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QUANTITATIVE NEUROMUSCULAR MONITORING –  NECESSITY OR TECHNOLOGY OVERDONE?

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THE ANESTHESIA CONSULTANT
THE ANESTHESIA CONSULTANT
Physician anesthesiologist at Stanford at Associated Anesthesiologists Medical Group
Richard Novak, MD is a Stanford physician board certified in anesthesiology and internal medicine.Dr. Novak is an Adjunct Clinical Professor in the Department of Anesthesiology, Perioperative and Pain Medicine at Stanford University, the Medical Director at Waverley Surgery Center in Palo Alto, California, and a member of the Associated Anesthesiologists Medical Group in Palo Alto, California.
emailrjnov@yahoo.com
THE ANESTHESIA CONSULTANT
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A QUANTITATIVE NEUROMUSCULAR MONITOR

How do anesthesiologists monitor the degree to which a patient’s muscles are pharmaceutically paralyzed during an anesthetic? A recent publication in our specialty’s most prestigious journal urges the use of a QUANTITATIVE neuromuscular monitoring machine to do this when general anesthetics include a paralytic drug. The article was not a prospective randomized study, but rather a retrospective (from 2016 to 2020) practice initiative from a solitary medical center. The goal of the authors (Weigel et al) was to measure the reversal of neuromuscular paralysis in all anesthetized patients at the end of their anesthetic, and to document that reversal in the patient’s chart.

Their measured goal was to document a train-of-four ratio of greater than or equal to 0.9 prior to extubation in each anesthetized patient. What is a train-of-four? A locomotive with four cars? Alas no. A train-of-four ratio is a monitor of the level of neuromuscular blockade. Four consecutive electronic stimuli are delivered along the path of a patient’s nerve. The twitch response of the muscle is measured in order to evaluate stimuli that are blocked, versus those that are delivered. Four consecutive muscle contractions of equal strength (a score = 1.0) occur if there is no neuromuscular blockade. If neuromuscular blockade is present, there will be a loss of twitch height of the final twitch compared to the first twitch, and the resulting ratio of the final twitch height/first twitch height (e.g. 4/5 = 0.8) will indicate the degree of blockade. The clinical concern is that a ratio of lower than 0.9 correlates with a weak patient who may not safely ventilate himself/herself.

The conclusion of the Weigel study boldly states, “Anesthesia providers are solely responsible for properly rescuing patients from the states of paralyses they initiate. This should occur for ALL PATIENTS as verified by QUANTITATIVE measurement and documentation of train-of-four ratios greater than or equal to 0.9.” (Capital letters added by me.) 

Should the American Society of Anesthesiologists (ASA) add QUANTITATIVE neuromuscular monitoring as a standard of care? 

Hmm. This would be a marked change because, to my observation, almost no anesthesia providers routinely use QUANTITATIVE neuromuscular monitoring at this time.

The authors’ goal of documenting a train-of-four ratio greater than or equal to 0.9 requires the purchase of QUANTITATIVE neuromuscular monitoring equipment in every anesthetizing location. The cost of each monitor was approximately $1,995, with the disposable costs of $20 to $25 per patient. An example QUANTITATIVE neuromuscular monitor is shown here:  

TwitchView QUANTITATIVE neuromuscular monitor

The article states, “The dangers of paralyzing a patient with neuromuscular blocking drugs are well recognized. Despite advances in anesthetic management, approximately half of all patients arriving to the postanesthesia care unit (PACU) suffer from residual blockade defined as a train-of-four ratio less than 0.9.” They cite a previous article from Anesthesia and Analgesia in 2018 which stated: “whenever a neuromuscular blocker is administered, neuromuscular function must be monitored by observing the evoked muscular response to peripheral nerve stimulation. Ideally, this should be done at the hand muscles (not the facial muscles) with a quantitative (objective) monitor. Objective monitoring (documentation of train-of-four ratio ≥0.90) is the only method of assuring that satisfactory recovery of neuromuscular function has taken place. (Bold emphasis added by me.) The panel also recommends that subjective evaluation of the responses to train-of-four stimulation (when using a peripheral nerve stimulator) or clinical tests of recovery from neuromuscular block (such as the 5-second head lift) should be abandoned in favor of objective monitoring.”

