(Blogitorials are short, informal blogs that are written in the spirit of a tweetorial).
A normal human EEG should always have some activity, from birth to death. Even during sleep there is EEG activity (sleeping is an active process that includes integration of memory). That’s pretty amazing – the human brain is a perpetual motion machine that runs for decades.
Now let’s consider anesthesia for a surgical procedure. Deep anesthetics can completely silence EEG activity (aka, EEG suppression). That’s probably not terrific for the brain. But a normal brain can wake up promptly following anesthesia, when medications are stopped.
Things can get a bit more complex, though, when dealing with brains which are in the throes of delirium or other active neurologic disease.
In the ICU, I’ve encountered some delirious patients with the following attributes:
- Moderate doses of propofol cause nearly complete suppression of EEG activity. For most patients, a moderate dose of propofol wouldn’t cause complete flattening of the EEG. However, in the context of brain injury with tenuous consciousness, moderate doses of propofol can strongly suppress EEG activity.
- When propofol is discontinued for a trial of awakening, the patient becomes dangerously agitated (without regaining consciousness). This leads to immediate resumption of propofol sedation (to keep the patient safe).
A vicious spiral results:
This is SIESTA syndrome. The patient is locked in a cycle of unconsciousness, punctuated by brief episodes of agitation. Most of the time the patient is sedated to the point of having minimal EEG activity, which may hinder their ability to regain consciousness.
One solution is to transition from propofol to dexmedetomidine sedation. Using dexmedetomidine, these patients can be safely sedated – yet their EEG will now regain baseline activity. Anecdotally, following 24 hours of sedation on dexmedetomidine with an active EEG, the patient is often able to awaken and be extubated.
Propofol remains my front-line sedative for most patients, due to its ease of titration and lack of tachyphylaxis (if dexmedetomidine is used for many days, this may eventually lead to dependence and subsequent withdrawal). However, dexmedetomidine may be uniquely useful to facilitate extubation.
For patients on video EEG monitoring, SIESTA syndrome is easy to observe. However, most patients aren’t on continuous EEG activity. So the next time you see a patient who is on propofol sedation with persistent inability to extubate due to agitation, consider transitioning to dexmedetomidine. ✌️
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I would encourage folks to comment in the box below 👇, rather than on different social media platforms. This will allow a conversation between people who use different social media platforms.
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Do you have any experience of this approach working in the patient with history of recreational drug use (principally opioids, amphetamines and benzodiazepines)? I find these a particularly difficult group to successfully desedate and extubate, as they frequently become extremely agitated post extubation, often requiring frantic reintubation. I suspect they might be a different cohort of patients to the ones you are referring to in the blog, but perhaps not.
Hello!!
Useful blog. thank you for sharing to us.
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Awesome!
I missed these original and smart PulmCrit blogitorials.
Good thing on moving it from social media to classic FOAMed blogs!
Now, as a good portuguese from alentejo (portuguese region near spain with the same epicureal traditions), going to my daily SIESTA…
Great information
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