The Journal of Bone & Joint Surgery

The Journal of Bone & Joint Surgery, Volume 92, Issue 1

Scientific Articles | January 01, 2010

Risk Factors for Spinal Cord Injury During Surgery for Spinal Deformity

Michael G. Vitale, MD, MPH¹; Derek W. Moore, MD²; Hiroko Matsumoto, MA¹; Ronald G. Emerson, MD³; Whitney A. Booker, BS¹; Jaime A. Gomez, MD⁴; Edward J. Gallo³; Joshua E. Hyman, MD¹; David P. Roye, Jr., MD¹

¹ Division of Pediatric Orthopaedic Surgery, Department of Orthopaedic Surgery, Morgan Stanley Children's Hospital of New York-Presbyterian, Columbia University Medical Center, 3959 Broadway, Room 800 North, New York, NY 10032. E-mail address for M.G. Vitale: mgv2@columbia.edu
² Department of Orthopaedic Surgery, The Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021
³ Department of Neurology, Columbia University, 710 West 168th Street, New York, NY 10032
⁴ Department of Orthopaedic Surgery, Columbia University, 622 West 168 Street, PH11-Center, New York, NY 10032

View Disclosures and Other Information

Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity.

Investigation performed at the Columbia University Medical Center, New York, NY

J Bone Joint Surg Am, 2010 Jan 01;92(1):64-71. doi: 10.2106/JBJS.H.01839

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Abstract

Background:

Spinal cord monitoring is now considered standard care during surgery for spinal deformity. Combined somatosensory and motor evoked potential monitoring allows the detection of early spinal cord dysfunction in most patients. The purpose of the current study was to identify clinical factors that increase the risk of intraoperative electrophysical changes and to provide management recommendations.

Methods:

The records of 162 consecutive patients who underwent surgery for the treatment of spinal deformity at a tertiary referral center were reviewed. Electrophysical monitoring of these patients was considered to have been successful if reproducible signals had been obtained. Relevant electrophysical changes included a reduction, as compared with baseline, of >50% in the amplitude of the somatosensory evoked potentials; an increase, as compared with baseline, of >10% in the latency of the somatosensory evoked potentials; a loss of motor evoked potentials; and an abrupt decrease of >75% in the motor evoked potentials.

Results:

One hundred and fifty-one (93%) of the 162 patients were monitored successfully. Four of the eleven patients with unsuccessful monitoring had neuromuscular scoliosis. Twelve of the 151 successfully monitored patients had a true electrophysical event, and two of them were found to have new postoperative neurologic deficits that represented a change from the findings of their preoperative neurologic examination. The determined causes of these electrophysical events included curve correction in eight patients, hypotension in two, direct cord trauma in one, and malposition of a pedicle screw in one. The patients with a true electrophysical event had a significantly higher rate of neurologic events than did the patients who did not have a true electrophysical event (p < 0.001). The rate of true electrophysical events was significantly higher in the patients with cardiopulmonary comorbidities than it was in the patients with no comorbidities (p = 0.011).

Conclusions:

Combined somatosensory and motor evoked potential monitoring effectively prevents neurologic injury in most children undergoing surgery for spinal deformity. Despite the potential for false-positive results, we recommend setting a low threshold for defining relevant electrophysical changes. Rapid intervention can reverse these changes and avoid potentially serious neurologic complications. Patients with cardiopulmonary comorbidities may be at a higher risk for having relevant electrophysical events.

Level of Evidence:

Diagnostic Level III. See Instructions to Authors for a complete description of levels of evidence.

Figures in this Article

Introduction

Paralysis and other major neurologic injuries are the most feared complications of pediatric surgery for the treatment of spinal deformity. The incidence of major neurologic injury following surgery for spinal deformity has been reported to range from 0.01 to 0.05%¹. Neurologic injury can be due to direct trauma or an ischemic insult to the spinal cord. Some investigators have noted that postoperative sensory deficits are more likely to be caused by direct trauma to the dorsal columns^2,3, whereas paraplegia is more likely to result from an ischemic insult to the anterior and central portions of the cord^3,4. Spinal cord monitoring was developed to allow the early detection and reversal of such neurologic complications and is now considered the standard of care during pediatric surgery for spinal deformity.

