Pitfalls of electromyography (EMG) in parathyroidectomy: a case report of unrecognized pseudocholinesterase deficiency

Introduction

Background

Nationwide, approximately 17,000 parathyroidectomies are performed annually in the United States as the standard curative option for primary hyperparathyroidism (1). The most common complication related to this surgery is recurrent laryngeal nerve (RLN) injury (2). This injury may manifest as hoarseness, respiratory distress, or even airway compromise requiring intervention. The incidence of permanent injury ranges from 0.5% to 5%, whereas transient injury can occur with an incidence ranging from 1% to 30% (3). In order to reduce the overall incidence, neuromonitoring has become more widely accepted and more frequently used whenever RLN injury is possible amongst our newest generation of surgeons (4).

For surgery to the anterior neck, electromyography (EMG) of the vocalis muscle is routinely used (5). Any deterioration of the EMG signals suggests a neural injury, and immediate intraoperative identification of the insult can allow for an early correction (6-8). During EMG monitoring, the surgeon stimulates suspected neural structures with a probe to elicit a response, which is detected via electrodes embedded in the endotracheal tube near the vocal folds. Concomitantly, electrodes embedded within the endotracheal tube, in close proximity to the muscles of the vocal cord, record electrical activity. When the probe directly contacts neural tissue, the neurons depolarize, and individual muscle units innervated by those neurons contract and a compound muscle action potential (CMAP) is generated and recorded. This CMAP can then be quantified in terms of voltage it produces after each stimulation. A voltage of greater than 100 microvolts is generally considered a positive response and indicative of an intact neuro-muscular pathway. During EMG monitoring, a post dissection evoked potential of at least 200 µV is considered normal, and a value of less than 200 µV is considered abnormal (9).

Pseudocholinesterase (PChE) is an enzyme that metabolizes choline esters in the body. Succinylcholine is hydrolyzed almost exclusively by PChE, making its pharmacokinetics highly sensitive to enzyme activity. Individuals with PChE deficiency have a prolonged duration of action of succinylcholine and thus prolonged neuromuscular blockade and weakness (10). The overall incidence of PChE deficiency is approximately 1 in 500 (heterozygous for the abnormal enzyme) to 1 in 2,000 to 1 in 5,000 (homozygous for the abnormal enzyme) individuals. Typical duration of neuromuscular blockade following standard dosing is 5–10 minutes. Heterozygotes for PChE deficiency experience a 30% increase in duration blockade and homozygotes have an increased duration of 2–3 hours (11). PChE deficiency can be displayed from either an inherited pattern or acquired cause. Acquired causes include certain medications, chronic infections, kidney or liver disease, malnutrition, severe burns, cancer, or pregnancy. Anesthesia providers must understand the pathophysiology of PChE deficiency and be prepared to safely and effectively manage patients who show signs and symptoms consistent with the disorder after the use of the indicated neuromuscular blocking drugs (12).

Rationale and knowledge gap

In this case report, we present the diagnostic challenges in a patient with unknown PChE deficiency undergoing parathyroidectomy. It is known that preoperatively unrecognized PChE deficiency will lead to prolonged paralysis after a depolarizing muscle relaxant such as succinylcholine has been administered and current literature states that this will invalidate an EMG monitoring system (13). However, PChE deficiency will only suppress the EMG signal for a certain amount of time, representing a major pitfall of EMG monitoring during parathyroid surgery. In fact, not being able to identify the RLN during surgery is not uncommon and such scenario could easily mask a PChE deficiency. We were unable to find any case reports in the literature describing a similar scenario, pointing out this critical diagnostic dilemma.

Objective

We discuss the multifactorial components of a negative EMG signal which can be challenging at times. We would like to emphasize the human component not being able to identify the nerves during surgery. We suggest establishing a state-of-the-art anesthesia checklist for patients undergoing parathyroid surgery with EMG monitoring. If the EMG signal is missing in the early phase during surgery and if EMG signal amplitudes increase over time, suspicion for PChE deficiency should be high and twitch monitors should be used to evaluate for any weakness before the patients wake up from anesthesia. We present this case in accordance with the CARE reporting checklist (available at https://atm.amegroups.com/article/view/10.21037/atm-25-89/rc).

