Palliative sedation?

[NurseDude1966]

As a nursing student, during one of our rotations I noticed that a lot of stage 4 cancer patients/ terminally ill patients were sedated with anesthetics such as midazolam or propofol and they referred to it as "paliative sedation." We were told that the two most common reasons for the sedation are due to persistent/ treatment resistant pain or nausea/vomiting.

I understand how sedation can help the pain because you cannot feel pain if you are asleep, but how does it help with nausea/vomiting? People can still vomit in their sleep as we often see with people who are overly intoxicated. Wouldn't being sedated just put them at risk for aspiration?

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[WholeLottaGame7]

I've mostly heard of opioid infusions, or ketamine, or dexmedetomidine infusions for palliative purposes. Neither of those drugs you mentioned are analgesics and wouldn't be my first (or second or third) choice for pain. Anxiolysis, sure. The propofol might be run at a low-dose for N/V as it does have anti-emetic properties. I've never seen high dose propofol for sedation for palliative purposes, that would be fairly unusual, I believe.

 

[NurseDude1966]

I've mostly heard of opioid infusions, or ketamine, or dexmedetomidine infusions for palliative purposes. Neither of those drugs you mentioned are analgesics and wouldn't be my first (or second or third) choice for pain. Anxiolysis, sure. The propofol might be run at a low-dose for N/V as it does have anti-emetic properties. I've never seen high dose propofol for sedation for palliative purposes, that would be fairly unusual, I believe.

Yeah they use opioids for the pain but for the actual sedation they use either midazolam or Propofol. But still that doesn't answer my question of how does being sedated stop refractory nausea and vomiting? It was said that deep sleep shuts down the vomiting center of the brain but people could still vomit in their sleep can't they?

 

[kidthor]

I haven't seen people palliated with propofol myself. There's a fine line between palliation and termination sedation. Propofol has such a narrow window that it'd quickly get into terminal sedation.

Once dying patients patients are less and less responsive, I think emesis is either uncommon or a non-issue. (perhaps because dying people are not usually eating). Also you may be confounding nausea and emesis...

Often I think we overdo it with drugs and complicated strategies when it comes to end-of-life care... and on a related note we as anesthesiologists are skilled with certain palliative care drugs and related issues - but we aren't palliative care physicians as such. So this question might be better suited to their forum.

 

[IMGASMD]

Stanford list it as 10mg/hr. Yes folks.
Obviously with bolus and increase rate as needed.

 

[Planktonmd]

Actually sedation does alleviate centrally triggered nausea and vomiting very effectively. All CNS depressants will work on that including Benzos, Propofol, Neuroleptics...

 

[NurseDude1966]

I haven't seen people palliated with propofol myself. There's a fine line between palliation and termination sedation. Propofol has such a narrow window that it'd quickly get into terminal sedation.

Once dying patients patients are less and less responsive, I think emesis is either uncommon or a non-issue. (perhaps because dying people are not usually eating). Also you may be confounding nausea and emesis...

Often I think we overdo it with drugs and complicated strategies when it comes to end-of-life care... and on a related note we as anesthesiologists are skilled with certain palliative care drugs and related issues - but we aren't palliative care physicians as such. So this question might be better suited to their forum.

I will post there. Thank you!

 

[NurseDude1966]

Actually sedation does alleviate centrally triggered nausea and vomiting very effectively. All CNS depressants will work on that including Benzos, Propofol, Neuroleptics...

Thank you for the reply! How does sedation stop nausea/vomiting though? And since it stops it, how do people vomit and possibly aspirate when asleep under anesthesia or really intoxicated?

Also, you mentioned centrlly acting nausea and vomiting. So like vomiting from a stomach tumor wouldn't be stopped as well with sedation as vomiting in lets say the brain?

 

[Planktonmd]

Thank you for the reply! How does sedation stop nausea/vomiting though? And since it stops it, how do people vomit and possibly aspirate when asleep under anesthesia or really intoxicated?

Also, you mentioned centrlly acting nausea and vomiting. So like vomiting from a stomach tumor wouldn't be stopped as well with sedation as vomiting in lets say the brain?

The vomiting center in the brainstem receives triggering signals from peripheral sources (stomach, intestine, biliary and urinary tracts...) and it also receives triggering signals from higher areas in the brain itself (odors, visions, memories, vestibular receptors...)
So suppressing cerebral activity can actually suppress that centrally triggered nausea.
When people vomit and aspirate under sedation or anesthesia the cause is usually reaching an anesthetic depth where the vomiting center is not fully suppressed while airway reflexes are impaired and unable to protect the airway.
The brainstem vomiting center is actually resistant to sedation but it has serotonin and dopamine receptors which explains the actions of currently used antiemetics.
I hope this helps.

