Neck Surgery. Brendan C. Stack, Jr., Mauricio A. Moreno, MD

24. Intraoperative Neural Monitoring in Neck Dissection

Bradley R. Lawson, Dipti Kamani, and Gregory W. Randolph Abstract

Intraoperative nerve visualization is the accepted gold standard for prevention of neural injury during neck dissection. However, a structurally intact nerve does not always correlate with a postoperatively functioning nerve. Intraoperative neural monitoring has emerged as an adjunctive and additive tool for nerve identification and prognostication of postoperative function. While much of the existing data focus on surgery of the central neck compartment, we present emerging applications for monitoring of the nerves at risk in lateral compartment neck dissection.

Keywords: neural monitoring, thyroidectomy, central neck dissection, lateral neck dissection

24.1 Introduction

Neck dissection is a technically demanding operation that may present risk to numerous nerves during the course of a single procedure. Nerve visualization during surgery has long been considered the gold standard for the prevention of neural injury. However, an intraoperatively visualized and structurally intact nerve does not always correlate with a postoperatively functioning nerve. Neural monitoring has garnered increasing attention from thyroid and parathyroid surgeons worldwide, largely due to its prognostic information regarding postoperative nerve function. This technology has also been applied to lateral neck dissection. Emerging data are beginning to support the hypothesis that neural monitoring can reduce the incidence of neural injury. This chapter focuses on the history of intraoperative neural monitoring (IONM), its impact on surgical practice, standards of IONM, and application of IONM to lateral neck dissection.

24.2 Historical Overview

In 1848, Du Bois-Reymond became the first to demonstrate nerve action potentials and describe electrical activity of muscle with electromyography (EMG).1 IONM allows for localization of neural structures, tests the function of these structures, and provides early detection of neural injury. The goal of IONM is to identify neural injury prior to the onset of irreparable damage, thereby allowing immediate corrective actions to be taken.1 Historically, IONM has been most commonly used by spine surgeons, with neurosurgeons, vascular surgeons, orthopedic surgeons, urologists, and otolaryngologists all utilizing monitoring to some extent. The most common procedures in which IONM is applied include spine surgery, carotid endarterectomy, selected brain surgeries, and ENT procedures such as vestibular schwannoma resection, parotidectomy, thyroidectomy, parathyroidectomy, and neck dissection. Shedd and Durham in 1966 published the first report of electrical stimulation of the recurrent laryngeal nerve (RLN) and superior laryngeal nerve (SLN) in a canine model via endolaryngeal balloon spirog- raphy. A pressure recording from a balloon in the larynx consistently demonstrated recognizable changes upon stimulation of the RLN, thereby providing a means for its electrical identification. The authors were then able to confirm in two human patients that the endolaryngeal balloon pressure recording provided a clear signal of RLN and SLN stimulation.2 In 1970, Riddell published a 23-consecutive-year experience of electrical identification of the RLN, with the addition of laryngeal palpation as a confirmatory safety measure.3

Different IONM techniques have been developed over the past four decades, including laryngeal palpation, glottic observation, intramuscular vocal cord electrodes, postcricoid surface electrodes, anterior laryngeal electrodes, and endotracheal tube (ETT)- based surface electrodes.4,5 Due to the ease of setup and use as well as their noninvasive nature, ETT-based surface electrodes have become popular for IONM in central neck surgery.4,5,6,7 While intramuscular electrodes deliver higher amplitudes, they are more complicated to insert, may be placed in the wrong location, may migrate during surgery, and may even break in some cases.