Two commonly used forms of spinal cord monitoring include assessments of somatosensory evoked potentials and transcranial motor evoked potentials. Somatosensory evoked potential monitoring assesses the sensory pathways of the dorsal columns. Although widely used and less sensitive to the effects of general anesthesia, somatosensory evoked potential monitoring is limited in that it can best detect injury to the dorsal columns and may fail to detect injury limited to the anterior motor tracts^5,6. Although paralysis is uncommon, there have been reports of paralysis despite normal results of somatosensory monitoring⁷.

Motor evoked potential monitoring assesses the motor pathways of the anterior and central portions of the spinal cord and therefore has the potential to detect injuries to the motor pathways. Although motor evoked potential monitoring is more sensitive to the depressant effect of general anesthetics on the excitability of both cortical and spinal motor neurons, it has been sensitive to changes in the corticospinal tracts^8-12.

Recent advances in both anesthetic and electrophysical monitoring techniques have led to an improvement in the reliability of motor evoked potential monitoring. The benefits of combining motor evoked potential monitoring with somatosensory evoked potential monitoring have been clearly demonstrated in the context of spinal surgery¹³. Combined somatosensory and motor evoked potential monitoring has several theoretical advantages over single-modality methods, including (1) the ability to monitor a larger proportion of patients, (2) increased accuracy provided by complementary information from two independent systems with a reduced risk of false-negative results, and (3) increased sensitivity to detect early spinal cord dysfunction¹³.

Effective spinal cord monitoring is somewhat dependent on the skills and experience of the monitoring staff. One challenge is optimizing the sensitivity of the technique. If monitoring is too sensitive, false-positive results may lead to unnecessary intraoperative interventions such as steroid administration, modification of instrumentation, and unnecessary wake-up tests and may extend surgical time^14-17. If the technique is not sensitive enough, damage to the neural elements may be missed, resulting in a permanent neurologic deficit¹⁸. The objectives of this study were to review the performance characteristics of combined somatosensory and motor evoked potential monitoring and identify patient characteristics that might place patients at increased risk for having a relevant and true change in somatosensory or motor evoked potential signals.

Materials and Methods

The study protocol was approved by the Columbia University Medical Center institutional review board. The study was a retrospective case series in which we examined our institution's experience with motor and somatosensory evoked potential monitoring during pediatric surgery for correction of spinal deformity. From 1999 to 2005, we identified 295 children and adolescents who had had surgery for the treatment of a spinal deformity. The patients had anterior and/or posterior spinal fusion and instrumentation. Our start date was established by the first year in which routine motor evoked potential monitoring was performed and both motor and somatosensory evoked potential data were stored digitally. One hundred and thirty-three patients (fifty-five with idiopathic scoliosis, thirty-two with neuromuscular scoliosis, twenty-three with congenital scoliosis, fourteen with kyphosis, eight with syndromal scoliosis, and one with spondylolisthesis) were excluded from the study because of inadequate medical records. Chi-square analysis confirmed that there was no significant difference in diagnosis between the patients who were included and those who were excluded from this study (p = 0.672). A total of 162 patients were included in the study.

Anesthetic Methodology

In the majority of cases, anesthesia was induced with propofol (mean dose, 140 mg; range, 50 to 250 mg) and maintained with a propofol infusion (6 to 10 mg/kg/hr). Invasive blood-pressure monitoring, pulse oximetry, and monitoring of cardiac activity, end-tidal carbon dioxide concentration, and temperature were performed. The patients were actively warmed throughout the procedure. A single bolus of nondepolarizing muscle relaxant (rocuronium, vecuronium, or atracurium) was given at the time of induction to facilitate tracheal intubation and ventilation. This was followed in each case by an infusion of the relaxant titrated to provide one or two clearly visible twitches of the thumb with use of a train of four supramaximal stimuli (0.2-msec duration, 50 mA, 2 Hz) delivered to the ulnar nerve at the wrist.