 

[Hork Bajir]

Propofol (and to a lesser degree midazolam) both have intrinsic antiemetic properties. Neither is first-line to treat nausea, but in a refractory palliative situation I could see there being a role. The subanesthetic doses of either agent that would be used in this context will likely depress airway protective reflexes and increase the likelihood of an aspiration event if/when the patient vomits... But if the patient is close to death and treating refractory nausea is a bigger concern, that may be an acceptable risk. I haven’t seen prop or midaz used in that way, but I suppose you could make a case for it.

If the patient has a mechanical gastric outlet (or small bowel) obstruction, which I assume is what you mean when you say “stomach cancer”, then no amount of any anti-emetic is going to stop the patient from puking up their gastric secretions. Decompressing the stomach with an OGT, NGT, venting PEG, etc will be far more effective for relieving nausea in that context (by relieving the distention of the hollow viscus which activates stretch receptors in the wall of the stomach/bowel, which is a crazy potent stimulus for nausea).

Hope this helps. As others have said, you may have more luck with your question on a palliative care forum.

 

[NurseDude1966]

The vomiting center in the brainstem receives triggering signals from peripheral sources (stomach, intestine, biliary and urinary tracts...) and it also receives triggering signals from higher areas in the brain itself (odors, visions, memories, vestibular receptors...)
So suppressing cerebral activity can actually suppress that centrally triggered nausea.
When people vomit and aspirate under sedation or anesthesia the cause is usually reaching an anesthetic depth where the vomiting center is not fully suppressed while airway reflexes are impaired and unable to protect the airway.
The brainstem vomiting center is actually resistant to sedation but it has serotonin and dopamine receptors which explains the actions of currently used antiemetics.
I hope this helps.

This actually was very helpful and I appreciate you taking the time to write this. So if the vomiting Center is resistant to sedation, then how does the sedation suppress it? Once it reaches a certain threshold that Center no longer is resistant to it? So would you say it is moderate or deep sedation that it would take to suppress it?

 

[Planktonmd]

This actually was very helpful and I appreciate you taking the time to write this. So if the vomiting Center is resistant to sedation, then how does the sedation suppress it? Once it reaches a certain threshold that Center no longer is resistant to it? So would you say it is moderate or deep sedation that it would take to suppress it?

Sedation actually suppresses the central signals that come from the brain to the vomiting center in the brainstem (odors, visions, vestibular signals...) not the center itself.
To suppress the vomiting center in the brainstem you need general anesthesia. But there are anti emetics that work on the serotonin and dopamine receptors in the vomiting center.

 

[NurseDude1966]

Sedation actually suppresses the central signals that come from the brain to the vomiting center in the brainstem (odors, visions, vestibular signals...) not the center itself.
To suppress the vomiting center in the brainstem you need general anesthesia. But there are anti emetics that work on the serotonin and dopamine receptors in the vomiting center.

Oh oh I see! So even if that center is not depressed itself, there's no input into it from the rest of the brain being suppressed in order to trigger it?

 

[NurseDude1966]

Sedation actually suppresses the central signals that come from the brain to the vomiting center in the brainstem (odors, visions, vestibular signals...) not the center itself.
To suppress the vomiting center in the brainstem you need general anesthesia. But there are anti emetics that work on the serotonin and dopamine receptors in the vomiting center.

So if somebody was vomiting due to a peripheral reason as opposed to central such as gastroenteritis or a bowel obstruction, etc? Sedation wouldn't work to stop that since the signals are coming from the body and not the brain?

 

[Hork Bajir]

@NurseDude1966

Afferent input “from the body” gets transmitted centrally to the brain. Most anesthetics work by modulating neurotransmission in the central nervous system (brain and spinal cord).

I commend you for you enthusiasm and curiosity... But what has been written above is already way more than you need to know for nursing school purposes. Keep asking questions and working in understanding what you’re seeing in the hospital... But it seems like your time might be better spent learning basic anatomy, pharmacology, and physiology than by trying to take a deep dive on side effects of IV anesthetic agents without having the background knowledge firmly in place. Just my 0.02

 

[WholeLottaGame7]

Stanford list it as 10mg/hr. Yes folks.
Obviously with bolus and increase rate as needed.