Case presentation

We report the perioperative management of a 74-year-old, 76 kg woman with American Society of Anesthesiologists (ASA) Physical Status Classification 3 presenting for a parathyroidectomy for primary hyperparathyroidism. Her surgical history included dental and cosmetic procedures under local anesthesia. Her comorbidities included a history of hypertension, sleep apnea and primary hyperparathyroidism. Thus, she underwent an elective parathyroidectomy for definitive management.

Induction of anesthesia was performed with the administration of propofol 200 mg (2.6 mg/kg) and succinylcholine 100 mg (1.3 mg/kg). To facilitate adequate intubating conditions while avoiding residual neuromuscular blockade during surgery with intraoperative EMG, succinylcholine was the neuromuscular blocker of choice in this case. Endotracheal intubation was performed with a 7.0 mm EMG (Xomed, Jacksonville, FL, USA) recording endotracheal neural integrity monitor (NIM) tube. Proper placement was confirmed via a video laryngoscope, evaluating the monitoring electrodes at the vocal cords. Sevoflurane [~0.5 minimal alveolar concentration (MAC)] and infusions of propofol (25 mcg/kg/min) and remifentanil (0.1 mg/kg/min) were utilized for maintenance of anesthesia. The patient was hemodynamically stable throughout the case with blood pressures running around 140/70 mmHg. Normothermia (36.7 ℃), normocarbia (35 mmHg), and normoxia (SpO₂ 97%) were maintained throughout the case (see Figure 1).

Figure 1 Timeline. Overview of the surgical procedure and neuromonitoring events. “*” denotes where a normal EMG signal was detected during the case for the first case. EMG, electromyography; OSA, obstructive sleep apnea; PACU, post anesthesia care unit.

During the surgery, free EMG evaluation concluded that neuropraxic or neurotonic discharges did not occur in either vocal cord throughout the procedure. Also, no inadvertent surgical stimulation of the RLN was noted in the surgical record. Triggered EMG evaluation concluded that direct stimulation with 0.5 or 1 mA of current of the vocalis muscle by the surgical team showed progressively larger EMG responses throughout the entirety of the surgery which is not unusual in a routine case (see Figure 2). We would like to emphasize the diagnostic dilemma that was created here, as EMG signals improved over time, which could be misinterpreted as normal recovery of nerve function rather than delayed recovery from succinylcholine. Moreover, the time from anesthesia-induction to the end of the surgery was approximately 2.5 hours.

Figure 2 Electromyography signals during parathyroid surgery in a patient with pseudocholinesterase deficiency who received succinylcholine for anesthesia induction. (A) 75 minutes after succinylcholine administration, amplitude measured at 135 µV. (B) At 90 minutes, amplitude was 205 µV. (C) At 120 minutes, amplitude was recorded as 340 µV. (D) At 135 minutes, amplitude reached 506 µV.

During emergence, the patient exhibited significant and clinically relevant weakness, which was evidenced by the inability to lift her head for prolonged periods of time or move her arms with definitive purpose. As such residual neuromuscular blockade was suspected, the anesthetic was deepened, and the train-of-four ratio (TOFR) was evaluated. Upon evaluation, the patient exhibited a TOFR of 0.8 and a significant fade with tetanic stimulation. To exclude inadvertent administration of muscle relaxants, 200 mg of sugammadex was administered, which, however, had no effect, as it only reverses amino steroid agents such as rocuronium. Mechanical ventilation continued until the patient eventually had full muscle recovery as evidenced by sustained tetanus using a twitch monitor, approximately 3–4 hours post-succinylcholine administration. The patient was later transferred to post anesthesia care unit (PACU) without further complications. Following this incident, PChE levels were later evaluated, and the patient was found to have a level of 952 U/L (normal, 2,900–7,100 U/L). This was consistent with a diagnosis of homozygous PChE deficiency.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

Intraoperative EMG monitoring is increasingly used in parathyroidectomy surgeries, but it is not routinely utilized nationwide (14-19). To facilitate adequate intubating conditions while avoiding residual neuromuscular blockade during surgery with intraoperative EMG, succinylcholine is often the neuromuscular blocker of choice. Given the known pharmacokinetics of succinylcholine, many anesthesiologists will assume that its neuromuscular blocking properties have dissipated after a certain period, especially when adequate neuromonitoring signals are achieved initially.