Electrophysical Methodology

Bilateral somatosensory evoked potentials were elicited by alternately stimulating the tibial nerve at each ankle with surface electrodes. Popliteal responses were measured as an internal control. Recording was performed with use of sterile subcutaneous needle electrodes positioned at the P39, P30, A1, and A2 cortical positions. Motor evoked potentials were stimulated with use of standard scalp electrodes placed at C3, C4, and Cz. Recording leads were positioned over large muscles of both lower extremities. Baseline data were obtained after induction of anesthesia and were used as the control. Once optimal parameters of transcranial electrical stimulation were established, a minimum of eight consecutive baseline motor evoked potentials was recorded during stable conditions of neuromuscular blockade that permitted one or two clearly visible twitches of the thumb, general anesthesia, and physiologic parameters, including blood pressure and body temperature. Motor and somatosensory evoked potentials were then monitored throughout the operation and recorded. A reduction in the amplitude of the somatosensory evoked potentials of >50% or an increase in the latency of >10%, as compared with baseline, was regarded as relevant. Loss of motor evoked potentials or an abrupt decrease in their amplitude of >75% of baseline values were considered indicative of a relevant change provided that the levels of neuromuscular blockade and general anesthesia were unchanged. Whenever a relevant electrophysical change occurred, the surgeon, anesthesiologist, and supervising neurophysiologist were notified and a standard protocol for evaluation of possible technical problems was initiated (Fig. 1). If the electrophysical changes did not resolve after an appropriate investigation and action, a wake-up test was performed for those patients who were able to follow instructions and to move voluntarily. In some cases, the electrophysical changes completely resolved coincident with the wake-up test.

Fig. 1

Flow chart showing actions in response to electrophysical (EP) changes. SEP = somatosensory evoked potential, and MEP = motor evoked potential.

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Statistical Analysis

To investigate the patient characteristics and rates of successful monitoring, electrophysical changes, actions taken, and neurologic events, variables were examined with use of descriptive analysis. Chi-square tests were performed to explore the differences in the likelihoods of successful electrophysical monitoring and electrophysical change among various diagnostic and comorbidity groups. All statistical tests were two-tailed, and a p value of <0.05 was considered to be significant.

Source of Funding

No funding source played a role in this investigation.

Results

Patient Characteristics

The demographics of our cohort are presented in Table I. The mean age was 15.7 years old (range, three to twenty-five years old). The primary diagnoses are listed in Table II. Seventy-eight patients had idiopathic scoliosis, thirty-six had neuromuscular scoliosis, twenty-six had congenital scoliosis, thirteen had kyphosis, six had syndromal scoliosis, and three had spondylolisthesis. Of the thirteen cases of kyphosis, three were idiopathic, six were neuromuscular, two were congenital, and two were due to Scheuermann disease. Fourteen of the thirty-six patients with neuromuscular scoliosis and three of the six with neuromuscular kyphosis had cerebral palsy; thus, a total of seventeen patients had cerebral palsy.

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TABLE I Patient Characteristics

	No. (%) of Patients (N = 162)
Sex
Female	113 (70)
Male	49 (30)
Diagnosis
Idiopathic scoliosis	78 (48)
Neuromuscular scoliosis	36 (22)
Congenital scoliosis	26 (16)
Kyphosis	13 (8)
Syndromal scoliosis	6 (4)
Spondylolisthesis	3 (2)

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TABLE I Patient Characteristics

	No. (%) of Patients (N = 162)
Sex
Female	113 (70)
Male	49 (30)
Diagnosis
Idiopathic scoliosis	78 (48)
Neuromuscular scoliosis	36 (22)
Congenital scoliosis	26 (16)
Kyphosis	13 (8)
Syndromal scoliosis	6 (4)
Spondylolisthesis	3 (2)

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TABLE II Success of Electrophysical Monitoring and True Electrophysical Events Based on Diagnosis