Yeah, that's not propofol for sedation, that's being used as an anti-emetic. I've heard of propofol PCAs for N/V that utilize similar very low doses of propofol.

 

[IMGASMD]

Yeah, that's not propofol for sedation, that's being used as an anti-emetic. I've heard of propofol PCAs for N/V that utilize similar very low doses of propofol.

https://palliative.stanford.edu/palliative-sedation/medications-of-choice/

 

[NurseDude1966]

@NurseDude1966

Afferent input “from the body” gets transmitted centrally to the brain. Most anesthetics work by modulating neurotransmission in the central nervous system (brain and spinal cord).

I commend you for you enthusiasm and curiosity... But what has been written above is already way more than you need to know for nursing school purposes. Keep asking questions and working in understanding what you’re seeing in the hospital... But it seems like your time might be better spent learning basic anatomy, pharmacology, and physiology than by trying to take a deep dive on side effects of IV anesthetic agents without having the background knowledge firmly in place. Just my 0.02

Well yeah but thats what i meant, peripheral originating triggers can still trigger the vomiting center under sedation (since the vomiting center is more resistant to sedation) where as centrally originating triggers cannot since those of central origin are suppressed by the sedation. Sorry if I made that confusing before.

 

[WholeLottaGame7]

https://palliative.stanford.edu/palliative-sedation/medications-of-choice/

Not sure what you meant by your reply since you didn't elaborate. I didn't say "I don't believe Stanford uses propofol," I said 10mg/hr is not a dose that produces sedation.

Since they don't list a max dose, presumably they can just keep going higher until they get into sedative doses and finally anesthetic doses. Obviously a lot of conflicting factors in these patients (high tolerance, but also on other synergistic meds), but I would think you'd have to be at least 100mg/hr to start getting a sedating effect (that's about 15-30 mcg/kg/min depending on weight).

On a semi-related note, this is one reason I love dexmedetomidine in kids, anecdotally I think it decreases PONV (even though I haven't seen a great study to address that question specifically).

 

[NurseDude1966]

@NurseDude1966

Afferent input “from the body” gets transmitted centrally to the brain. Most anesthetics work by modulating neurotransmission in the central nervous system (brain and spinal cord).

I commend you for you enthusiasm and curiosity... But what has been written above is already way more than you need to know for nursing school purposes. Keep asking questions and working in understanding what you’re seeing in the hospital... But it seems like your time might be better spent learning basic anatomy, pharmacology, and physiology than by trying to take a deep dive on side effects of IV anesthetic agents without having the background knowledge firmly in place. Just my 0.02

So would this same principle of sedation work for relentless vomiting due to lets say gastric cancer or gastroenteritis since the triggering nausea signal into the vomiting center of the brain stem is originating in the body as opposed to the brain? I know its not something I need to know its just something I'm curious about that I could not find an answer to lol.

 

[IMGASMD]

Not sure what you meant by your reply since you didn't elaborate. I didn't say "I don't believe Stanford uses propofol," I said 10mg/hr is not a dose that produces sedation.

Since they don't list a max dose, presumably they can just keep going higher until they get into sedative doses and finally anesthetic doses. Obviously a lot of conflicting factors in these patients (high tolerance, but also on other synergistic meds), but I would think you'd have to be at least 100mg/hr to start getting a sedating effect (that's about 15-30 mcg/kg/min depending on weight).

On a semi-related note, this is one reason I love dexmedetomidine in kids, anecdotally I think it decreases PONV (even though I haven't seen a great study to address that question specifically).

I didn’t really have a great point; just pointing out that some of these people who are writing the protocols probably shouldn’t. (Unfamiliarity of the drug). I truly believe they think 10mg/hr is enough.

 

[NurseDude1966]

So would this same principle of sedation work for relentless vomiting due to lets say gastric cancer or gastroenteritis since the triggering nausea signal into the vomiting center of the brain stem is originating in the body as opposed to the brain? I know its not something I need to know its just something I'm curious about that I could not find an answer to lol.

Can somebody answer this question please?

 

[nimbus]

Can somebody answer this question please?

With enough sedation, all physical symptoms go away. It could be pruritus, nausea, pain, anxiety, dyspnea, whatever.

 

[Hork Bajir]

Or another way of looking at things is this: nociceptive transmission occurs whether you are awake or asleep. Pain is a subjective, conscious experience (usually but not always resulting from that nociceptive input). If you are unconscious, you cannot consciously experience pain- despite the fact that nociceptive transmission is still occurring, as is the autonomic and neurohormonal stress response to that input.