In light of these many different techniques for IONM, standardization became a priority in order to promote uniform application of this emerging technology. The International Neural Monitoring Study Group (INMSG) was founded in 2006 to guide the emerging field of neurophysiologic monitoring, particularly of the vagus and laryngeal nerves in thyroid and parathyroid surgery.8

Vagal and RLN monitoring have gained widespread acceptance within the global surgical community. A recent study from Pennsylvania State University indicates that IONM is used by 80% of otolaryngologists and 48% of general surgeons who perform thyroid and parathyroid surgery at academic centers in the United States.9 Neural monitoring has become the standard of care in Germany; 93% of thyroidectomies were performed with RLN monitoring according to a national survey in 2010.10 Exposure to IONM during training is associated with a 3.1 times greater likelihood of using it in practice.11 Of note, use of IONM is actually more common among high-volume thyroid surgeons (>100 cases per year). This suggests that IONM is not being used as a substitute for anatomical knowledge and surgical skill, but rather as a useful adjunctive tool to those who are most surgically experienced.11.12

Data continue to be discordant regarding the impact of neural monitoring on rates of neural injury in thyroid and parathyroid surgery. In a study of more than 850 patients undergoing revision surgery, Barczynski et al found transient and permanent RLN injuries in 2.6 and 1.4% of nerves with IONM versus 6.3 and 2.4% of nerves without IONM, respectively. The rate of transient paralysis was statistically significantly reduced when neural monitoring was used.13 Thomusch et al compared visual RLN identification with neural monitoring in over 5,000 procedures; they found rates of transient and permanent paralysis of 1.4 and 0.4% of nerves at risk with IONM versus 2.1 and 0.8% of nerves at risk with visual identification alone. A multivariate logistic regression confirmed that use of neural monitoring decreased the rate of postoperative transient (p <0.008) and permanent (p <0.004) RLN palsy as an independent factor by 0.58 and 0.30, respectively.14 However, Pisanu et al performed a meta-analysis of over 35,500 nerves at risk and found no statistically significant difference in the rates of transient and permanent RLN paralysis with and without neural monitoring.15

Dralle et al looked into this issue and found that an adequately powered study would require 9 million patients per arm for benign goiter and 40,000 patients per arm for thyroid malignancy surgery to detect statistical differences in the rate of RLN palsy with or without IONM.16 The argument for selective versus routine use of IONM continues to evolve among the community of surgeons who use it. We perform IONM in all cases in order to distribute the benefit of this additional information to all patients. Dionigi et al have also articulated the point that difficult cases may not always be apparent preopera- tively.7 Routine use of IONM provides greater experience in interpreting the data, along with improved troubleshooting skills with the device itself should difficulties arise during a particularly challenging case. Current INMSG guidelines recommend the routine use of IONM for thyroid and parathyroid surgery, including central neck dissection.4 Currently, no guidelines exist for the use of IONM in lateral neck dissection.

24.3 Benefits of Intraoperative Neural Monitoring Application

The discussion relating to rates of RLN paralysis represents a single and rather limited perspective for evaluation of the use of IONM and its benefits to patients. Overall benefits offered by IONM include (1) nerve identification/neural mapping, (2) aid in dissection following nerve identification, and (3) injury iden- tification/postoperative neural prognostication. When one appreciates the electrical information provided by IONM as additive and confirmatory to visual information, these benefits become rather apparent. Neural monitoring does not replace but adds to anatomic knowledge and surgical skill, and it provides a new functional dynamic. The need for visual identification of the nerve is not replaced by IONM; this technology is not intended to be used as a “divining rod.”

24.3.1 Neural Identification and Mapping

The RLN can be mapped out in the paratracheal region through linear stimulation with the neural probe. Visual identification then follows using directed dissection in the process referred to as neural mapping. Multiple studies report nerve identification rates of 98 to 100% using such neural mapping.5 Chiang et al reported a 100% identification rate, including nerves (25% of the total) that were classified as difficult to identify visually because of their complex anatomy.17 The previsualization neural mapping allows for rational and directed dissection, which may be a substantial advantage in scarred operative fields and cases with complex anatomy (such as ramified nerves, large goiters, revision surgeries, etc.).18

24.3.2 Aid in Neural Dissection

After the nerve has been visually identified, intermittent stimulation of the nerve versus adjacent nonnerve tissue can be helpful in tracing the nerve and its branches through the surgical field. This is analogous to intermittent facial nerve stimulation during parotidectomy. Accurate delineation of the medial border of the RLN can be very useful during ligament of Berry’s dissection.