The American Society of Anesthesiologists (ASA) sets the standard of care for intraoperative monitoring. The ASA Standard of Anesthesia Monitoring currently does not mandate any form of neuromuscular monitoring. The ASA Standard of Anesthesia Monitoring is the gold standard for all operating room monitoring, is followed by all training programs, and is referred to in courts of law as the standard of care should an adverse anesthesia outcome occur. 

A 2010 survey of anesthesia providers documented that 19.3% of Europeans and 9.4% of Americans never use neuromuscular monitors. The majority of respondents from the US (64.1%) and Europe (52.2%) estimated the incidence of clinically significant postoperative residual neuromuscular weakness to be <1% (P<0.0001). Most respondents in this study reported that “neither conventional nerve stimulators nor quantitative train-of-four monitors should be part of minimum monitoring standards.”

I suggest three values in anesthetic care: Do the right thing, be safe, and Keep It Simple Stupid (the KISS principle). Rather than strapping a thumb monitor onto every one of my patients, I’m a disciple of qualitative neuromuscular monitoring—a less technologically complex form of monitoring. When I was serving my residency training in anesthesiology at Stanford in the 1980s, each resident was equipped with a MiniStim nerve stimulator, which is a qualitative neuromuscular monitor. 

MiniStim qualitative neuromuscular monitor

A qualitative neuromuscular monitoring device is simple to use. When the two terminals are applied to the facial nerve lateral to the eye of a sleeping patient and the green button is pushed, the orbital muscles will twitch if unparalyzed, and they will not twitch if paralyzed. With experience one can easily discern whether the patient is paralyzed or not, and one can estimate the degree of paralysis. The MiniStim also has a tetanus feature. When the two terminals are applied to the facial nerve lateral to the eye of a sleeping patient and the red button is pushed, a sustained electrical energy is emitted between the two terminals. The orbital muscles will show a sustained contraction if unparalyzed, and will not contract at all if fully paralyzed. If partially paralyzed, the muscles will contract and then the contraction will fade away in seconds. With experience, one can estimate to what degree the patient is paralyzed. The qualitative neuromuscular monitor does not give you the exact data, i.e. a decimal number between 0.0 (totally paralyzed and 1.0 (no paralysis) that a QUANTITATIVE neuromuscular monitor does. 

I still carry a MiniStim, and have used one for the entire 38 years I’ve practiced anesthesia, and for the 30,000 patients I’ve anesthetized. I would not start a case without a neuromuscular qualitative monitor. I would not want to be a patient receiving a neuromuscular paralytic drug if the anesthesiologist did not utilize a neuromuscular monitoring device similar to the MiniStim. The MiniStim is no longer manufactured, but other similar qualitative neuromuscular monitors are easily purchased, e.g. as depicted below, for $251, with no additional disposable costs.

SunStim qualitative neuromuscular monitor

Why is the topic of reversing neuromuscular blockade seeing this kind of scrutiny in 2022? Residual neuromuscular paralysis is less a problem now than at any time since the paralyzing medications were discovered. Why? Because in 2015 the United States Food and Drug Administration (FDA) approved the new intravenous drug sugammadex, a reliable, specific, and safe agent for the reversal of neuromuscular paralysis. Sugammadex can eliminate neuromuscular paralysis rapidly. A rocuronium molecule, bound within sugammadex’s lipophilic core, is rendered unavailable to bind to the acetylcholine receptor at the neuromuscular junction, and paralysis is reversed in seconds. 

