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 Table of Contents  
ORIGINAL ARTICLES
Year : 2021  |  Volume : 4  |  Issue : 1  |  Page : 113-120

Position-related neurovascular injuries detected by intraoperative monitoring


Department of Neurology, Baylor College of Medicine, Houston, Texas, USA

Date of Submission18-Aug-2019
Date of Decision07-Jul-2020
Date of Acceptance26-Aug-2020
Date of Web Publication28-Jan-2021

Correspondence Address:
Shaila Gowda
Department of Neurology, Baylor College of Medicine, 7200 Cambridge Street, Houston, TX.
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ISJ.ISJ_59_19

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  Abstract 

Background: Poor patient positioning during surgeries can result in vascular and peripheral nerve injuries. The purpose of this study was to analyze the various etiologic factors related to positioning detected by intraoperative monitoring (IOM) and make recommendations for prevention of comorbidities. Materials and Methods: The data for a total of 4450 consecutively monitored patients who underwent orthopedic and neurosurgical procedures were retrospectively reviewed. Patients with signal changes related to positioning detected by IOM were analyzed for position, modalities, timing of interventions, duration of surgery, and etiologic factors. Deficit and non-deficit groups were further compared using Wilcoxon rank sum test. Results: Intraoperative evidence of impending neurologic injury was seen 1.1% times, most frequently due to malpositioning of upper extremities (57%) in prone position (55%). Shoulder tape, bootstrap, thigh/hip pads, sitting and lower extremity malpositioning were other etiologic factors. Appropriate intervention was performed within 3min 66% of the time. Four patients developed new postoperative deficits: brachial plexopathy (n = 3) and bilateral sciatic neuropathy (n = 1). The deficit group had longer duration of surgery (P = 0.031), and neurophysiological (NP) signal changes persisted for an increased time interval (P = 0.0084) when compared to the non-deficit group. Conclusion: Prolonged duration of surgery and persistence of NP signal changes can increase the risk of potential neurovascular injury. Intraoperative neurovascular injuries due to positioning can occur in various settings. Early recognition of signal changes during monitoring and immediate intervention is likely to prevent neurological deficits.

Keywords: Intraoperative monitoring, neurophysiological change, neurovascular injury, somatosensory evoked potentials, transcranial electric motor evoked potentials


How to cite this article:
Gowda S. Position-related neurovascular injuries detected by intraoperative monitoring. Indian Spine J 2021;4:113-20

How to cite this URL:
Gowda S. Position-related neurovascular injuries detected by intraoperative monitoring. Indian Spine J [serial online] 2021 [cited 2021 May 12];4:113-20. Available from: https://www.isjonline.com/text.asp?2021/4/1/113/308201




  Introduction Top


Patient positioning is the joint responsibility of the surgeon and the anesthesiologist. Vascular and peripheral nerve injuries can occur during surgeries due to poor positioning. These are preventable complications but continue to occur. Numerous reports have shown the utility of upper extremities (UEs) somatosensory evoked potentials (SSEP) in predicting impending neural injury related to positioning in spine surgeries.[1],[2],[3],[4],[5] Several studies have validated the role of intraoperative monitoring (IOM) with SSEP and transcranial motor evoked potentials (tc-MEP) in the prevention of injury to neural structures.[6],[7],[8] A meta-analysis of pooled published cases reported IOM as 94% sensitive and 96% specific when used as diagnostic modality for potential neurologic injury.[9] The purpose of this study was to collectively analyze the various etiologic factors related to positioning detected by IOM in a single institution in patients undergoing orthopedic and neurosurgical procedures. The intent was to present exemplary case scenarios related to positioning responsible for impending neurovascular injuries detected by IOM and to make necessary recommendations for improved outcomes. The clinical utility of this study may help potentially decrease perioperative position related comorbidities when utilizing additional tools like IOM during surgeries.


