site of compression, close patient observation is adequate.

Cheh et al16 advocated prompt elevation of mean arterial blood pressure >80 mm Hg and early release of correction in the event of a complete loss of neuromonitoring signals during correction of thoracic kyphosis. The correction was released before neurologic function was assessed with a wake-up test. The authors cited as a rationale for early release of correction the high accuracy rate of modern neuromonitoring coupled with the likely vascular etiology of the neurologic deficit, secondary to anterior column lengthening. All nine patients who demonstrated complete loss of neuromonitoring signals had a prompt return of signals and subsequent negative wake-up test after prompt release of surgical correction.

Steroid Protocol
Although its use is debated, methylprednisolone is currently the only recognized pharmacologic intervention for the treatment of acute SCI.39 Use of steroids has not been extensively studied in the intraoperative setting; however, we currently administer steroids to patients who have a continued negative wake-up test (ie, absence of motor function) after release of tension from corrective and distractive maneuvers.15,18,27

In the laboratory and in animal models, methylprednisolone has been shown to reduce inflammation and stabilize cell membranes. An influx of free radicals occurs in the acutely injured spinal cord, leading to lipid peroxidation, which results in cell membrane instability as well as ionic derangement of calcium, sodium, and potassium. Methylprednisolone is thought to act by membrane stabilization via its postulated inhibition of lipid peroxidation and calcium ion influx.

The current recommended protocol is a loading intravenous bolus dose of 30 mg/kg administered over 15 minutes, followed by 5.4 mg/kg/hr as a 23-hour infusion (if started within 3 hours from the time of injury).39 The use of methylprednisolone for the management of intraoperative SCI is not well documented. Thus, the surgeon is faced with the dilemma of weighing the potential benefits of improved neurologic recovery against a possible increased risk of infection. The American Association of Neurological Surgeons/Congress of Neurological Surgeons (AANS/CNS) Joint Section on Disorders of the Spine and Peripheral Nerves Guidelines Committee has indicated that methylprednisolone for either 24 or 48 hours is an option in the treatment of patients with acute spinal cord injuries that should be undertaken only with the knowledge that the evidence suggesting harmful side effects is more consistent than any suggestion of clinical benefit.40

Intravenous lidocaine (2 mg/kg) for vasodilatation has been described for treatment of a postulated ischemic spinal cord after segmental vessel ligation.41 In experimental models, intrathecal and intravenous vasodilators have been shown to enhance spinal cord perfusion and neuronal protection. Although the authors of this review have no clinical experience with controlled hypothermia, this has been reported to show promising results in an animal model.42

	Postoperative Management

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
A patient with an intraoperative neurologic insult should be admitted to the intensive care unit postoperatively for close monitoring of hemodynamic parameters as well as for neurologic examinations. Mean arterial blood pressure must be maintained at >80 mm Hg with the judicious use of intravenous fluid replacement, blood transfusion (if indicated), and/or vasopressors when necessary to maintain cord perfusion.43 A β-agonist (eg, dopamine) can be used to maintain mean arterial blood pressure if fluid replacement alone is insufficient.16 A neurologic examination should be performed and documented every hour for the first 12 to 24 hours. This may pose a problem if the patient remains intubated and sedated. In this case, it is paramount that the patient be lightened from sedation on an hourly basis for effective assessment of neurologic function.

	Delayed Postoperative Neurologic Complications

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
Neurologic complications in the postoperative period should be managed with the same diligence and meticulous care as described for an intraoperative SCI. Although relatively uncommon, delayed postoperative SCI may be attributed to progressive spinal cord ischemia secondary to traction or to the development of an epidural hematoma.

As with any acute SCI, adequate perfusion of the spinal cord is paramount (Figure 2). Blood pressure should be meticulously monitored, and mean arterial blood pressure should be maintained at >80 mm Hg in an effort to sustain spinal cord perfusion.15,43 Vasopressors (eg, dopamine) may be required to attain adequate blood pressure and cord perfusion. Hemoglobin levels should also be checked and corrected to avoid excessive postoperative anemia. Patient temperature should be maintained above 36.5° C (97.7°F). A steroid protocol may be initiated as indicated above for the patient with continued neurologic loss.

View larger version (19K): [in this window] [in a new window]   Figure 2 Algorithm for management of delayed, postoperative neurologic injury following surgery to treat the patient with scoliosis. ICU = intensive care unit, MAP = mean arterial blood pressure

	Summary

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 
Iatrogenic SCI secondary to spinal surgery is a devastating event. In an effort to minimize the prevalence of this complication, the surgeon should maintain a thorough and systematic preoperative, intraoperative, and postoperative regimen. In addition to screening for high-risk patients preoperatively, such diligence will aid in identifying and comprehensively managing intraoperative and/or postoperative complications that may arise in an effort to decrease the risk of permanent neurologic injury. Although no randomized, double-blind, prospective studies have been done to provide absolute treatment pathways, we believe that the information contained herein may be used as a general guideline for the management of neurologic injury resulting from the surgical management of scoliosis.

	Figures

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 

	References

Top Abstract Prevalence of Iatrogenic Spinal... Mechanisms of Neurologic Injury Patient Evaluation and... Intraoperative Preparation Intraoperative Neuromonitoring Intraoperative Neurologic... Postoperative Management Delayed Postoperative Neurologic... Summary Figures References

 

Evidence-based Medicine: Levels of evidence are described in the table of contents. References 15 and 39 are level I studies. References 17 and 37 are level II studies. Level III studies include references 2, 4, 7, 9, 12, 13, 22, 25, 38, and 43. Level IV studies include references 1, 3, 5, 8, 10, 11, 16, 18, 21, and 28-32. References 6, 20, 23, 27, and 33 are level V studies. The remaining references are review articles, case reports, and animal studies.Citation numbers printed in bold type indicate references published within the past 5 years.


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