24.3.3 Injury Identification and Prognostication of Postoperative Function

While monitoring is helpful in neural identification and is an excellent adjunct during nerve dissection, the key utility of IONM is the intraoperative prediction of postoperative function. A structurally intact nerve is not necessarily equivalent to a functional nerve. Blunt and stretch injury to the nerve may not always be visually detectable. Several studies have suggested that the visualization of the nerve by the surgeon is a poor judgment of RLN injury intraoperatively. Only 10 to 14% of injured nerves are identified as being such during the course of the sur- gery.19.20 Bergenfelz et al, when reviewing the Scandinavian endocrine quality register in over 3,660 cases, noted that they were able to intraoperatively identify nerve injury only in 11.3% of injured nerves. In addition, bilateral RLN injury was only identified during the operation in 16% of cases when it oc- curred.21 Snyder et al have also recently concluded that the majority of injured nerves are judged to be visually intact during surgery.22 Thus, visual examination is vastly insufficient to prognosticate postoperative RLN function.

In contrast, postoperative neural function prediction with IONM has been associated with uniformly high negative predictive values for injury ranging from 92 to 100%.23 Criteria supported by the INMSG for neurapraxic injury include a 50% or greater decline in amplitude and a 10% or greater increase in latency. In the absence of these conditions, the nerve is judged to retain normal physiologic function. This predictive ability of IONM is of particular importance in bilateral thyroid surgery, because both nerves governing the laryngeal airway introitus are at risk with one surgery. If neurapraxic injury identified on the initial side of surgery does not quickly recover, operative strategy may be rationally changed. Goretzki et al found that when loss of signal was identified on the first side, surgery could be terminated and a staged contralateral procedure performed at a later date with complete avoidance of bilateral nerve paralysis. However, when the surgeon continued to contralateral side surgery after loss of signal on the first side, 19% of patients developed bilateral vocal cord paralysis.24 The prognostic ability of IONM in the avoidance of the major morbidity of bilateral vocal cord paralysis is evident. This advantage is not amenable to statistical analysis but is likely one of the main reasons for IONM application.

24.3.4 Prognostic Testing Errors and Their Avoidance

As discussed previously, multiple recent studies report very high negative predictive value, making IONM vastly superior to visual identification of nerve injury. However, the following categories of errors may occur and should be considered by all monitoring surgeons. In these terms, we define positive (+) test as EMG loss of signal at the end of surgery (i.e., the test for the disease of postoperative vocal cord paralysis is positive), and we define negative (-) test as maintained EMG at the end of surgery (i.e., the test for vocal cord paralysis is negative).

1. False positives (i.e., loss of signal with intact neural function postoperatively). The causes of false positives include the following:

a) Various equipment problems on both the stimulation (i.e., faulty probe, inaccurate probe connection to monitor) and recording (i.e., ETT malposition or displacement) sides.

b) Neuromuscular blockade.

c) Blood or fascia obscuring the stimulated nerve segment.

d) Early-response elimination due to the monitor’s latency cutoff period for recording artifact suppression.

e) Vocal cord paralysis with early neural recovery.

Note that the majority of prognostic testing false positives relate to tube malpositioning.

2. False negatives (i.e., a good EMG with postoperative vocal cord paralysis).

a) Stimulation distal to the injured nerve segment (canine models suggest distal segments maintain electrical stimul- ability for up to 3 days). This is the primary rationale for vagal stimulation at the end of surgery.

b) Injuries subsequent to the final neural stimulation such as during wound irrigation, suctioning, and closure.

c) Delayed neurapraxia. One hypothesis is that progressive edema may affect the RLN at an intralaryngeal location such as the cricothyroid joint articulation.

d) Posterior RLN branch injury. Robust ETT electrode waveform confirms anterior branch RLN integrity. Posterior branches may be disrupted despite strong amplitude with stimulation, and such patients may have an abduction deficit postoperatively.25.26

e) Vocal cord immobility secondary to nonneural issues such as arytenoid cartilage dislocation or laryngeal edema.