Diagnosis	Somatosensory Evoked Potential Monitoring Successful* (N = 149)	P Value†	Motor Evoked Potential Monitoring Successful* (N = 134)	P Value†	Either Somatosensory or Motor Evoked Potential Monitoring Successful* (N = 151)	P Value†	True Electrophysical Events*‡ (N = 12)	P Value†
Idiopathic scoliosis (n = 78)	74 (95 ± 4.9)	—	72 (92 ± 5.9)	—	74 (95 ± 4.9)	—	3 (4 ± 4.5)	—
Neuromuscular scoliosis (n = 36)	30 (83 ± 12.2)	0.052	26 (72 ± 14.6)	0.006	32 (89 ± 10.3)	0.217	3 (9 ± 10.1)	0.255
Congenital scoliosis (n = 26)	25 (96 ± 7.4)	0.633	21 (81 ± 15.2)	0.102	25 (96 ± 7.4)	0.633	3 (12 ± 12.7)	0.167
Kyphosis (n = 13)	12 (92 ± 14.5)	0.546	9 (69 ± 25.1)	0.033	12 (92 ± 14.5)	0.546	2 (17 ± 21.1)	0.141
Syndromal scoliosis (n = 6)	5 (83 ± 29.8)	0.316	4 (67 ± 37.7)	0.099	5 (83 ± 29.8)	0.316	0 (0)	0.820
Spondylolisthesis (n = 3)	3 (100)	0.857	2 (67 ± 53.3)	0.240	3 (100)	0.857	1 (33 ± 53.3)	0.150
Subgroup analysis
Cerebral palsy (neuromuscular scoliosis: n = 14; kyphosis: n = 3)	13 (77 ± 20.2)	0.031	8 (47 ± 23.7)	<0.001	15 (88 ± 15.3)	0.287	3 (20 ± 20.2)	0.057

*The values are given as the number with the percentage and 95% confidence interval in parentheses.
†The p value is for the significance of the difference compared with the group with idiopathic scoliosis.
‡The percentage is of the patients monitored successfully (with either somatosensory or motor evoked potential monitoring).

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TABLE II Success of Electrophysical Monitoring and True Electrophysical Events Based on Diagnosis

Diagnosis	Somatosensory Evoked Potential Monitoring Successful* (N = 149)	P Value†	Motor Evoked Potential Monitoring Successful* (N = 134)	P Value†	Either Somatosensory or Motor Evoked Potential Monitoring Successful* (N = 151)	P Value†	True Electrophysical Events*‡ (N = 12)	P Value†
Idiopathic scoliosis (n = 78)	74 (95 ± 4.9)	—	72 (92 ± 5.9)	—	74 (95 ± 4.9)	—	3 (4 ± 4.5)	—
Neuromuscular scoliosis (n = 36)	30 (83 ± 12.2)	0.052	26 (72 ± 14.6)	0.006	32 (89 ± 10.3)	0.217	3 (9 ± 10.1)	0.255
Congenital scoliosis (n = 26)	25 (96 ± 7.4)	0.633	21 (81 ± 15.2)	0.102	25 (96 ± 7.4)	0.633	3 (12 ± 12.7)	0.167
Kyphosis (n = 13)	12 (92 ± 14.5)	0.546	9 (69 ± 25.1)	0.033	12 (92 ± 14.5)	0.546	2 (17 ± 21.1)	0.141
Syndromal scoliosis (n = 6)	5 (83 ± 29.8)	0.316	4 (67 ± 37.7)	0.099	5 (83 ± 29.8)	0.316	0 (0)	0.820
Spondylolisthesis (n = 3)	3 (100)	0.857	2 (67 ± 53.3)	0.240	3 (100)	0.857	1 (33 ± 53.3)	0.150
Subgroup analysis
Cerebral palsy (neuromuscular scoliosis: n = 14; kyphosis: n = 3)	13 (77 ± 20.2)	0.031	8 (47 ± 23.7)	<0.001	15 (88 ± 15.3)	0.287	3 (20 ± 20.2)	0.057

The primary comorbidities were grouped into six categories: none, cardiopulmonary, neuromuscular, anatomic, developmental, and syndromic (Table III).

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TABLE III Comorbidity Subgroups

No comorbidity	66
Cardiopulmonary	23
Congenital heart disease	14
Restrictive/obstructive pulmonary disease	7
Other chronic pulmonary pathological condition	2
Neuromuscular	36
Cerebral palsy	11
Cerebral palsy and seizure	6
Duchenne muscular dystrophy	2
Encephalopathy	1
Muscular dystrophy	3
Other neuromuscular disorder	7
Seizure disorder	1
Spinal muscular atrophy	3
Spina bifida and syringomyelia	2
Anatomic	11
Congenital abnormality	2
Other growth abnormalities	1
Neoplasias	1
Scheuermann syndrome	3
Spondylolisthesis	4
Developmental	8
Attention-deficit hyperactivity disorder	2
Developmental delays	6
Syndromic	18
Down syndrome	1
Wolf-Hirschhorn syndrome	3
Neurofibromatosis I	1
Developmental delays	4
Klippel-Feil syndrome	2
Dysgenesis of corpus callosum	1
Kabuki syndrome	1
Jarcho-Levin syndrome	1
VACTERL	1
DiGeorge syndrome	1
Trisomy 8	1
Angelman syndrome	1