Emetogenic input can still occur whether you are awake or asleep; nausea is a subjective sensation that requires you to be awake in order to experience. Reflex expulsion of gastric contents in response to an emetogenic stimulus can still happen regardless of whether or not someone is awake enough to experience nausea.

Some anesthetic agents- propofol for example- have direct anti-emetogenic properties (they supposedly blunt the feeling of nausea as well as the vomiting reflex in response to emetogenic input). All anesthetic agents, if given in high enough doses to cause a loss of consciousness, will prevent someone from feeling subjective nausea (because there is no subjective experience at all when a patient is under deep general anesthesia).

Again, though, I would separate mechanical causes for nausea/vomiting from central ones. If you have a small bowel obstruction, no amount of anti-emetic in the world is going to overcome such a strong stimulus for nausea. Even if you make that person unconscious so that they don’t “feel” nausea, they will still vomit.

 

[NurseDude1966]

With enough sedation, all physical symptoms go away. It could be pruritus, nausea, pain, anxiety, dyspnea, whatever.

Right, but my question is how? So like how does sedation put an end to relentless vomiting that hasnt responded to antiemetics as in the case of patients with cyclic vomiting syndrome of advanced cancer? As I mentioned (I'm not sure if it was here or elsewhere) but we see that people who are under anesthesia can still vomit or people who are intoxicated to a point where they are unconscious can still vomit (and risk aspirating at that). So how does sedation stop vomiting and not just cause the patient to vomit in their sleep?

 

[siliso]

All symptoms stop with deep enough sedation because they require conscious awareness to be symptoms at all. You can manage gastric output with an NG, nothing to vomit. You can’t itch or be in pain or dyspneic or nauseated or agitated if you’re unconscious. It’s a last resort, though.

 

[NurseDude1966]

Or another way of looking at things is this: nociceptive transmission occurs whether you are awake or asleep. Pain is a subjective, conscious experience (usually but not always resulting from that nociceptive input). If you are unconscious, you cannot consciously experience pain- despite the fact that nociceptive transmission is still occurring, as is the autonomic and neurohormonal stress response to that input.

Emetogenic input can still occur whether you are awake or asleep; nausea is a subjective sensation that requires you to be awake in order to experience. Reflex expulsion of gastric contents in response to an emetogenic stimulus can still happen regardless of whether or not someone is awake enough to experience nausea.

Some anesthetic agents- propofol for example- have direct anti-emetogenic properties (they supposedly blunt the feeling of nausea as well as the vomiting reflex in response to emetogenic input). All anesthetic agents, if given in high enough doses to cause a loss of consciousness, will prevent someone from feeling subjective nausea (because there is no subjective experience at all when a patient is under deep general anesthesia).

Again, though, I would separate mechanical causes for nausea/vomiting from central ones. If you have a small bowel obstruction, no amount of anti-emetic in the world is going to overcome such a strong stimulus for nausea. Even if you make that person unconscious so that they don’t “feel” nausea, they will still vomit.

But again, and this is where i get confused and where the discrepency comes in. Deep sedation CAN stop the sensation of nausea as well as the subsequent reflex of vomiting as we see in the case of cyclic vomiting syndrome. When a patient fails to respond to antiemetics they abort the episode via sedating them with lorazepam to stop the vomiting and bring it under control. Or another example is palliative sedation. So like the example of severe vomiting from cancer that won't respond to antiemetics, they sedate the person with midazolam or something to bring the symptoms under control.

When I read, it was said that the vomiting reflex is triggered by neurons in your brain not your stomach, so naturally if you sedate (aka shut down) the brain it'll slow and stop the vomiting. Just like your other reflexes (people can't sneeze or cough when they are deeply sedated right)? And this makes total sense BUT (and here is the part that confuses me)... We see that individuals who are under general anesthesia csn still vomit which is why they tell u not to eat before surgery. Or people who are way too drunk/ intoxicated can vomit while unconscious and risk aspirating.

So how can being sedated/ asleep help stop vomiting in one sense but in another sense (anesthesia, being drunk) womt stop it and will just put you at risk? Does it depend on the level or depth of sedation?

 

[NurseDude1966]

All symptoms stop with deep enough sedation because they require conscious awareness to be symptoms at all. You can manage gastric output with an NG, nothing to vomit. You can’t itch or be in pain or dyspneic or nauseated or agitated if you’re unconscious. It’s a last resort, though.