24.4 Intraoperative Neural Monitoring Standards Guidelines

Despite the increasingly broad use of IONM, a review of the literature and clinical experience demonstrates there is significant variability in the application of neural monitoring across different centers. Variation exists in the use of pre- and postoperative laryngeal examination, a variety of stimulation probes and recording electrodes, and in monitor output with some providing only audio tone and others generating quantitative laryngeal EMG waveforms. Heterogeneity also exists regarding technique of ETT placement and the troubleshooting algorithm enacted when loss of signal occurs. The literature suggests that this nonstandard application of monitoring techniques leads to a significant rate of monitoring inaccuracies, most notably due to equipment-related problems such as ETT malposition in 3.8 to 23% of patients.27,

24.4.1 Basic System Setup

Recording ground and nerve stimulator anode electrodes are placed on the patient’s shoulder and are interfaced with the monitor through a connector box (Fig. 24.1). The recording electrodes from the right and left vocal cords exit the ETT proximally and are also interfaced with the connector box. Finally, the nerve stimulator cathode electrode (i.e., the probe) is placed on the sterile surgical field and connected to the box underneath the sterile drapes.

24.4.2 Anesthesia

Close partnership with anesthesiology is absolutely essential in a successful neural monitoring program.32.33 Anesthetic needs must be discussed prior to the case. Since IONM requires accurate and robust EMG response, neuromuscular blockade must be avoided without exception. Any neuromuscular blockade after induction could interfere with EMG activity; therefore, it is advisable to utilize short-acting neuromuscular blockade and to allow this to wear off following intubation.34.35

The ETT should be inserted without the use of lidocaine or any lubricant jelly. Pooled saliva may obscure the EMG signals, and using suction and possibly a drying agent may be helpful. The electrodes should abut very closely to the vocal cords; hence, the largest possible size tube for intubation should be used. Appropriate ETT electrode contact with the vocal cords must be confirmed after the patient is fully positioned. The INMSG has suggested two options for confirmation of optimal tube position prior to the start of surgical dissection. The first is to observe spontaneous respiratory variation, which is defined as the spontaneous bilateral EMG waveforms between 30 and 70 microvolts which is observed after the paralytic induction agent has worn off but before the inhalational plane of anesthesia becomes deep. Respiratory variation is typically present as the patient resumes spontaneous breathing and may be observed in conjunction with spontaneous movement or “bucking” (Fig. 24.2). When respiratory variation is present unilaterally, this is an indication that the electrode has lost contact with the vocal cord due to rotation. Tube rotation may then be performed until bilateral waveforms are observed. The second option is to perform repeat laryngoscopy in order to visually ensure adequate ETT positioning. The video-laryngoscope may again be helpful for this post-positioning examination. Repeat laryngoscopy is recommended in all cases when respiratory variation cannot be identified. A recently published study by our unit found that identification of respiratory variation was possible in 91% of their patients, whereas the remaining 9% required a repeat laryngoscopy.33,34,35

Fig. 24.1 Standard Monitoring Equipment Set-up (ref 2011 guidelines). ET, endotracheal tube; GND, ground electrodes; REC, recording electrodes.

After successful positioning of the ETT, the monitor setting should be assessed; low impedance values suggest good electrode-patient contact. The impedance of the electrodes should be less than 5 П and the imbalance between the two sides should be less than 1 Q; monitor event threshold should be at 100 pV and the stimulator probe should be set to a pulsatile output of 4 per second with stimulating current set between 1 and 2 mA. At the onset of surgery, the stimulation of strap muscles resulting into a gross muscle twitch can be performed to confirm the absence of neuromuscular blockade as well as an intact stimulatory pathway. Vagal stimulation (V1) is performed prior to formal surgical dissection of the central neck compartment. It is only when the vagus nerve is stimulated and provides robust EMG activity that the surgeon may be assured that the system is fully functional and that the RLN can be safely sought after through the neural mapping technique. Only once the vagus nerve has been positively stimulated (true positive) can a subsequent negative response be regarded as a true negative. For each patient, IONM data must essentially include preoperative laryngeal exam (L1), an initial intraoperative suprathreshold vagal nerve stimulation (V1), an initial intraoperative RLN stimulation (R1), and also a similar set of events (R2 and V2) should be recorded at the end of the surgery followed by a postoperative laryngeal exam (L2).