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TABLE III Comorbidity Subgroups

No comorbidity	66
Cardiopulmonary	23
Congenital heart disease	14
Restrictive/obstructive pulmonary disease	7
Other chronic pulmonary pathological condition	2
Neuromuscular	36
Cerebral palsy	11
Cerebral palsy and seizure	6
Duchenne muscular dystrophy	2
Encephalopathy	1
Muscular dystrophy	3
Other neuromuscular disorder	7
Seizure disorder	1
Spinal muscular atrophy	3
Spina bifida and syringomyelia	2
Anatomic	11
Congenital abnormality	2
Other growth abnormalities	1
Neoplasias	1
Scheuermann syndrome	3
Spondylolisthesis	4
Developmental	8
Attention-deficit hyperactivity disorder	2
Developmental delays	6
Syndromic	18
Down syndrome	1
Wolf-Hirschhorn syndrome	3
Neurofibromatosis I	1
Developmental delays	4
Klippel-Feil syndrome	2
Dysgenesis of corpus callosum	1
Kabuki syndrome	1
Jarcho-Levin syndrome	1
VACTERL	1
DiGeorge syndrome	1
Trisomy 8	1
Angelman syndrome	1

Successful Monitoring

Somatosensory and motor evoked potential monitoring was attempted in all patients. The monitoring was defined as technically successful when it was able to conduct reproducible signals on the sensory or motor pathway under surgical conditions. Somatosensory evoked potential monitoring was successful in 149 (92%) of the 162 cases, motor evoked potential monitoring was successful in 134 cases (83%), either motor or somatosensory evoked potential monitoring was successful in 151 cases (93%) (Fig. 2), and both motor evoked potential monitoring and somatosensory evoked potential monitoring were successful in 83% of cases.

Fig. 2

Flow chart showing numbers of patients with successful monitoring, electrophysical changes, actions taken, and neurologic events. EP = electrophysical.

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Patients with neuromuscular scoliosis were significantly less likely than patients with idiopathic scoliosis to have successful motor evoked potential monitoring (p = 0.006) and had a trend toward being significantly less likely to have successful somatosensory evoked potential monitoring (p = 0.052) (Table II). Successful motor evoked potential monitoring was less likely in patients with kyphosis than it was in those with idiopathic scoliosis (p = 0.033). Additionally, both somatosensory evoked potential (p = 0.031) monitoring and motor evoked potential (p < 0.001) monitoring were significantly less likely to be successful in patients with cerebral palsy. However, with the number of patients studied, we could not identify a significant difference in the success of combined monitoring (i.e., either somatosensory or motor evoked potential monitoring was successful) between patients with neuromuscular scoliosis (p = 0.217), kyphosis (p = 0.546), or cerebral palsy (p = 0.287) and those with idiopathic scoliosis.

When compared with patients without any comorbidities, patients with neuromuscular comorbidities had a significantly lower rate of success of motor evoked potential monitoring (p = 0.001) and a trend toward a lower rate of successful somatosensory evoked potential monitoring (p = 0.064) (Table IV). However, there was no identifiable difference in the rates of successful monitoring with somatosensory and motor evoked potential techniques combined between patients with neuromuscular comorbidities and those without comorbidities (p = 0.239). Patients with anatomic comorbidities were significantly less likely than patients without comorbidities to have successful somatosensory evoked potential monitoring alone (p = 0.035), successful motor evoked potential monitoring alone (p = 0.020), or successful combined monitoring (p = 0.035) (Table IV).

