This is in response to Reuben Strayer's comments on ketamine-associated laryngospasm on the August episode of EM:RAP. I am what many would consider a "high utilizer" of Ketamine in our academic emergency department. I believe it to be one of the safest analgesia and sedation medications in emergency medicine, and I push very hard for my residents to use it regularly for these indications so they can be comfortable with it when they graduate. One of the reasons I push so hard is that this medication, above all others, suffers from so much disinformation on that part of physicians, nurses, and the media, that training providers often shy away from it. I took some issue with the discussion on "laryngospasm" by Reuben Strayer (whom I have learned extensively about ketamine from) because I don't think the piece highlighted the fact enough that what many people consider to be laryngospasm is just a relaxation of upper airway structures. He does mention this and compares it to OSA patients, but then talks about the primary treatments as treatments for laryngospasm, which is most often what is not actually happening. Dr Strayer was 100% correct that simple jaw thrust and oxygenation almost always helps, but that is because we are aiming to lift the glottic structures off the airway, not relax spasmed vocal cords. I think it important for listeners to understand this fact, because the whole idea of "laryngospasm" is what often scares providers away from Ketamine and (I have seen many times) leads providers to panic and rush to paralytics and intubation, when the simple knowledge that you are usually treating upper airway relaxation and NOT laryngospasm helps to ease their tension.
Hi Andrew, thanks for your comment. I am in complete agreement that some providers shy away from using ketamine, to the detriment of their patients. One of my primary objectives in that segment was to reduce this anxiety, as it pertains to laryngospasm, by describing laryngospasm as an event not to be feared, but rather prepared for, as it is so readily treated. I'm not sure we know exactly what's going on, at the level of the glottis, during airway obstruction. I suspect you are correct that some of the obstruction you see in ketamine PSA is muscle relaxation, however it's worth noting 1. ketamine-related laryngospasm, or what is often described as laryngospasm, is much more commonly in kids, who are less likely to have typical OSA-type obstructive physiology. 2. ketamine is the PSA agent _least_ likely to lead to airway obstruction from lack of muscle tone, because among PSA agents, ketamine is most likely to preserve airway reflexes and laryngeal muscle tone. It has been speculated that the reason that jaw thrust is effective in laryngospasm is not because you are lifting the airway structures off the glottis, but that you are stretching the cricothyroid muscle.
In any case, a key principle in executing PSA is that the management of hypoventilation is the same, regardless of cause, I call it the "PSA Intervention Sequence," which you see on the back of my PSA checklist.
So whether the obstruction (as evidenced by sonorous respirations or hypoventilation) is caused by relaxation of tone or laryngospasm or if those two processes are intertwined, proper head/neck positioning, followed by a jaw thrust, will be effective most of the time.
Thanks for your comments, glad to have you as a ketamine ally.
reuben
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Andrew Schmidt - October 3, 2022 4:26 PM
This is in response to Reuben Strayer's comments on ketamine-associated laryngospasm on the August episode of EM:RAP. I am what many would consider a "high utilizer" of Ketamine in our academic emergency department. I believe it to be one of the safest analgesia and sedation medications in emergency medicine, and I push very hard for my residents to use it regularly for these indications so they can be comfortable with it when they graduate. One of the reasons I push so hard is that this medication, above all others, suffers from so much disinformation on that part of physicians, nurses, and the media, that training providers often shy away from it. I took some issue with the discussion on "laryngospasm" by Reuben Strayer (whom I have learned extensively about ketamine from) because I don't think the piece highlighted the fact enough that what many people consider to be laryngospasm is just a relaxation of upper airway structures. He does mention this and compares it to OSA patients, but then talks about the primary treatments as treatments for laryngospasm, which is most often what is not actually happening. Dr Strayer was 100% correct that simple jaw thrust and oxygenation almost always helps, but that is because we are aiming to lift the glottic structures off the airway, not relax spasmed vocal cords. I think it important for listeners to understand this fact, because the whole idea of "laryngospasm" is what often scares providers away from Ketamine and (I have seen many times) leads providers to panic and rush to paralytics and intubation, when the simple knowledge that you are usually treating upper airway relaxation and NOT laryngospasm helps to ease their tension.
Reuben Strayer (@emupdates) - October 5, 2022 3:08 PM
Hi Andrew, thanks for your comment. I am in complete agreement that some providers shy away from using ketamine, to the detriment of their patients. One of my primary objectives in that segment was to reduce this anxiety, as it pertains to laryngospasm, by describing laryngospasm as an event not to be feared, but rather prepared for, as it is so readily treated. I'm not sure we know exactly what's going on, at the level of the glottis, during airway obstruction. I suspect you are correct that some of the obstruction you see in ketamine PSA is muscle relaxation, however it's worth noting 1. ketamine-related laryngospasm, or what is often described as laryngospasm, is much more commonly in kids, who are less likely to have typical OSA-type obstructive physiology. 2. ketamine is the PSA agent _least_ likely to lead to airway obstruction from lack of muscle tone, because among PSA agents, ketamine is most likely to preserve airway reflexes and laryngeal muscle tone. It has been speculated that the reason that jaw thrust is effective in laryngospasm is not because you are lifting the airway structures off the glottis, but that you are stretching the cricothyroid muscle.
https://accessanesthesiology.mhmedical.com/content.aspx?bookid=974§ionid=61589165#:~:text=The%20cricothyroid%20muscle%20is%20the%20only%20tensor%20of,to%20allow%20passage%20of%20some%20flow%20with%20CPAP.
In any case, a key principle in executing PSA is that the management of hypoventilation is the same, regardless of cause, I call it the "PSA Intervention Sequence," which you see on the back of my PSA checklist.
https://emupdates.com/emergency-department-procedural-sedation-checklist-v2/
So whether the obstruction (as evidenced by sonorous respirations or hypoventilation) is caused by relaxation of tone or laryngospasm or if those two processes are intertwined, proper head/neck positioning, followed by a jaw thrust, will be effective most of the time.
Thanks for your comments, glad to have you as a ketamine ally.
reuben