  Materials and Methods Top


The database was retrospectively reviewed for positive neurophysiological changes during IOM for surgeries performed between April 2003 and April 2014. A total of 9436 surgeries used IOM during this period, of which 4886 used electromyography (EMG) only and were excluded from the study. The remaining 4550 cases were further reviewed to include only those cases with positive SSEP and/or tc-MEP changes due to positioning. Signal changes due to anesthetics, temperature fluctuations, or blood pressure variability were excluded. The data were then analyzed for the following: modalities monitored, type and duration of neurophysiological (NP) change persistence when encountered, time of occurrence since onset of surgery, length of surgery, causative factors, type of intervention performed by surgical/IOM team with or without any resolution. Medical records were reviewed for patient demographics, surgical procedure, and postoperative course. SSEP monitoring was performed with stimulation of median nerve (MN) or ulnar nerve (UN) at the wrist, posterior tibial nerves (PTN), and/or peroneal nerves (PN) at the ankles/knees. Stimulus was delivered using 13-mm disposable subdermal needle electrodes with a 300 microsecond square wave electrical pulse at the rate of 2.66 Hz with constant current output of 25–40 mA in the upper and 40–70 mA in the lower extremities so as to maximize the SSEP amplitude for each patient. Stimulus delivery was interleaving. Potentials were recorded using disposable 13-mm subdermal needle electrodes affixed to Cz/Cpz, C3/Cp3, and C4/Cp4, and referenced to Fz/FPz (all electrodes placed according to international 10–20 system). A significant change in SSEP response was considered with 10% latency prolongation and/or 50% decrease in amplitude from baseline response. The tc-MEP stimulation was performed using disposable subdermal corkscrew electrodes placed 2 cm anterior to C3 and C4 with voltages between 300 and 600 V, pulse width of 50 microseconds, train of 3–6 square wave pulse, and interpulse interval of 1–4 microseconds. The responses were recorded from sterile subdermal needles placed in the muscles of upper and lower extremities.

A significant tc-MEP change was defined if there was an acute unilateral or bilateral amplitude loss of >70% that was repeatable.[10] A complete loss of tc-MEP and SSEP was interpreted as loss of response. All cases that used IOM before June 2004 had only SSEP studies, and tc-MEPs were performed in subsequent cases. Anesthesia was induced with propofol and rocuronium or succinylcholine and maintained with isoflurane/±nitrous oxide or with propofol/remifentanil and vecuronium titration to maintain at least 2–3/4 train-of-four twitches. The study was conducted after the institutional review board (IRB) approval was obtained.


  Results Top


A total of 4450 consecutive patients who underwent orthopedic and neurosurgical procedures utilizing IOM were analyzed. Orthopedic procedures were further classified into spine and hip procedures. Of total cases, 84% cases were spine, 6.5% were hip (acetabulum) surgeries, and 9.5% were craniotomies. All had SSEP monitoring, and tc-MEPs were performed in 67% of the cases.

Intraoperative evidence of impending neurologic injury was seen 1.1% times (49 patients); most frequently due to malpositioning of UE (57%) in prone position (55%). Patient positions during surgery were supine (n = 15), prone (n = 27), lateral (n = 1), lateral decubitus/prone (n = 4), and sitting (n = 2). There were 37 males and 12 females, the average age was 45.3 ± 21.6 years. Of the total 49 patients, 78% were spine, 14% hip, and 8% were craniotomy cases, and 27% cases were identified in the last 1 year of the study period. Modalities monitored included SSEP (n = 49), tc-MEP (n = 20) with or without EMG depending on the case and surgeon preference.

Changes included UN or MN SSEP (n = 37), PTN or PN SSEP (n = 7), combination of SSEP and tc-MEP changes (n = 4), and tc-MEP change only (n = 1). Improper extremity position rectified with appropriate positioning was grouped as malpositioning. The rest was classified based on the etiologic factor identified as the cause [Table 1]. The mean duration of surgery for the entire group was 237.2 ± 26min, and the mean total duration the signal changes lasted before significant or complete resolution was 33.76 ± 49.85min. Time of occurrence of NP signal changes was at 64.65 ± 63.05min since incision. The mean time taken to intervene after the alert was 17.4 ± 40.05min. Two-thirds of the time, the intervention was performed within 3min, 82% of the time within 15min. There was no intervention performed in one case. Repositioning or addressing the causative factor showed some improvement or complete resolution of signal changes in 47 of 49 patients. Three patients (3/47) had new postoperative deficit: brachial plexus palsy (n = 2) and bilateral sciatic neuropathy (n = 1). In the remaining two who did not improve: one had new postoperative brachial plexopathy(n = 1) and one could not be evaluated due to postoperative confusion and death. In total, four patients (4/49) had new postoperative deficits. Patient details are highlighted in [Table 2]. There was a gradual loss of UN SSEP signals in Patient 1 [Figure 1] operated in the prone position for scoliosis surgery, 73min into surgery. As part of troubleshooting, the IOM technologist moved the recording electrode to axilla, and a peripheral response was recorded, which was presumed as normal Erb’s point response, and monitoring was considered stable. There was a gradual loss of tc-MEPs [Figure 2] starting approximately 4h later. Patient 2 underwent right-sided acoustic neuroma resection in supine position. There was a loss of right UN SSEP 52min into surgery. Initial intervention with arm repositioning was done at 7min with some improvement in latency and amplitude. Latency was however prolonged at 22%, and amplitude was at 48% of baseline values. Recurrent loss of right UN SSEP occurred at 134 and 327min into surgery. Attempts to reposition were made immediately after the signal changes and intermittently as part of troubleshooting. However, the latencies and amplitude continued to remain at the values aforementioned. Patient 3 was operated in the left lateral decubitus/prone position for kyphosis surgery. There was a loss of unilateral UN SSEPs twice during the course of surgery. The latency and amplitude improved but did not return to baseline values. The latency showed 20% prolongation, and amplitude was 42% of baseline values.
Table 1: Etiologic factors and modalities affected during surgical procedure