Prior to 2015, the only reversal agent for pharmaceutical paralysis with a non-depolarizing neuromuscular blocker such as rocuronium was the drug neostigmine. Neostigmine can cause the side effect of severe bradycardia (slowing of the heart rate), and had to be administered intravenously in combination with glycopyrrolate (Robinul) or atropine. If a surgery was concluding and the patient had residual neuromuscular paralysis, the anesthesia provider needed to administer the combination of neostigmine/Robinul well before the wakeup-time, because the peak effect of neostigmine occurs at 10 minutes after administration.  If the patient was markedly paralyzed, e.g. the qualitative neuromuscular monitor showed no significant twitch or tetanus activity, neostigmine could not adequately reverse the neuromuscular paralysis in a short time. Sometimes it took 20-30 minutes before a deep neuromuscular paralysis could be reversed with neostigmine. If an anesthesia provider erroneously chose to awaken a patient prior to the time their neuromuscular paralysis was reversed or worn off, the patient would be too weak to breathe normally. A medical complication of hypoventilation or of awake paralysis could occur. 

Because of sugammadex, the risk of untreated residual neuromuscular paralysis has never been lower. Unreversed neuromuscular paralysis at wake-up should be a never-event now that sugammadex exists. There is virtually no circumstance in which an attending anesthesia provider should have unreversed neuromuscular paralysis at the present time. Why, in 2022, should we advocate for a QUANTITATIVE neuromuscular monitor which is bulky, expensive, and can only be strapped onto the thumb? The thumb location is a disadvantage, because many anesthetics, for example laparoscopies, require the arms to be tucked at a patient’s sides during surgery, and a thumb monitor is not practical. The qualitative neuromuscular monitors work on any peripheral nerve: e.g. the ulnar nerve at the wrist, the facial nerve lateral to the eye, or the posterior tibial nerve in the ankle, and provide a more versatile monitor than the QUANTITATIVE neuromuscular thumb monitor.

Qualitative neuromuscular monitoring is useful, easy, versatile, and inexpensive. QUANTITATIVE neuromuscular monitoring has the appeal of a score—a number between 0 and 1.0—that can be added to the already burdensome printout of the Electronic Medical Record (EMR), and may seem satisfying to those addicted to the dubious wonders of the EMR, or to those who want to see QUANTITATIVE neuromuscular monitors reported in the medical literature. But the addition of QUANTITATIVE neuromuscular monitoring to the required ASA list of monitors at this time is premature.

Where is the science? Where is the prospective, randomized trial of QUANTITATIVE neuromuscular monitoring versus qualitative neuromuscular monitoring in the age of sugammadex? Does anyone really believe that qualitative neuromuscular monitoring will be inaccurate and lead to significant anesthetic complications in an era when sugammadex is available? 

Qualitative neuromuscular monitoring was always a solid idea. I made this point twelve years ago when I wrote, “During residency or during the years afterward, a MiniStim and a stethoscope are arguably the only tools of your own you need to carry into an operating room to conduct a 21st-century general anesthetic.”

Until prospective scientific evidence demonstrates that QUANTITATIVE neuromuscular monitoring improves outcomes, mandating the extra technology of QUANTITATIVE neuromuscular monitoring as a required standard is not the correct path for the ASA to take in 2022 or at any time in the future. 

The most popular posts for laypeople on The Anesthesia Consultant include:
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READ ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM

LESSONS LEARNED REGARDING SUGAMMADEX

THE ANESTHESIA CONSULTANT 1 Comment
THE ANESTHESIA CONSULTANT
THE ANESTHESIA CONSULTANT
Physician anesthesiologist at Stanford at Associated Anesthesiologists Medical Group
Richard Novak, MD is a Stanford physician board certified in anesthesiology and internal medicine.Dr. Novak is an Adjunct Clinical Professor in the Department of Anesthesiology, Perioperative and Pain Medicine at Stanford University, the Medical Director at Waverley Surgery Center in Palo Alto, California, and a member of the Associated Anesthesiologists Medical Group in Palo Alto, California.
emailrjnov@yahoo.com
THE ANESTHESIA CONSULTANT
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8-2040-01

Regarding sugammadex and residual neuromuscular blockade: I’m aware of two cases of residual neuromuscular blockade which occurred during the past year. Both cases involved obese patients who required emergency reintubation. Both cases were near misses for brain death. Both of these near misses would never have occurred if sugammadex had been used.