But being sedated will stop the sensation of nausea but will it stop the vomiting reflex itself? As mentioned I see that being sedated is a last resort option for refractory vomiting and will stop it by basicaly turning the brain off (your reflexes stop when you are sedated enough, like your ability to sneeze, cough, withdraw from pain, etc) but at the same time we see that sometimes people can vomit under general anesthesia or if they are too intoxicated and unconscious. How can that be? That sedation can stop it in some cases byt other times doesnt?

 

[siliso]

Vomiting is just expulsion of gastric contents PO. It can be managed mechanically by suction if the reflex isn’t suppressed. If the person is unconscious, they won’t experience any sensations related to the evacuation of gastric contents by tube or by reverse peristalsis, so they won’t experience nausea or vomiting. Under anesthesia people generally have OG, you can keep stomach empty by hook or by crook, so the point is more or less moot in a palliative sedation or anesthetic context. Intoxicated/ODing people vomit and aspirate it because they’re too unconscious to care...just like people who are very sedated don’t clear secretions from their airway and rattle because they’re too sleepy and comfortable to care about clearing their secretions. This is a good thing to be able to explain to families when their loved one is rattling because it does sound to the layperson like their loved one is choking, and they’re not.

 

[NurseDude1966]

Vomiting is just expulsion of gastric contents PO. It can be managed mechanically by suction if the reflex isn’t suppressed. If the person is unconscious, they won’t experience any sensations related to the evacuation of gastric contents by tube or by reverse peristalsis, so they won’t experience nausea or vomiting. Under anesthesia people generally have OG, you can keep stomach empty by hook or by crook, so the point is more or less moot in a palliative sedation or anesthetic context. Intoxicated/ODing people vomit and aspirate it because they’re too unconscious to care...just like people who are very sedated don’t clear secretions from their airway and rattle because they’re too sleepy and comfortable to care about clearing their secretions. This is a good thing to be able to explain to families when their loved one is rattling because it does sound to the layperson like their loved one is choking, and they’re not.

But again (and maybe I'm not explaining it the right way as I'm getting various answers) but HOW DOES DEEP SEDATION OR ANESTHESIA STOP THE VOMITING REFLEX? They do use it for that purpose in refractory cases of vomiting so how exactly does it work?

So in the case I brought up of during anesthesia, since the reflex is suppressed, is it more of a passive thing (the food regurgitates and passively enters the esophagus) as opposed to actually vomiting and it being an active process ( again, simce the reflex is suppressed?)

 

[nimbus]

But again (and maybe I'm not explaining it the right way as I'm getting various answers) but HOW DOES DEEP SEDATION OR ANESTHESIA STOP THE VOMITING REFLEX? They do use it for that purpose in refractory cases of vomiting so how exactly does it work?

So in the case I brought up of during anesthesia, since the reflex is suppressed, is it more of a passive thing (the food regurgitates and passively enters the esophagus) as opposed to actually vomiting and it being an active process ( again, simce the reflex is suppressed?)

You answered your own question multiple times. Vomiting and nausea are 2 related but separate things.

And you are correct, if a patient vomits under anesthesia it is usually passive regurgitation. Active wrenching and vomiting is most often caused during anesthesia when somebody triggers the vomiting reflex (eg by attempted intubation) before the patient is deep enough or before they are paralyzed.

May I ask why you are so fixated on this particular topic? Seems like it’s the only thing you post about in 3 different forums. Hopefully you are not here for medicolegal research.

 

[IMGASMD]

But again (and maybe I'm not explaining it the right way as I'm getting various answers) but HOW DOES DEEP SEDATION OR ANESTHESIA STOP THE VOMITING REFLEX? They do use it for that purpose in refractory cases of vomiting so how exactly does it work?

So in the case I brought up of during anesthesia, since the reflex is suppressed, is it more of a passive thing (the food regurgitates and passively enters the esophagus) as opposed to actually vomiting and it being an active process ( again, simce the reflex is suppressed?)

Deep enough? It’s like porn, I know when I see it?
I know I sound like a douche when I give that answer. But there are too many factors to really account for. Some medications such as propfol has some intrinsic properties that will suppress brain activities or morphine which has metabolites that will activate brain and make patient nauseous. There are even more factors that will contribute to the act of vomit, such as activation of chemoreceptor trigger zone by whole lot of compounds or mechanical forces, such as dilated bowel due to obstruction, what we like to consider in anesthesia, decrease in LES tone.
Circling back to the question what you are DYING TO KNOW. Honestly, I don’t have the answer you want. But if they’re in the state of “deep sedation”* without other electrolyte imbalance**, or other mechanical problems, you’re probably fine.