Fig. 24.2 Respiratory variation waveform: (a) Upper line—baseline noise (between 10 and 20 pV). Lower line—baseline coarsening by respiratory variation (30-70 pV) occurring when the patient is at the onset of bucking in the early anesthesia period). (b) Left and right baseline tracings in a patient with known right vocal cord palsy. The left vocal cord shows typical respiratory variation. The right vocal cord is electrically silent.

24.5 Monitoring Safety

Multiple studies have demonstrated the safety of repetitive stimulation of the facial nerve in neurotologic surgery, provided that the patient is appropriately isolated and grounded.36.37.38 Multiple investigators have also demonstrated the safety of repetitive RLN stimulation during thyroidectomy/central neck dissection.39,40,41,42,43,44,45,46 In the authors’ experience, stimulation of individual nerves can be performed hundreds of times with constant current pulses of 1 to 2 mA without ill effects. Friedman et al have reported that in both dogs and humans, vagal and RLN stimulation in the 2- to 4-mA range at 10 to 25 Hz (with a pulse duration of 500 ps) was well tolerated without laryngeal or cardiorespiratory symptoms.47 In both canine and porcine models, continuous, prolonged vagal stimulation has been shown not to be associated with any change in vagal or RLN stimulability or any significant cardiopulmonary effect.48 On the basis of a literature review and the cumulative experience of its members, the INMSG has released a statement that repetitive stimulation of the RLN and vagus nerves is not associated with neural injury; the group specifically noted that vagal stimulation is not linked with bradyarrhythmias or bronchospasm.24

Several studies have supported the success and safety of neural monitoring performed with minimally invasive surgical approaches. A needle electrode placed through the cricothyroid membrane to monitor the bilateral vocal cords has been described and allows neural monitoring to be performed during local anesthesia (Snyder, personal communication, 2012).

24.6 Normative Human Monitoring Data

Normative data of RLN and vagus nerve stimulation during IONM is well reported in the literature.48,49,50,51

24.7 Threshold

Threshold is defined as the current that, applied to the nerve, initially starts to elicit recognizable EMG activity. The response amplitude produced at stimulation threshold is lower than the maximum amplitude that may be achieved as the stimulation current is increased. At a certain level of stimulation, all nerve fibers are depolarized, and maximum EMG amplitude is achieved. Beyond this point, increasing the stimulating current does not lead to further increases in recorded EMG amplitude. The human RLN maximally depolarizes at 0.8 mA. This serves as the rationale for stimulating at 1 mA during the bulk of the case since this represents safe suprathreshold stimulation. The use of 2 mA does not produce any higher EMG amplitude, but it depolarizes a larger sphere of tissue around the probe tip and can be quite useful during initial searching and mapping of the RLN.

24.8 Amplitude

The typically biphasic waveform represents the summated motor unit action potentials of the ipsilateral vocalis as recorded by vocal cord surface electrodes at the level of the glottis. Measures of amplitude may be correlated with the number of muscle fibers participating in the polarization during laryngeal EMG. Using existing standards in EMG monitoring physiology, we define amplitude as the vertical height from the apex of the positive waveform deflection to the nadir of the negative deflection (i.e., peak to peak). Mean RLN (both RLNs) amplitude is reported as 891.6 mV (± 731) and mean vagal amplitude as 739.7 mV (±433.9).51

24.9 Latency

Latency is generally believed to represent the speed of stimulation-induced depolarization and therefore depends on the distance of the stimulation point to the ipsilateral vocalis muscle. We define latency as the time from the stimulation spike to the first evoked waveform peak. Given the significant difference in length of the vagus nerve on both sides, latency is significantly longer on the left compared to the right side with vagal stimulation. This is evident in the study of normative EMG by Sritharan et al in which the difference between the mean left vagal latency (8.14 ms) and mean right vagal latency (5.47 ms) was statistically significant (p < 0.0001).50 Analysis of normative data shows that RLN latencies are significantly shorter compared to vagal latencies.44,52 In addition, the non-RLN has a shorter latency than the RLN. The non-RLN may be electrically identified when high vagal stimulation produces laryngeal response but more distal (i.e., caudal) stimulation does not.44,52