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TABLE IV Success of Electrophysical Monitoring and True Electrophysical Events Based on Primary Comorbidities

	Somatosensory Evoked Potential Monitoring Successful* (N = 149)	P Value†	Motor Evoked Potential Monitoring Successful* (N = 134)	P Value†	Either Somatosensory or Motor Evoked Potential Monitoring Successful* (N = 151)	P Value†	True Electrophysical Events*‡ (N = 12)	P Value†
None (n = 66)	63 (96 ± 5.0)	—	61 (92 ± 6.4)	—	63 (96 ± 5.0)	—	2 (3 ± 4.1)	—
Cardiopulmonary (n = 23)	22 (96 ± 8.3)	1.00	21 (91 ± 11.5)	1.00	22 (96 ± 8.3)	1.00	5 (23 ± 16.9)	0.011
Neuromuscular (n = 36)	30 (83 ± 12.2)	0.064	23 (64 ± 15.7)	0.001	32 (89 ± 10.3)	0.239	4 (13 ± 10.3)	0.175
Anatomic (n = 11)	8 (73 ± 26.3)	0.035	7 (64 ± 28.4)	0.020	8 (73 ± 26.3)	0.035	1 (13 ± 17.0)	0.305
Syndromic (n = 18)	18 (100)	1.00	14 (78 ± 19.2)	0.094	18 (100)	1.00	0 (0)	1.00
Developmental (n = 8)	8 (100)	1.00	8 (100)	1.00	8 (100)	1.00	0 (0)	1.00

*The values are given as the number with the percentage and 95% confidence interval in parentheses.
†The p value is for the significance of the difference compared with the group with no comorbidities.
‡The percentage is of the patients monitored successfully (with either somatosensory or motor evoked potential monitoring).

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TABLE IV Success of Electrophysical Monitoring and True Electrophysical Events Based on Primary Comorbidities

	Somatosensory Evoked Potential Monitoring Successful* (N = 149)	P Value†	Motor Evoked Potential Monitoring Successful* (N = 134)	P Value†	Either Somatosensory or Motor Evoked Potential Monitoring Successful* (N = 151)	P Value†	True Electrophysical Events*‡ (N = 12)	P Value†
None (n = 66)	63 (96 ± 5.0)	—	61 (92 ± 6.4)	—	63 (96 ± 5.0)	—	2 (3 ± 4.1)	—
Cardiopulmonary (n = 23)	22 (96 ± 8.3)	1.00	21 (91 ± 11.5)	1.00	22 (96 ± 8.3)	1.00	5 (23 ± 16.9)	0.011
Neuromuscular (n = 36)	30 (83 ± 12.2)	0.064	23 (64 ± 15.7)	0.001	32 (89 ± 10.3)	0.239	4 (13 ± 10.3)	0.175
Anatomic (n = 11)	8 (73 ± 26.3)	0.035	7 (64 ± 28.4)	0.020	8 (73 ± 26.3)	0.035	1 (13 ± 17.0)	0.305
Syndromic (n = 18)	18 (100)	1.00	14 (78 ± 19.2)	0.094	18 (100)	1.00	0 (0)	1.00
Developmental (n = 8)	8 (100)	1.00	8 (100)	1.00	8 (100)	1.00	0 (0)	1.00

*The values are given as the number with the percentage and 95% confidence interval in parentheses.
†The p value is for the significance of the difference compared with the group with no comorbidities.
‡The percentage is of the patients monitored successfully (with either somatosensory or motor evoked potential monitoring).

True Electrophysical Events and Neurologic Events

Of the 151 patients who were successfully monitored with either the motor or the somatosensory evoked potential technique, twenty (13%) had changes on electrophysical monitoring leading to an alert (Fig. 2). Of these twenty alerts, seven were caused by excessive paralytic agent and one was triggered by an altered lead position (see Appendix). These eight alerts were deemed false-positive electrophysical changes. Therefore, twelve of the 151 successfully monitored patients had a true electrophysical event, and two of them were found to have new postoperative neurologic deficits that represented a change from the findings on their preoperative neurologic examination. None of the 139 patients who did not have a true electrophysical event had new postoperative neurologic deficits. Therefore, the patients with a true electrophysical event had a significantly higher rate of neurologic events than did the patients who did not have a true electrophysical event (p < 0.001). Finally, the ability of electrophysical monitoring to detect neurologic deficits was found to have a sensitivity of 100% (95% confidence interval, 19.8% to 100%) and a specificity of 87.9% (95% confidence interval, 81.3% to 92.5%). The prevalence of detected neurologic deficits in the 151 successfully monitored patients was 1.3% (95% confidence interval, 0.2% to 5.2%).