Explanations of findings

Patients with normal PChE activity will show rapid recovery from succinylcholine compared to PChE deficient patients (10,11). In patients with normal PChE activity, EMG signals would be seen within minutes after succinylcholine and each subsequent EMG signal would be consistent in amplitude as long as the same amount of neural tissue is stimulated. In practice, this amplitude does vary slightly from stimulation to stimulation. In contrast, patients with PChE deficiency exhibit a delayed onset of EMG signals, with gradually increasing amplitude as neuromuscular function recovers over several hours. Clinically the PChE deficient patient would exhibit profound weakness initially, then progressively improve over the course of hours (20). From a neuromonitoring perspective, we observed EMG signals which were small when they first appeared but became increasingly large as the case went on. This trend was demonstrated by representative EMG signals seen throughout the case in Figure 2. While there was insufficient neuromuscular recovery at the end of the case to support adequate respiration without a ventilator, there was, however, enough recovery to obtain large and reliable EMG signals. Of note, this increase in amplitude is not uncommon and as such is not specific to progressive neurologic recovery, but it could be useful information to share with the care team if a neuromonitoring technician or the supervising attending observes a pattern of late initial EMG signals followed by steady improvement in amplitude.

Comparison with similar case reports

To our knowledge there are no case reports in the literature describing a similar scenario. Moreover, we could not find a previous report describing a detailed checklist for EMG signals during parathyroid surgery (21). In fact, literature claims that PChE deficiency would invalidate an EMG monitoring system (13). However, our case suggests that this assumption may be overly simplistic. In fact, we observed a completely normal course of EMG signals throughout. The attesting attending who finalized the neuromonitoring report stated that large EMG responses were present throughout the surgical procedure, bilateral EMG responses were present at the end of the procedure and thus the conclusion was that surgical stimulation of the RLN was achieved. It was further noted that postoperatively no new deficits were found.

Limitations

While this scenario has never been described before, PChE deficiency is quite rare. However, while PChE deficiency is rare, it is a critical diagnostic consideration during neuromonitoring that may otherwise go unrecognized. Furthermore, with the availability of sugammadex, some providers have omitted the use of succinylcholine completely. However, succinylcholine remains the agent of choice in these cases due to its speed, reliability and quick neuromuscular recovery time. Another limitation is that current best practice recommends neuromuscular monitoring prior to emergence in all patients receiving neuromuscular blockers, including succinylcholine (22). However, in our scenario with a “normal” EMG signal course, most anesthesiologists would have not tested for residual neuromuscular blockade.

Conclusions

Implications and actions needed

A consensus statement on the perioperative use of neuromuscular monitoring recommends that neuromuscular function should be monitored whenever a blocking drug is administered (22). This needs are to be emphasized in our daily practice and when training new anesthesia providers. We further emphasize the importance of obtaining detailed history prior to any intervention or surgery requiring monitored anesthesia care or general anesthesia. In addition, a family history of complications during general anesthesia may help identify patients at risk (23). Regardless, based on our case report we suggest establishing an evidence-based anesthesia checklist for patients undergoing parathyroid surgery with EMG monitoring. If the EMG signal is missing in the early phase or if EMG amplitudes increase over time, suspicion for PChE deficiency should be high and twitch monitors must be used to evaluate for any weakness before the patients wake up from anesthesia (see Figure 3).

Figure 3 Recommended checklist for EMG using an EMG NIM tube for recurrent laryngeal nerve monitoring during parathyroid surgery. EMG, electromyography; NIM, neural integrity monitor.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://atm.amegroups.com/article/view/10.21037/atm-25-89/rc

Peer Review File: Available at https://atm.amegroups.com/article/view/10.21037/atm-25-89/prf

Funding: Research reported in this publication was supported by the National Heart, Lung, and Blood Institute (No. R56HL156955 to T.d.l.G.E.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-25-89/coif). T.d.l.G.E. serves as an unpaid editorial board member of Annals of Translational Medicine from November 2023 to October 2025. T.d.l.G.E. reports receiving funding from National Heart, Lung, and Blood Institute for this study (No. R56HL156955). The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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