24.10 Monitor Problem Solving: Loss of Signal Algorithm

When loss of signal occurs, a surgeon must rule out equipment- related issues, and hence the surgeon’s first response is to palpate the larynx while stimulating the vagus (Fig. 24.3, Fig. 24.4). Laryngeal twitch is a simple method of intraoperative palpation of the posterior cricoarytenoid muscle.40 Presence of laryngeal twitch confirms that the stimulation side of the monitoring system is adequately operational, and the majority of recording side issues are related to ETT malposition. The corrective maneuver consists of stimulation of the vagus as the anesthesiologist repositions the ETT until EMG signal is obtained.

If laryngeal twitch is not present during nerve stimulation, then the stimulation side connections should be inspected. The status of neuromuscular blockage should also be considered if stimulation current is absent. If the current in the range of 1 to 2 mA is being distributed to the patient, the strap or sternocleidomastoid (SCM) muscles are then stimulated. If the strap or SCM muscles respond, contralateral vagus stimulation should be attempted; if EMG response is present, consider ipsilateral neural injury.

An event must satisfy the following conditions to be labeled as true LOS:

1. Presence of a satisfactory EMG at the beginning (R1 = 500 pV) of the monitoring and prior to the event (> 100 pV).

2. No or low response (i.e., 100 pV or lower) with stimulation at 1 to 2 mA in a dry field.

3. Absence of laryngeal twitch on ipsilateral vagal stimulation.

4. Presence of contralateral nerve response on contralateral vagal stimulation.

Fig. 24.3 Intraoperative LOS evaluation standard.

Fig. 24.4 Laryngeal palpation technique.

A true LOS should prompt the surgeon to identify the site of injury. It provides the opportunity to identify and treat the nerve injury if possible.

If signal is lost, the surgeon should stimulate the most distal point of the RLN (i.e., the laryngeal entry site) and serially stimulate proximally along the nerve to determine if a neurapraxic segment can be identified.24 The identification of such a segment, termed “type I RLN injury—segmental injury,” allows the surgeon to review the management of this portion of the nerve as it relates to excessive traction, compression, clamping, or other injury. Should this method of retrograde mapping show the entire course of the RLN to be nonconductive, the injury is defined as type II RLN injury—global injury.4 When true loss of signal occurs, the surgeon should then reconsider bilateral surgery in order to avoid the potential of bilateral nerve paralysis.

24.11 Continuous Neural Vagal Monitoring

The intermittent nature of intraoperative monitoring theoretically allows the nerve(s) to be at risk of damage between stimulations. Herein lies the principal methodological limitation of intermittent stimulation: it only allows the surgeon to identify neural injury once the damage has already been inflicted. Continuous vagal stimulation allows the establishment of baseline EMG amplitude and latency for each individual patient at the start of the case. A “combined event” involves concordant 50% or more decrease in baseline amplitude and 10% or more increase in initial baseline latency.53.54 These combined electrophysiologic events typically precede postoperative vocal fold palsy, and they have been shown in a study of over 1,300 nerves at risk to be reversible in 82% of cases upon termination of the offending surgical maneuver.55 Signal recovery to > 50% of baseline amplitude during surgery signifies normal postoperative vocal fold function in all cases when a “combined event” does occur.56 The current recommendation is to allow an injured nerve a minimum wait time of 20 minutes, prior to either moving on with contralateral surgery or terminating the operation.56,52

A major difference in continuous monitoring is that it requires opening of the carotid sheath for placement of a vagal electrode at the level of the cricoid cartilage. A variety of electrode configurations have been designed to allow the placement of a dedicated electrode on the vagus nerve for the purpose of continuous stimulation that provides ongoing amplitude and latency data.