*deep sedation is in quotes, because I would like to use ASA’s definition there, not just a term people like to throw around. There is an actual definition of this.
**i invoke electrolyte imbalance here because when you’re under alcohol intoxication, I would assume you’re not “balanced”. So that would be a different conversation.

 

[NurseDude1966]

You answered your own question multiple times. Vomiting and nausea are 2 related but separate things.

And you are correct, if a patient vomits under anesthesia it is usually passive regurgitation. Active wrenching and vomiting is most often caused during anesthesia when somebody triggers the vomiting reflex (eg by attempted intubation) before the patient is deep enough or before they are paralyzed.

May I ask why you are so fixated on this particular topic? Seems like it’s the only thing you post about in 3 different forums. Hopefully you are not here for medicolegal research.

No not medicolegal research, im still in school! Im asking based off of what i was observing during rotation and what I learned. But i felt there wasnt anough info (for my liking) and I wanted to delve deeper but nobody vould answer.

 

[NurseDude1966]

Deep enough? It’s like porn, I know when I see it?
I know I sound like a douche when I give that answer. But there are too many factors to really account for. Some medications such as propfol has some intrinsic properties that will suppress brain activities or morphine which has metabolites that will activate brain and make patient nauseous. There are even more factors that will contribute to the act of vomit, such as activation of chemoreceptor trigger zone by whole lot of compounds or mechanical forces, such as dilated bowel due to obstruction, what we like to consider in anesthesia, decrease in LES tone.
Circling back to the question what you are DYING TO KNOW. Honestly, I don’t have the answer you want. But if they’re in the state of “deep sedation”* without other electrolyte imbalance**, or other mechanical problems, you’re probably fine.

*deep sedation is in quotes, because I would like to use ASA’s definition there, not just a term people like to throw around. There is an actual definition of this.
**i invoke electrolyte imbalance here because when you’re under alcohol intoxication, I would assume you’re not “balanced”. So that would be a different conversation.

Ok to put it simple because I get all these various answer that domt really address the question.
When deeply sedated/ anesthetized, peoples reflexes/ bodily actvities (cough, sneezing, response to pain, beathing, etc) diminish and get suppressed as the body and brain slow down and get "turned of" from the sedation... Vomiting is a reflex therefor does vomiting (not nausea, not just the sensation of vomiting) but does the act/reflex of vomiting itself get suppressed like all the other reflexes in the body?

 

[Hork Bajir]

Yes. The vomiting reflex (active reverse peristalsis that pushes gastric contents up and out) does get suppressed by anesthesia, like with all other reflexes.

However as has been pointed out repeatedly, gastric contents can still reflux up and out even without reverse peristalsis. Anything that creates a pressure gradient from stomach to outside world (when the lower esophageal sphincter is relaxed) will cause gastric contents to go up and out.

Because you keep bringing up alcohol and low dose sedative agents (Valium, etc)... in order to make reflexes like the cough, gag, and vomiting reflexes go away, you need to be under a deep plane of general anesthesia. Unless you become an SRNA, that won’t apply to any of the patients you are seeing. Under lighter planes of sedation, certain reflexes are actually exaggerated (for example please go read about laryngospasm, which is an exaggerated glottic closure reflex that usually manifests when a patient is under a light plane of anesthesia). So low dose propofol like you are describing is NOT likely to “shut down” any reflexes.

Dude, this (and the above information) is the best you’re going to get. Your question has been answered. If you still don’t get it, I encourage you to go read more about the things that have been said above.

 

[IMGASMD]

Ok to put it simple because I get all these various answer that domt really address the question.
When deeply sedated/ anesthetized, peoples reflexes/ bodily actvities (cough, sneezing, response to pain, beathing, etc) diminish and get suppressed as the body and brain slow down and get "turned of" from the sedation... Vomiting is a reflex therefor does vomiting (not nausea, not just the sensation of vomiting) but does the act/reflex of vomiting itself get suppressed like all the other reflexes in the body?

If you’re asking “does reflexes get suppressed under deep sedation?” Yes.

Re-read what has been said already Or ask simpler questions. Even yes or no questions for now? that will help clarify some concepts. There are precise definition of sedation and reflex in medical usage, maybe that’s where some of the frustrations arise from.

Moreover, if you’re trying to clarify definition of sedation and its effect on reflexes, you’re in the world of hurt. Because how the stage/plane/level of sedation is being defined as such that some of the normal reflexes are extinguished.