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Table 2: Demographics of patients with deficits

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Figure 1: (A) Gradual loss of left ulnar nerve somatosensory evoked potentials. (B) Complete loss with peripheral axillary response (bottom notched arrow). (C) Water fall showing loss on the left side and retained responses on the right

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Figure 2: (A) Presence of transcranial motor evoked potential (tc-MEP) in the left upper extremity at baseline. (B) Loss of tc-MEPs. (C) Waterfall showing loss in the left side and preserved MEPs in the right side

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Two patients (Patients 4 and 5) were operated in the sitting position for cervical spondylosis. Patient 4 was postoperatively clinically diagnosed with bilateral sciatic neuropathy. Analysis of the PTN SSEP data showed the presence of normal peripheral popliteal fossa (PF) responses with gradual loss of subcortical and cortical responses bilaterally. No electrodiagnostic studies were available for review.

Second patient (Patient 5) was a 64-year-old male with diagnosis of cervical spondylosis with myelopathy who underwent a posterior cervical laminectomy in the sitting position. There was a swift loss of right PTN cortical and subcortical SSEP response and tc-MEPs in right lower extremity when patient was moved from supine to sitting position. This was approximately 30min from the time of initial baseline recording of NP signals in supine position. The signals returned when patient was laid back in the supine position at the end of the procedure [Figure 3]. This patient did not incur any postoperative deficits.
Figure 3: Bilateral posterior tibial nerve (PTN) somatosensory evoked potentials: Normal baseline response in supine position (line arrow), with swift loss of subcortical and cortical response in sitting position ( broad arrow) and return of signals in right PTN (notched arrow); popliteal fossa responses remain unchanged (open arrow)

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All four patients with deficits showed clinical improvement before discharge. The deficit and non-deficit groups were further compared using the Wilcoxon rank sum tests [Table 3]. Patients who experienced deficits had longer duration of surgery (P = 0.031), and the NP changes persisted for an extended duration (P = 0.0084). The differences in the time taken to intervene between the two groups and the number of recurrences of signal changes was not large to achieve statistical significance.
Table 3: Comparison of deficit and non-deficit groups

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  Discussion Top


Neurologic injury is a common perioperative morbidity as a result of improper patient positioning.[11] Peripheral nerve injury is the second most common cause of professional liability and patient injury in the practice of anesthesiology.[12] A total of four patients in this series had neurological deficits postoperatively. Three patients had unilateral brachial plexopathy due to malpositioning of UE. Failure to identify the diminishing amplitudes of SSEP signals, lack of adequate analysis, and appropriate troubleshooting to restore the potentials prevented timely intervention in Patient 1. IOM provides real-time assessment of the status of nervous system, which allows for the surgeon to modify the surgical course if it is indicative of impending injuries.[13],[14],[15] This case was being monitored by a newly trained (<6 months) technologist with no additional supervision. The risk of neurologic injury with spine surgeries was reported to be less than half if monitoring was performed by an experienced team (monitored cases >300/year) compared to an inexperienced team (cases <100/year).[3] Although the total number of cases performed in this institution was over at least 500 cases/year, the monitoring technologist had limited experience. In a survey by Stecker and Robertshaw,[16] 75% of the respondents providing IOM data interpretation had less than 1 year of experience in IOM, and 28% provided only descriptions and not data interpretation of wave forms. Unfortunately, guidelines for data description or the extent of communication of data interpretation during IOM are not uniform across institutions. There is a lack of adequately trained and certified technologists and physicians, which has led to significant barrier to more widespread use of IOM.[14],[16],[17] Recent monitoring guidelines by Medicare for physicians practicing in United States have posed additional challenges.[18] Surgeon-driven neuromonitoring system was examined and reported as safe and effective for spinal deformity surgeries and to provide an option in the absence or unavailability of monitoring personnel.[19] However, this study did not include SSEPs as part of the diagnostic modality. Additional studies are needed to validate this approach.