These may be categorized according to the extent of dissection required around the vagus nerve for their placement. Repetitive pulsed stimulation (typically at 1 mA and < 1 Hz) is performed via the vagal electrode, and there is no further need to interrupt surgery to stimulate the vagus nerve. Randolph et al demonstrated that a vagal electrode can be placed without complications in a matter of seconds.52

Implantable electrodes for the stimulation of the vagus nerve have been used for many years to treat a variety of chronic conditions such as epilepsy, depression, migraine, and Alzheimer’s disease. No clinically relevant side effects have been observed with permanent vagus nerve stimulators.57.58 Terris et al, in a small series conducted during the onset of use of CIONM in their group, reported a single episode of bradycardia; noticeably this study had a concomitant very high vagal electrode dislocation rate.59 Numerous animal and human studies have supported the safety of continuous vagal monitoring for central neck surgery. Basic animal research has shown that a current of 1 mA recruits efferent type A motor fibers and myelinated type B autonomic fibers without activating thin, demyelinated vagal type C fibers. The vagal type C fibers are believed to mediate vasovagal symptoms causing cardiac (arrhythmias, bradycardia), pulmonary (bronchospasm), gastrointestinal (nausea, vomiting), or central (headache, numbness) side effects.55 59.60

24.12 Superior Laryngeal Nerve Monitoring

Damage to the external branch of the SLN can result in significant voice changes, particularly in singers, which are typically described as reduction in pitch, inability to reach higher registers, and decreased voice projection. Robinson et al, in a study of 35 patients with laryngeal EMG, found that SLN paresis/paralysis was associated with significant decreases in maximum phonation time and frequency range, along with increases in mean flow rate, jitter, shimmer, and noise-to-harmonic ratio.61,62 Eisele reported estimated rates of SLN paralysis from 9 to 14%, and Cernea et al described rates up to 28%.63,64

Neural monitoring can be used to intraoperatively identify the external branch of the SLN. In 20% of cases, the external branch is hidden beneath the fascia of the inferior constrictor muscle and not seen directly.64,65,66 Despite this, a nerve stimulator passed along the inferior constrictor can reliably elicit a discrete twitch. The laryngeal head of the sternothyroid muscle serves as an excellent landmark for the linear oblique path of the external branch as it traverses down along the inferior constrictor toward the cricothyroid muscle. The external branch of the SLN can be found within 1 to 2 mm of this obliquely oriented line (the laryngeal head of the sternothyroid, which inserts onto the thyroid cartilage lamina) with a high degree of certainty (Fig. 24.5). Even when the nerve is deep to the fascia of the inferior constrictor, blind stimulation in this area will identify a linear path that results in discrete cricothyroid muscle contraction. Following this technique, neural stimulation should be able to identify the external branch of the SLN in 100% of cases.

EMG recording with ETT surface electrodes reveals a smaller amplitude and shorter latency with stimulation of the external branch of the SLN. On average, the average amplitude of the SLN is 34% of the ipsilateral RLN amplitude, consistent with canine data reported by Nasri et al.67 It should be noted that the monitor’s event threshold setting may need to be lowered and the stimulation rejection setting may need to be shortened in order to capture this early, low-amplitude waveform. Recent studies suggest that monitoring of the external branch of the SLN is associated with improved ability to identify the nerve and a lower rate of adverse voice parameters postoperatively.68 To facilitate understanding and standardization of EBSLN monitoring, in 2013 INMSG has published guidelines for EBSLN monitoring.69

Fig. 24.5 Superior laryngeal nerve path indicated by laryngeal head of sternothyroid muscle.

24.13 Nerve Monitoring in Lateral Compartment Dissection

As previously discussed, neck dissection may present risk to multiple nerves during the course of a single operation. Neural monitoring allows the surgeon to perform the function of neural mapping as previously discussed in relation to the RLN, in addition to assessing the functional status of motor nerves within the operative field in real time. There is currently no application for neural monitoring in relation to sensory nerves (i.e., lingual nerve) or special nerves (i.e., cervical sympathetic chain) that may be at risk of injury during neck dissection.