 

[siliso]

I am a clinical pragmatist who has practiced a good deal of practical palliative care. Do you have a practical clinical/management question that hasn’t been answered? If your question is whether it’s theoretically possible to vomit despite deep sedation, the answer is it doesn’t matter and why do you care.

 

[NurseDude1966]

Yes. The vomiting reflex (active reverse peristalsis that pushes gastric contents up and out) does get suppressed by anesthesia, like with all other reflexes.

However as has been pointed out repeatedly, gastric contents can still reflux up and out even without reverse peristalsis. Anything that creates a pressure gradient from stomach to outside world (when the lower esophageal sphincter is relaxed) will cause gastric contents to go up and out.

Because you keep bringing up alcohol and low dose sedative agents (Valium, etc)... in order to make reflexes like the cough, gag, and vomiting reflexes go away, you need to be under a deep plane of general anesthesia. Unless you become an SRNA, that won’t apply to any of the patients you are seeing. Under lighter planes of sedation, certain reflexes are actually exaggerated (for example please go read about laryngospasm, which is an exaggerated glottic closure reflex that usually manifests when a patient is under a light plane of anesthesia). So low dose propofol like you are describing is NOT likely to “shut down” any reflexes.

Dude, this (and the above information) is the best you’re going to get. Your question has been answered. If you still don’t get it, I encourage you to go read more about the things that have been said above.

Makes sense. Glad we spread this out and gave examples. Only thing though, is valium and midazolam and lorazepam for that matter often used to create a deep plane of sedation in the icu and or other areas? I mean i know for midazolam they even use that for induction of anesthesia sometimes.

 

[WholeLottaGame7]

Makes sense. Glad we spread this out and gave examples. Only thing though, is valium and midazolam and lorazepam for that matter often used to create a deep plane of sedation in the icu and or other areas? I mean i know for midazolam they even use that for induction of anesthesia sometimes.

Midazolam can be used for conscious (light) sedation.
Midazolam can be used for moderate sedation.
Midazolam can be used for deep sedation.
Midazolam can be used for general anesthesia.

It all depends on what dose you use, the size of the patient, how tolerant they are, etc. The same can be said for basically any sedative medication. ICUs generally shoot for light or moderate sedation. Occasionally deep sedation. Very rarely general anesthesia.

 

[NurseDude1966]

Midazolam can be used for conscious (light) sedation.
Midazolam can be used for moderate sedation.
Midazolam can be used for deep sedation.
Midazolam can be used for general anesthesia.

It all depends on what dose you use, the size of the patient, how tolerant they are, etc. The same can be said for basically any sedative medication. ICUs generally shoot for light or moderate sedation. Occasionally deep sedation. Very rarely general anesthesia.

Thank you

What level of sedation is usually required to suppress intractable vomiting?

 

[abolt18]

Thank you

What level of sedation is usually required to suppress intractable vomiting?

The people to whom you are directing this question do not regularly give SEDATION for vomiting. I don’t know who on here can truly answer this question because I would say that most of the individuals would give one of the more accepted medicines/treatments for nausea that won’t cause (as much) sedation, including but not limited to ondansetron, metoclopramide, promethazine, prochlorperazine, haloperidol, dexamethasone, aprepitant, ephedrine IM, scopolamine patch, NG tube, acupressure, alcohol swabs under the nose, and possibly low-dose benzos. But I would say that in the world of anesthesia, someone with intractable nausea and vomiting is not getting SEDATION as their treatment, as that’s just asking for a major aspiration event. My point in all of this is to say that your question is flawed to begin with. Rather, maybe you should be asking if there’s a better treatment for this ailment than sedation.

 

[WholeLottaGame7]

Thank you

What level of sedation is usually required to suppress intractable vomiting?

Patients who are under the maintenance phase of general anesthesia do not vomit. Going into or coming out of general anesthesia, sure. Anything short of general anesthesia, I would assume that they could vomit, and potentially now do not have airway reflexes to protect themselves.

Nobody's getting a GA to keep them from vomiting. So the question is, do other depths of anesthesia suppress nausea and vomiting? Sure, to varying degrees. Does it mean they can't or won't vomit if the stimulus is strong enough? No. Is it worse if they do vomit while sedated? Probably. Do the palliative care docs care? At that point in the game/decision-making process, probably not.

