Intraop analgesics

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GassmanMD

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I was recently speaking to some co residents about how we manage intraoperative opioids for long, painful, non tiva cases. We do not see how each other practices so it was interesting to find out that I am one who gives much less opioid throughout the duration of my long cases on opioid naive patients. Most of my co residents will load the receptors way earlier than I would. I will give opioids if the hemodynamics dictate, but I don't just blindly bolus narcotics. I tend to load at the end with opioids and go with a multi modality approach. What do you guys do and why?

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I trained with some attendings that liked to start longer cases with a "good narcotic base," and would give 2mg of dilaudid shortly after induction. Usually, little else was required for several hours. I also had an attending that believed that pain is only a phenomenon of the conscious mind, and would remove your opioids from the room after induction, only letting you have then back for emergence. Most attending were somewhere in the middle. We also had a robust Acute Pain service, so we had a lot of pathways involving multimodal analgesia, used oral premeds like gabapentin, a good bit of regional, and lots of ketamine.

From this, I developed my practice, in which I tend to use a lot less opioid than my colleagues. I use ketamine and magnesium for NMDA activity (especially in chronic pain patients, frequent flyers, and long painful procedure), ketorolac and acetaminophen for most procedures where it would add something of value, and am not afraid to let some brief period of intense stimulation go untreated (or treated with small doses of beta-blocker), if the analgesic would greatly outlast the untreated pain. In the end, the PACU nurses may have to give an extra dose or two of fentanyl to my patients, as compared to my colleagues,' but mine also leave the PACU faster and more alert.
 
Thanks for the response. Sounds like your way of practicing is very similar to mine. Speaking of PACU, we get quarterly reports regarding our average initial PACU pain score (0-10 visual analog scale). I am usually slightly above average, in a bad way. The co resident I spoke to said he is consistently below average . Not sure about PACU discharge times, that would be good to compare.
 
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You will always get better pain control and a smoother general anesthesia if you give long-acting narcotics early (in long cases). It will prevent/diminish the sympathetic/inflammatory response. There is a reason why we say that it's much easier to prevent pain than to treat pain, after all those mediators are already circulating. Of course, the other side of the coin, the side effect, is that the patient might get oversedated; there is a fine line you'll have to learn to walk.

Giving narcotics at the beginning of/during the case (vs the end) allows you to also better gauge the patient's response and tolerance. You can fine tune the dose during the entire procedure. There is a reason this is called balanced anesthesia; we want to maximize the advantages and minimize the disadvantages of every drug. I give (long-acting) narcotics so that I can use less hypnotic agent; they usually give a faster and better wake-up than when you control pain just with hypnotic agents, and less nausea then short-acting narcotics. Similarly, I don't use muscle relaxants only to help the surgeon, or to look good because the patient does not move; I use them mainly so that I don't have to keep the patient deeper than needed.

You can balance anesthesia any way you want, not necessarily with narcotics (I use toradol whenever I can), as long as the pain control lasts after emergence. Learn to use every agent for its advantages; in case of long-acting narcotics, there is that inherent advantage of long-term pain and sympathetic reaction control. Why not use that advantage by starting the medication early enough that it lasts through the surgery, and stopping it late enough so that it lasts even after the surgery? Why expose the patients to nurse-controlled analgesia? Yes, they might be slightly more awake, but at what cost? Would you like waking up in pain after surgery?

By the time s/he hits the PACU, a patient should be both awake and pain-free. If you learn how to do that, you will enjoy every day at work. Learn from your patients, from every wake-up, from every mistake.

During my residency, I was considered "heavy handed" with narcotics just because I titrated meds to the patient's needs, regardless of what was politically correct. I once had a chronic pain ortho patient having regular surgeries. He was on the acute pain service in between, and they had a tough time controlling his post-op pain. Even the patient told me that I had no chance. He was taking about 300 mg morphine equivalent daily, at baseline. I still remember that, besides running him on low-dose ketamine, I titrated in about 20-30 mg of Dilaudid equivalent during the 2-3 hour-surgery. I would push 2 mg at a time and it would be like water. He woke up slightly groggy, pain-free for the first time in many surgeries (his words). I would do it again in a heartbeat. Of course one can argue about hyperalgesia, NMDA antagonists, gabapentin etc., but the idea here is to do what's the best for the patient, and do it early. I hate our narcomania, but that doesn't stop me from treating and preventing pain with narcotics when needed.
 
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It's amazing that I have been doing this for a little over a year and no attending has ever taken a look at my anesthetic record which they are signing and commented on my analgesia strategy.
 
Of course every case is different and I have only been an attending for a year, but I almost never give long acting narcotics early on in a case. You can never predict how a patient will respond and I would bet the people that are so heavy handed with the opioids also wind up having to give narcan more than you do.