Identifiable Exposures and Actions Taken

All of the twelve patients with a true electrophysical event had an identifiable exposure, defined as an intraoperative action (by either the surgeon or the anesthesiologist) that anatomically and temporally could explain the true electrophysical event. In no case was there a true electrophysical event that could not be explained by an identifiable exposure. The identifiable exposure was the act of curve correction in eight patients, hypotension in two, malposition of a pedicle screw in one, and direct spinal cord trauma (the suction device was seen to strike the posterior aspect of the spinal cord) in one.

An action to reverse the identifiable exposure was taken in eleven of the twelve patients. (The exception was the one who had direct spinal cord trauma.) An increase in the blood pressure was the primary intervention in five of the eleven patients, although the blood pressure was increased in all eleven. The curve correction was relaxed in five patients, and a pedicle screw was removed in one.

The action taken resulted in a return of the altered electrophysical values to baseline in eight of the patients. The electrophysical values did not return to baseline in four patients. In two of them, the somatosensory evoked potentials were improving at the end of the operation. One of these patients awoke with positive neurologic findings, which completely resolved in five days. Postoperatively, the second patient had no neurologic change from the preoperative status. The two patients who did not have intraoperative resolution of the episode had severe cerebral palsy and did not have a detectable neurologic change postoperatively.

Type of Spinal Deformity and Comorbidities

With the numbers of patients studied, we did not identify a significant difference between the rate of true electrophysical events in the patients with idiopathic scoliosis and the rate in any of the other groups (Table II). The rate of true electrophysical events in the patients with cardiopulmonary comorbidities was significantly higher than that in the patients with no comorbidities (p = 0.011) (Table IV).

Discussion

Somatosensory evoked potential monitoring was successful in 95% of our patients with idiopathic scoliosis and motor evoked potential monitoring was successful in 92% of those patients, rates that are consistent with those in prior reports^13,18. In the literature, the reliability of electrophysical monitoring in patients with spinal deformity with a neurogenic cause has been questioned. Owen et al.¹⁹ stated in 1994 that somatosensory evoked potential monitoring is unreliable and nonspecific in patients with neuromuscular scoliosis. However, subsequent technological and methodological improvements, including new anesthetic protocols, multiple-site monitoring, and new computer algorithms, have improved the efficacy of somatosensory evoked potential monitoring in this group of patients. We demonstrated an 83% success rate with somatosensory evoked potential monitoring and a 72% success rate with motor evoked potential monitoring in patients with neuromuscular deformity, rates that are consistent with those in the recent literature¹³. These rates were significantly lower than those for the patients with idiopathic scoliosis. It should be stated, however, that we performed multiple comparisons and this increases the probability of documenting a significant difference when one does not exist. Either motor or somatosensory evoked potential monitoring was successful in 89% of our patients with a neuromuscular disorder and in 89% of those with neurologic comorbidities. This rate was not significantly different from that seen in the patients with idiopathic scoliosis. Therefore, despite the difficulties, we were able to reliably monitor the majority of patients with neuromuscular scoliosis.

Our study documented true electrophysical events in 8% (twelve) of 151 patients, a rate that was lower than the 15% rate reported by Pelosi et al.¹³. In addition, we observed a lower rate of postoperative neurologic deficits in patients with a documented electrophysical event (17%; two of twelve) than did Pelosi et al. (37%). In this study, electrophysical monitoring detected neurologic deficits with a sensitivity of 100%, a specificity of 87.9%, and a prevalence of 1.3%. In the study by Pelosi et al., the sensitivity was 100%, the specificity was 91.5%, and the prevalence was 4.8%. In both studies, electrophysical changes had a 100% sensitivity—i.e., all of the neurologic deficits were preceded by detection of electrophysical changes. The specificity in our study (87.9%) was slightly lower than that in the study by Pelosi et al. (91.5%). These results show a clear relationship between electrophysical changes and neurologic events, leading to the conclusion that electrophysical events are an early sign of neurologic injury.

In our study, normal motor evoked potentials at the conclusion of the surgery always predicted the absence of motor deficits. In one case, the electrophysical findings deteriorated and then returned to baseline, but the patient still had a postoperative neurologic deficit. In this patient, the injury was the result of a medially placed pedicle screw and led to an L5 radiculopathy. It is known that somatosensory and motor evoked potential monitoring is not specific for individual nerve roots, and therefore it is possible for the results of motor and somatosensory evoked potential monitoring to be normal in the presence of a nerve root injury.