 

[NurseDude1966]

The people to whom you are directing this question do not regularly give SEDATION for vomiting. I don’t know who on here can truly answer this question because I would say that most of the individuals would give one of the more accepted medicines/treatments for nausea that won’t cause (as much) sedation, including but not limited to ondansetron, metoclopramide, promethazine, prochlorperazine, haloperidol, dexamethasone, aprepitant, ephedrine IM, scopolamine patch, NG tube, acupressure, alcohol swabs under the nose, and possibly low-dose benzos. But I would say that in the world of anesthesia, someone with intractable nausea and vomiting is not getting SEDATION as their treatment, as that’s just asking for a major aspiration event. My point in all of this is to say that your question is flawed to begin with. Rather, maybe you should be asking if there’s a better treatment for this ailment than sedation.

Its not flawed, people who have intractable vomiting that does not respond to s cocktail of antiemetics/ various therapies (aka cyclic vomiting syndrome, cancer, etc) are often sedated to prorvide relieve from the vomiting that will not stop otherwise.

 

[NurseDude1966]

Patients who are under the maintenance phase of general anesthesia do not vomit. Going into or coming out of general anesthesia, sure. Anything short of general anesthesia, I would assume that they could vomit, and potentially now do not have airway reflexes to protect themselves.

Nobody's getting a GA to keep them from vomiting. So the question is, do other depths of anesthesia suppress nausea and vomiting? Sure, to varying degrees. Does it mean they can't or won't vomit if the stimulus is strong enough? No. Is it worse if they do vomit while sedated? Probably. Do the palliative care docs care? At that point in the game/decision-making process, probably not.

Yeah this is along the lines of what i was referring to. So like those refractory cyclic vomiting syndrome patients or end stage cancer patients who have intractable vomiting that cannot be controlled with antiemetics or other means and end up having to be sedated (aka palliative sedation) to terminate their symptoms, the depth of sedation is relative to the perosn and depends on what it will tske to relieve them.

 

[siliso]

Far more often people who can’t stop puking get an NG TO SUCTION

 

[NurseDude1966]

Far more often people who can’t stop puking get an NG TO SUCTION

But that doesn't stop the actual retching. It just eliminates the possibility of food coming up.

 

[evilbooyaa]

I can almost guarantee you that the people using the term 'palliative sedation' are NOT anesthesiologists, and 'sedation' to non-anesthesiologists means something quite different than 'sedation' to anesthesiologists. To non-anesthesiologists, anybody who gets any benzo or propofol, is 'sedated'. To anesthesiologists, it depends on how much you give and the patient's response to determine their level of sedation.

At the end of the day, propofol and benzos have intrinsic anti-emetic capabilities (separate from their ability to knock you out, AKA anesthetize you). You delving into the levels of sedation and its relation to reflexes is losing sight of the forest for the trees and is beyond the scope of routine medical practice (nobody is doing general anesthesia, which is NOT the same as giving propofol or benzos on a drip, to fix someone's nausea). At the end of the day, what you believe to be 'sedation' is not what most people on this forum think of as 'sedation'.

I know I'm way out of my lane here, but I see two sides talking past each other for the past ~50ish posts.

 

[siliso]

But that doesn't stop the actual retching. It just eliminates the possibility of food coming up.

In my experience it does Why don’t you ask your preceptors if you are seeing specific clinical cases that you have questions about. Probably will be more productive for you.

 

[abolt18]

Its not flawed, people who have intractable vomiting that does not respond to s cocktail of antiemetics/ various therapies (aka cyclic vomiting syndrome, cancer, etc) are often sedated to prorvide relieve from the vomiting that will not stop otherwise.

It's as if you didn't even read a single word of my entire post except the one where I told you your questioning was flawed. This entire thread has been filled with people getting DEEP into the pathophysiology of nausea and vomiting and how they are both related and can also be completely separate. The answers have been more than thorough and you've been so hung up on this concept of "palliative sedation" for N/V, that you've neglected to understand that we are not palliative care doctors and we do not (except the intensivists on here) provide palliative care or palliative sedation.

We provide varying levels of sedation and anesthesia for people undergoing surgery/procedures/tests. It is our intention that our patients will wake up after surgery. It is a primary goal of what we do to protect the airway and prevent the patient from having their gastric contents end up in their lungs. We provide anesthesia as safely as possible. If someone has bad nausea and vomiting, they are NOT getting sedation as a treatment. Not from me anyway.

In the ICU or in parts of end-of-life care, someone may elect to give sedation, but that's not a normal component of practice for most of the participants in this section of SDN. So, how much sedation does it take to suppress cyclical vomiting syndrome? I don't know, and I don't intend to find out. Maybe ask the palliative care docs?

 

[POW16]

Can we close this thread?