24.14 Marginal Mandibular Nerve

The marginal mandibular branch of the facial nerve faces injury during the approach to level I dissection. The rate of temporary paresis is reported at 10%, with permanent paralysis occurring in less than 1% of cases.69 The result is asymmetric movement of the lower lip and possible oral incompetence. The marginal mandibular nerve travels in the superficial layer of the deep cervical fascia along the surface of the masseter muscle, passing over the facial vein and artery to innervate the lower lip. The inferior border of the submandibular gland serves as a landmark for the incision through the fascia in order to avoid marginal mandibular branch injury (Fig. 24.6). A nerve stimulator passed along the fascia just inferior to the body of the mandible will elicit lower lip twitch with high reliability. The fascial incision is then placed inferior to the stimulated location of the nerve, and the fascia is elevated broadly along the caudal aspect of the mandibular body.

Fig. 24.6 Marginal mandibular nerve injury can be avoided by reflecting fascia along with the marginal mandibular nerve up and off the gland.

24.15 Hypoglossal Nerve

The hypoglossal nerve is at risk of injury during the course of level Ib dissection. It may also be at risk in level II dissection as the nodal specimen is dissected away from the anterior aspect of the carotid sheath. Injury to this nerve results in deviation of the tongue and atrophy of its intrinsic musculature. Oral phase dysphagia occurs due to difficulty with food bolus manipulation. The hypoglossal nerve passes deep to the posterior belly of the digastric muscle. It is typically identified on the surface of the hyoglossus muscle when the lateral border of the mylohyoid muscle is retracted anteriorly during level Ib dissection (Fig. 24.7). In our experience, stimulation of the hypoglossal nerve is most beneficial to the surgeon as the nodal packet is dissected away from the carotid sheath in level II. Stimulation in a triangle defined by the internal jugular vein posteriorly, the superior thyroid artery inferiorly, and the posterior digastric belly superiorly reliably elicits contraction of the tongue and can help avoid inadvertent hypoglossal injury.

Fig. 24.7 Hypoglossal nerve exposed during lateral neck dissection.

24.16 Spinal Accessory Nerve

The spinal accessory nerve is at particular risk for traction injury during level II dissection (Fig. 24.8). A recent study of neck dissection for thyroid cancer reports temporary spinal accessory nerve paresis in 27% of cases.70.71 Injury leads to shoulder weakness when attempting to elevate the arm above the horizontal plane. Adhesive capsulitis of the glenohumeral joint and frozen shoulder may result if physical therapy is not initiated in a timely fashion. Transection of the spinal accessory nerve causes winged scapula. Stimulation of the spinal accessory nerve is particularly useful during lateral neck dissection, particularly when it is retracted for level IIb dissection. Periodic stimulation can be employed to monitor for possible neurap- raxic traction injury, allowing for immediate reversal of an offending maneuver. Neural mapping may also be employed to allow for early identification of the spinal accessory nerve, as the anterior aspect of the SCM is freed from the superficial layer of the deep cervical fascia.

24.17 Phrenic Nerve

The phrenic nerve may be at risk of injury during dissection of levels III and IV. This nerve lies between the anterior scalene muscle and the overlying deep layer of the deep cervical fascia (Fig. 24.8). The surgeon protects the phrenic nerve via preservation of the deep layer of the fascia. Phrenic nerve injury may result in hemidiaphragmatic paralysis and elevation, with up to a 25% reduction in lung capacity. Stimulation of the deep cervical fascia along the surface of the anterior scalene muscle will result in contraction of the diaphragm, which is palpable and often easily visible to the surgeon. Use of the neural mapping technique to trace the course of the phrenic nerve in the deep layer of fascia can be very useful for preservation of the fascia, notably when the surgeon is examining the compartment deep to the caudal aspect of the common carotid artery.

24.18 Vagus Nerve

Vagal nerve monitoring has been discussed in detail earlier in this chapter, but it merits mention that during dissection of levels II to IV, ligation and transection of the internal jugular vein presents particular risk to the vagus nerve. Continuous vagal nerve monitoring can provide significant benefit to the surgeon in the setting of retrocarotid nodal disease and invasion of the internal jugular vein.

24.19 Summary

Multimodality cranial nerve monitoring during neck procedures is rapidly becoming a new standard for safety and quality of care in head and neck surgery.

Fig. 24.8 Phrenic nerve and spinal accessory nerve preserved at the completion of lateral neck dissection.


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