Attempted curve correction was the identifiable exposure in eight (67%) of twelve patients in our study. This finding is consistent with that of Pelosi et al. (ten of sixteen patients; 63%). However, the rate of hypotension as the identifiable exposure in our study (two of twelve patients; 17%) was lower than the rate identified by Pelosi et al. (six of sixteen; 38%). In addition, our study shows that actions taken when an electrophysical event occurs are likely to result in a satisfactory neurologic outcome even when the actions do not lead to resolution of the electrophysical changes. This observation is also consistent with the findings of Pelosi et al. Therefore, electrophysical events reflect a potentially reversible neurologic injury, and action to reverse the identifiable exposure should be taken whenever an electrophysical event occurs with an identifiable exposure (such as curve correction or hypotension).

As noted in the Materials and Methods section, a wake-up test was performed for some patients with persistent electrophysical changes. The wake-up test is useful in several ways, and it can confirm the presence or absence of impaired spinal cord function. Foot movement during a wake-up test may occur even if electrophysical signals have not yet returned to baseline. Wake-up tests are not useful for patients who have substantial cognitive impairment or neurologic or primary muscle disease.

Our study showed relatively high rates of electrophysical events in patients with spondylolisthesis (33% [one of three]) and kyphosis (15% [two of thirteen]). These trends are in keeping with established knowledge^1,20 that patients with sagittal plane deformities may be at greater risk for neurologic injury during surgery for correction of spinal deformity.

There is ample evidence that ischemia secondary to systemic hypotension or vascular injury can lead to injury to the spinal cord. We hypothesized that patients with decreased cardiopulmonary reserve, as a result of either decreased cardiac output or an abnormality of the lungs compromising their ability to oxygenate the blood, may be at higher risk for ischemic injury to the spinal cord. In this study, patients with cardiopulmonary comorbidities demonstrated a higher rate of true electrophysical events than did those with no comorbidities (p = 0.011). This may be related to the relatively fragile circulation of the anterior corticospinal tracts that are supplied by the anterior spinal artery²¹. Physiologic variables, such as systemic blood pressure, intravascular volume, and blood hemoglobin concentration, that affect blood flow and oxygen delivery to the spinal cord may be influenced by congenital cardiopulmonary disease^22,23. Unfortunately, the methodology by which we assigned a primary comorbidity to patients was not robust and the number of subjects in our study was small. Therefore, our findings of a significant increase in electrophysical events in patients with cardiopulmonary comorbidities should be interpreted with caution. Clearly, a better study would be one in which the investigators determined cardiac output and pulmonary function by directly measuring oxygen saturation during the procedure or cardiac ejection fractions prior to and during surgery.

Combined somatosensory and motor evoked potential monitoring is technically feasible and effective at demonstrating neurologic injury during all types of pediatric spinal deformity surgery. Even though it is technically more difficult and less reliable in patients with neuromuscular scoliosis, it is reliable in the majority of cases and should be attempted in patients undergoing correction of spinal deformity. Such monitoring is effective at detecting early neurologic injury and provides the surgeon with an opportunity to reverse the neurologic injury. When an electrophysical event occurs during surgery and there is an identifiable exposure, action should be taken to reverse this exposure. Patients with kyphosis and those with cardiopulmonary comorbidities appear to be more prone to electrophysical events and should be approached with special caution and careful electrophysical monitoring. Patients with spondylolisthesis, although generally not at risk for cord injury, demonstrate a high rate of positive electrophysical change as well and need to be monitored carefully.

Appendix

A table showing details on all subjects with electrophysical changes is available with the electronic version of this article on our web site at jbjs.org (go to the article citation and click on "Supporting Data").

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Topics

comorbidity ; evoked potentials, motor ; spinal cord injuries ; trauma, nervous system ; spinal cord ; scoliosis, neuromuscular ; somatosensory evoked potentials ; spinal deformities

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Michael G. Vitale, Derek W. Moore, Hiroko Matsumoto, Ronald G. Emerson, Whitney A. Booker, Jaime A. Gomez, Edward J. Gallo, Joshua E. Hyman, David P. Roye, Jr.; Risk Factors for Spinal Cord Injury During Surgery for Spinal Deformity. The Journal of Bone & Joint Surgery. 2010 Jan;92(1):64-71.

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