The first case was a 50-year-old, 120 kilogram male for an endoscopic retrograde cholangiopancreatography (ERCP). The procedure was to be done in the prone position, and required endotracheal intubation. The intubation was easily performed, and was facilitated with 60 mg of rocuronium for paralysis. The patient was turned prone, and the procedure commenced. After only 15 minutes of operating time, the gastroenterologist announced that the procedure was over. Electrical nerve stimulation of the train of four (TOF) at the facial nerve with a Life Tech Mini Stim showed one twitch. The anesthesiologist injected 5 mg of neostigmine and 1 mg of glycopyrrolate IV, and the patient was turned supine. After ten minutes, the TOF nerve stimulation of the facial nerve showed four equal twitches, and the sevoflurane anesthesia was discontinued. The patient was allowed to return to spontaneous breathing, and he opened his eyes. The trachea was extubated. Within the first two minutes, the patient had inadequate strength for spontaneous respiration. On 100% oxygen via mask, his oxygen saturation dropped from 100% to 80%. 120 mg of succinylcholine was injected IV, and an emergency reintubation was performed. The repeat intubation was more difficult than the original intubation, and required two looks before the trachea was visualized. The nadir oxygen saturation was 60%. The patient was kept asleep for thirty additional minutes, until nerve stimulation at the ulnar nerve showed both TOF and sustained tetany without fade. At that point the trachea was extubated. The patient had no brain damage, and he was discharged home ninety minutes later.

The second case was a 45-year-old, 120 kilogram male with obstructive sleep apnea for a uvulopalatopharyngoplasty (UPPP) and tonsillectomy. The endotracheal intubation was easily done, and was facilitated with 70 mg of rocuronium for paralysis. The surgery lasted 60 minutes. The anesthesiologist injected 5 mg of neostigmine and 1 mg of glycopyrrolate IV fifteen minutes prior to the end of surgery. At the conclusion of surgery, electrical nerve stimulation of the facial nerve with a Life Tech Mini Stim showed four equal twitches in the TOF, and the sevoflurane anesthesia was discontinued. The patient was allowed to return to spontaneous breathing, and opened his eyes. The trachea was extubated. Within the first minute, the patient was awake and breathing, but had jerky breathing pattern and was unable to ventilate himself effectively. On 100% oxygen via mask, his oxygen saturation dropped from 100% to 70%. 200 mg of propofol and 120 mg of succinylcholine were injected IV, and an emergency reintubation was performed. The repeat intubation was more difficult than the original intubation because of blood in the mouth and the oral surgery, and required two looks before the trachea was visualized. The nadir oxygen saturation was 49%. The patient was kept asleep for thirty additional minutes until nerve stimulation at the ulnar nerve showed both TOF and sustained tetany without fade. At that point the trachea was extubated. The patient had no brain damage. He was a planned admission to the hospital, and the remainder of his hospital course was uncomplicated.

Several teaching points are warranted:

  1. If succinylcholine been used for the intubations, the large intubating doses of rocuronium would have been avoided, and the inadequate reversal of the rocuronium intubating doses would likely not have occurred.
  2. If smaller doses of rocuronium been used for intubation, the inadequate reversal of the rocuronium intubating doses would likely not have occurred.
  3. These two cases were done prior to sugammadex availability. In the era of sugammadex, beginning now in 2016, these two near misses should never occur. Sugammadex is a modified γ-cyclodextrin which shows a high affinity for rocuronium and vecuronium. Sugammadex forms a tight inclusion complex with either rocuronium or vecuronium, resulting in rapid reversal of neuromuscular blockade. Sugammadex is able to reverse a moderate profound neuromuscular blockade with a dose of 2.0 mg/kg, and a profound neuromuscular blockade with a dose of 4.0 mg/kg.(1) In my experience, these doses of sugammadex completely reverse rocuronium paralysis within 30-40 seconds. Inadequate neuromuscular blockade reversal should never occur in the era of sugammadex. The past practice of administering neostigmine plus glycopyrrolate to reverse neuromuscular blockade, and then waiting up to ten minutes, is an inferior pharmacologic measure when compared to sugammadex. Reversal with neostigmine plus glycopyrrolate is slow, unreliable, and at times incomplete. While it’s true that a 200 mg ampoule of sugammadex costs approximately $100, that sum of money is trivial when compared to the cost of the lawsuit that would have occurred if either of the two case studies above had resulted in brain death due to delayed or unsuccessful reintubation. In my medical-legal consulting practice I see multiple cases of failed or delayed endotracheal intubations that result in brain death and multimillion-dollar closed malpractice claims.
  4. Residual neuromuscular blockade cannot always be reliably excluded by using qualitative monitoring such as a Life Tech MiniStim device to monitor TOF. The TOF is monitored by comparing the amplitude of the fourth (T4) to the first (T1) evoked mechanical response at the facial nerve or the ulnar nerve. The T4/T1 ratio, or the TOF ratio, coincides with symptoms of peripheral muscle weakness.At a TOF ratio less than 0.60, signs of muscle weakness and ptosis are easily observed. When TOF ratios recover to 0.70, the majority of patients are able to sustain head lift and eye opening. A very low TOF ratio between 0.1 and 0.5 is easily detected by a qualitative nerve stimulator. However, TOF ratios between 0.5 and 1.0 can be difficult to discern visually. Many clinicians are unable to detect fade when TOF ratios exceed 0.30 to 0.4.(1) Qualitative neuromuscular monitoring of the facial nerve twitch can be deceiving. Applying the peripheral nerve stimulator to the ulnar nerve at the adductor pollicis is the gold standard, and this site must be used for the pre-reversal assessment even when the ulnar nerve and thumb are not accessible intraoperatively. Recovery from neuromuscular paralysis should be present when a TOF count without fade has been confirmed at the adductor pollicis.(2) In a partially paralyzed patient, a visually undetectable fade of the TOF at the facial nerve may coincide with a visually detectable fade in TOF when the ulnar nerve is tested. When a patient’s arms are tucked during surgery, or when the ulnar nerve area is distant from the anesthesiologist’s location, it may be impossible to test ulnar nerve stimulation intraoperatively. Prior to extubation, when the ulnar nerve is accessible, ulnar nerve stimulation will convey a more accurate assay of the level of neuromuscular reversal.
  5. Immediate reversal of neuromuscular blockade induced by rocuronium is possible with a larger dose of sugammadex of 16 mg/kg. To facilitate intubation, a dose of succinylcholine (1 mg/kg) will cause a neuromuscular blockade of 4 – 5 minutes in duration. If an airway is found to be difficult or if the intubation is found to be impossible, the anesthesiologist has no way to return the patient to spontaneous breathing until these 4 – 5 minutes elapse. To facilitate intubation, a dose of rocuronium (0.5 – 1 mg/kg), if immediately reversed by sugammadex 16 mg/kg, will cause a shorter duration of paralysis than if succinylcholine were used. It remains to be seen whether this fact will lead to increased use of rocuronium rather than succinylcholine in difficult endotracheal intubations in which a potential early return to spontaneous ventilation is deemed prudent.

 

Healthcare systems are likely to promote selective or infrequent utilization of the new neuromuscular paralysis antidote sugammadex because of its cost. For your practice, and for mine, use the drug when you need it. You’re not personally paying the $100 price for the dose of sugammadex. If you have a serious patient complication because of inadequate neuromuscular reversal by the old drug neostigmine, the adverse patient outcome and the resulting lawsuit may cost you a whole lot more than that $100.