Brachial plexus is prone for injury from malpositioning of UE[5] due to its long and superficial course in the axilla. Ischemia of intraneural capillaries from stretch and compression of the plexus is most frequently noted in prone position. Extreme abduction of shoulders with elbows flexed or arms raised above the head (reinforced to make room for surgeons) makes the plexus vulnerable to stretch injuries in prone position. Recommendations include limiting shoulder abduction to 90° or less. When shoulder abduction of 90° is necessary, then elbows must be bent at 90° and not fully extended.[20] In Patients 2 and 3, despite multiple efforts to reposition the arms, the SSEP signals improved but did not return to baseline, suggesting likely an ongoing ischemia and susceptibility of brachial plexus. However, some case reports suggest that even with arm positions with abduction of less than 90°, patients may be at risk for brachial plexus injury.[21],[22],[23],[24] Brachial plexus is also prone for injury from compression in the lateral decubitus position when the dependent arm and shoulder are positioned between the thorax and the table. Recommendations include positioning the dependent arm anterior to thorax,[25] and arms should not be suspended from an L-shaped bar.[26] Extension and lateral flexion of the head to one side widens the angle between the head and opposite shoulder in the lateral decubitus position but this should be avoided as this increases the stretch on brachial plexus.[27] When patient is in the supine position, elevating the elbow at least 6 inches above the table is recommended to prevent stretching of the brachial plexus.[26]

Two patients were operated in the sitting position for cervical spondylosis. Surgery in sitting position for patients undergoing posterior fossa or cervical lesions provides adequate access, lowers intracranial pressure, and allows gravity drainage of blood and CSF.[28] However, complications include venous air embolism, tension pneumocephalus, quadriparesis, hemodynamic instability, and in rare instances, sciatic nerve (SN) injury.[29],[30],[31] Patient 4 was diagnosed with bilateral sciatic neuropathy. SN injury as a complication of surgery performed in sitting position has been reported in earlier series[32],[33],[34],[35] but unlike the case in this study, there was no IOM performed. In another report, position-related SN injury was detected by SSEPs during spinal surgery.[36] However, patients were in kneeling and prone position, and none had deficits. Mechanism of SN injury during surgeries in sitting positions is not well known but proposed mechanisms include SN injury due to gluteal compartment syndrome,[34] stretch injury due to excessive hip flexion,[33] or compression against ischial tuberosity. Patient characteristics such as low body mass index (BMI), preexisting neuropathy due to diabetes or vascular disease, long duration of surgery, and anatomic variations have been identified as risk factors for perioperative neuropathy. The SSEP recordings do not specifically localize intraoperative changes to SN. However, when signals are lost above PF and iatrogenic injuries are ruled out, malpositioning affecting SN should be strongly considered. Proper patient positioning and increased awareness of the susceptibility of the SN compression injuries, especially during prolonged surgery, are needed to minimize intraoperative morbidities. Recommendations include limiting the degree of hip flexion and knee extension to prevent excessive SN stretching and adequate careful padding underneath buttocks to prevent compression from ischial tuberosity.[35]

Acute flexion of the neck in the sitting position in an anesthetized patient can stretch the cord and decrease local cord perfusion, especially if the mean arterial pressure is low. Appropriate intervening measure after signal changes are noted, is critical in preventing perioperative morbidity. In the second patient (Patient 5) operated in sitting position, surgeon prevented any intervention after the alert. Signal loss persisted for almost the entire length of surgery. In some instances, there is a lack of surgeon’s response to a warning after the alerts are communicated by the monitoring team. In a large IOM series,[37] surgeons responded by appropriate interventions in 26.4% of the cases only. In another study, 44% felt that surgeons responded to a warning less than 50% of the time and 25% felt the surgeons responded only 10% of the time. While most surgeons are aware of IOM, some do not have a clear understanding of what actions to undertake in the context of IOM signal changes. It was found that surgeons were more likely to respond to warnings issued by monitorist or physicians with higher degree of experience.[16] The experience and knowledge of the individual IOM technologist and/or supervising physician plays a major role in providing reliable timely warning criteria and its application to the surgical team.