For the record, I have no financial interest or investment in sugammadex. I just know a good product when I see one.

References:

  1. Murphy GS et al, Reversal (Antagonism) of Neuromuscular Blockade, Chapter 35, Miller’s Anesthesia, 8th Edition, 2015.
  2. Thilen SR, Qualitative Neuromuscular Monitoring: How to Optimize the Use of a Peripheral Nerve Stimulator to Reduce the Risk of Residual Neuromuscular Blockade, Curr Anesthesiol Rep. 2016;6:164-169.

 

The most popular posts for laypeople on The Anesthesia Consultant include:

How Long Will It Take To Wake Up From General Anesthesia?

Why Did Take Me So Long To Wake From General Anesthesia?

Will I Have a Breathing Tube During Anesthesia?

What Are the Common Anesthesia Medications?

How Safe is Anesthesia in the 21st Century?

Will I Be Nauseated After General Anesthesia?

What Are the Anesthesia Risks For Children?

 

The most popular posts for anesthesia professionals on The Anesthesia Consultant  include:

10 Trends for the Future of Anesthesia

Should You Cancel Anesthesia for a Potassium Level of 3.6?

12 Important Things to Know as You Near the End of Your Anesthesia Training

Should You Cancel Surgery For a Blood Pressure = 178/108?

Advice For Passing the Anesthesia Oral Board Exams

What Personal Characteristics are Necessary to Become a Successful Anesthesiologist?

 

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Published in September 2017:  The second edition of THE DOCTOR AND MR. DYLAN, Dr. Novak’s debut novel, a medical-legal mystery which blends the science and practice of anesthesiology with unforgettable characters, a page-turning plot, and the legacy of Nobel Prize winner Bob Dylan.

KIRKUS REVIEW

In this debut thriller, tragedies strike an anesthesiologist as he tries to start a new life with his son.

Dr. Nico Antone, an anesthesiologist at Stanford University, is married to Alexandra, a high-powered real estate agent obsessed with money. Their son, Johnny, an 11th-grader with immense potential, struggles to get the grades he’ll need to attend an Ivy League college. After a screaming match with Alexandra, Nico moves himself and Johnny from Palo Alto, California, to his frozen childhood home of Hibbing, Minnesota. The move should help Johnny improve his grades and thus seem more attractive to universities, but Nico loves the freedom from his wife, too. Hibbing also happens to be the hometown of music icon Bob Dylan. Joining the hospital staff, Nico runs afoul of a grouchy nurse anesthetist calling himself Bobby Dylan, who plays Dylan songs twice a week in a bar called Heaven’s Door. As Nico and Johnny settle in, their lives turn around; they even start dating the gorgeous mother/daughter pair of Lena and Echo Johnson. However, when Johnny accidentally impregnates Echo, the lives of the Hibbing transplants start to implode. In true page-turner fashion, first-time novelist Novak gets started by killing soulless Alexandra, which accelerates the downfall of his underdog protagonist now accused of murder. Dialogue is pitch-perfect, and the insults hurled between Nico and his wife are as hilarious as they are hurtful: “Are you my husband, Nico? Or my dependent?” The author’s medical expertise proves central to the plot, and there are a few grisly moments, as when “dark blood percolated” from a patient’s nostrils “like coffee grounds.” Bob Dylan details add quirkiness to what might otherwise be a chilly revenge tale; we’re told, for instance, that Dylan taught “every singer with a less-than-perfect voice…how to sneer and twist off syllables.” Courtroom scenes toward the end crackle with energy, though one scene involving a snowmobile ties up a certain plot thread too neatly. By the end, Nico has rolled with a great many punches.

Nuanced characterization and crafty details help this debut soar.

Click on the image below to reach the Amazon link to The Doctor and Mr. Dylan:

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LEARN MORE ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM BY CLICKING ON THE PICTURE BELOW:

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