Use of shoulder tape/brace or arm sled was associated with decreased UE SSEP signal in 11 patients. The upper shoulder and arm are often depressed and fixed with shoulder tape to get better exposure and access. Shoulder braces are often used in surgeries to prevent patient movement on the operating table. Arm sleds are used to securely hold patient’s arms and legs on the operating table and allow surgeons to lean against the guard without disturbing the anesthesia lines. Both stretching and compression of the brachial plexus are the principal mechanisms of injury here. Particular attention was paid to the shoulder tape release or brace adjustment or release of arm in the sled by the IOM technologist in this series. The safety of the braces has been questioned despite the use for over 50 years.[24] The risks of using shoulder tape, brace or arm sleds are difficult to quantify as it is impossible to know the total number of patients in whom these have been used and have been helpful.

Compression of deep peroneal nerve can occur at the ankle with the use of traction boots. Entrapment of PTN beneath the flexor retinaculum on the medial side of the ankle can cause tarsal tunnel syndrome. Entrapment may also include the two branches, the medial and lateral plantar nerves. Clinically, patients can present with aching, burning, numbness, and tingling involving the sole, the distal foot, the toes, and occasionally the heel. Loosening/removing the traction boot or ace wrap improved or returned the responses to baseline in three patients who underwent hip surgery, open reduction and internal fixation (ORIF) after they had ipsilateral loss of PTN/PN SSEPs in the operating limb [see [Figure 4]]. None had any postoperative deficits. Clinical significance of loss of signals in these types of cases is imperative for the prevention of peripheral nerve injuries.
Figure 4: Case of open reduction internal fixation for acetabulum fracture showing right posterior tibial nerve somatosensory evoked potentials (SSEPs) in the popliteal fossa (PF) (A) and cortical channels (B). Loss of SSEPs (bottom arrow) and return of signals (notched top arrow) when the boot traction was decreased

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An isolated case of bilateral femoral artery ischemia was detected by IOM during posterior scoliosis surgery operated in prone position.[38] Bilateral femoral artery occlusion was caused by distal placement of hip and thigh pads, resulting in gradual loss of LE SSEPs and eventually tc-MEPs. Similar case with right lower extremity monoplegia detected by loss of tc-MEPS only has been reported.[39] Hip pads must be carefully placed over the anterior superior iliac spines, and not distally where it can occlude femoral artery in prone position.

Position-related changes can occur anytime during the course of surgery. Repositioning should ideally reverse this and prevent perioperative injuries.[40] Nine patients had recurrence of loss or diminished amplitudes more than once during surgery: two patients being in the deficit group. Although an association of the number of recurrences was not a predictor of postoperative deficit, the significance of this needs to be determined in larger studies. Interventions were performed within 15 minutes after the alerts in 82% of the cases. The deficit group in this study had longer operative times and also showed increased duration of NP signal changes in the affected extremity, indicating prolonged exposure to neural injury. Longer operative times have been associated with peripheral nerve injuries.[41] Halogenated or nitrous oxide–based agents influence SSEP amplitude and latency, but SSEPs are generally more resistant to anesthetics than MEPs.[42] MEP responses have been noted to gradually decline under general anesthesia over the duration of surgery[43] despite stable doses of the anesthetic agents, described as “anesthetic fade”,[6] thus requiring higher degree of MEP stimulation parameters to offset this effect.[44] Interpretation of “anesthetic fade” is important as this can give rise to false-positive results. The changes encountered with anesthetic fade typically are gradual and global as opposed to iatrogenic. Surgical stage, spinal level, and type of signal changes encountered often help in differentiating the etiology.

Similar to other studies,[45] malpositioning of UE was the major cause of SSEP changes, but unlike others, only 1.1% of total patients in this study were identified as showing positional changes detected by IOM. This is felt to be due to substantial underreporting and variable technologist-documented response. This study is however limited due to its retrospective nature, small sample size of patients with neurologic deficits, lack of standardized institutional guidelines in place through most of the study period, and lack of postoperative satisfaction score for further analysis.


  Conclusion Top


This study collectively emphasizes the neurovascular injuries detected by IOM, related to positioning and the importance of timely detection and intervention. Longer duration of surgery increases the risk of neural injury. Persistence of neurophysiological changes is suggestive of ongoing neurovascular injury. The expertise of the monitoring technologist and/or supervising physician is important in providing careful interpretation of IOM data for timely intervention. Surgical teams should strive to prevent any position-related injuries on a case-by-case basis, especially when additional tools, such as intraoperative monitoring, are available.

Institution where the study was conducted

This study was conducted at William Beaumont Health System, Royal Oak, Michigan.

Institutional review board (IRB) approval was obtained.

Acknowledgements

We acknowledge the statistics department for their assistance in this study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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