I don't believe the "anti-inflammatory" effects of opioids have been shown to improve outcomes and if the case goes south you may need that sympathetic response to maintain bp; why burn the bridge? For your chronic pain patients, utilize your multimodal strategies, in addition to regional which many orthopedic procedures are amenable to.

Are people who are loading the patients up with a narcotic base, following them in the post op period? Following up on side effects like urinary retention, GI symptoms, post op delirium? Half of my patients are obese and have undiagnosed OSA. With the rampant narcotic dependence/abuse, this stuff is obviously not benign and not being judicious with it has after effects than we may not necessarily see.
 
I frequently use toradol, mag, ketamine, IV clonidine, decadron (4),preop acetaminophen, and occ preop gabapentin. Anything to keep those narcs down
 
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You will always get better pain control and a smoother general anesthesia if you give long-acting narcotics early (in long cases). It will prevent/diminish the sympathetic/inflammatory response. There is a reason why we say that it's much easier to prevent pain than to treat pain, after all those mediators are already circulating. Of course, the other side of the coin, the side effect, is that the patient might get oversedated; there is a fine line you'll have to learn to walk.

Giving narcotics at the beginning of/during the case (vs the end) allows you to also better gauge the patient's response and tolerance. You can fine tune the dose during the entire procedure. There is a reason this is called balanced anesthesia; we want to maximize the advantages and minimize the disadvantages of every drug. I give (long-acting) narcotics so that I can use less hypnotic agent; they usually give a faster and better wake-up than when you control pain just with hypnotic agents, and less nausea then short-acting narcotics. Similarly, I don't use muscle relaxants only to help the surgeon, or to look good because the patient does not move; I use them mainly so that I don't have to keep the patient deeper than needed.

You can balance anesthesia any way you want, not necessarily with narcotics (I use toradol whenever I can), as long as the pain control lasts after emergence. Learn to use every agent for its advantages; in case of long-acting narcotics, there is that inherent advantage of long-term pain and sympathetic reaction control. Why not use that advantage by starting the medication early enough that it lasts through the surgery, and stopping it late enough so that it lasts even after the surgery? Why expose the patients to nurse-controlled analgesia? Yes, they might be slightly more awake, but at what cost? Would you like waking up in pain after surgery?

By the time s/he hits the PACU, a patient should be both awake and pain-free. If you learn how to do that, you will enjoy every day at work. Learn from your patients, from every wake-up, from every mistake.

During my residency, I was considered "heavy handed" with narcotics just because I titrated meds to the patient's needs, regardless of what was politically correct. I once had a chronic pain ortho patient having regular surgeries. He was on the acute pain service in between, and they had a tough time controlling his post-op pain. Even the patient told me that I had no chance. He was taking about 300 mg morphine equivalent daily, at baseline. I still remember that, besides running him on low-dose ketamine, I titrated in about 20-30 mg of Dilaudid equivalent during the 2-3 hour-surgery. I would push 2 mg at a time and it would be like water. He woke up slightly groggy, pain-free for the first time in many surgeries (his words). I would do it again in a heartbeat. Of course one can argue about hyperalgesia, NMDA antagonists, gabapentin etc., but the idea here is to do what's the best for the patient, and do it early. I hate our narcomania, but that doesn't stop me from treating and preventing pain with narcotics when needed.

Good argument for early use of long acting opioids. Out of curiosity how often do you use low dose ketamine infusion as adjuvant? What dose are you running? Any benefit over using ketamine bolts precincts ion?
 
Good argument for early use of long acting opioids. Out of curiosity how often do you use low dose ketamine infusion as adjuvant? What dose are you running? Any benefit over using ketamine bolts precincts ion?

I am doing mostly outpatient cases nowadays, so I rarely get to use ketamine. For chronic pain patients, I used to run it at 0.2 mg/kg/h. You can give it as an infusion, or simply as an hourly bolus. The highest rate I have ever used for chronic pain has been 1 mg/kg/h, on the floor, in a CRPS patient, without any change in mental status, but she had a history of severe opiate tolerance and opiate-induced hyperalgesia.

I don't really understand the last question.
 
All roads lead to Rome, my friend. Find what works best for you and the patients. Mine depends on type of surgery, surgeon, etc. I in general tend to avoid up front, give some short-acting ones at incision, and titrate the longer-acting stuff to respiratory rate at the end and adjuvants 10 minutes before wake-up.
 
All roads lead to Rome, my friend. Find what works best for you and the patients. Mine depends on type of surgery, surgeon, etc. I in general tend to avoid up front, give some short-acting ones at incision, and titrate the longer-acting stuff to respiratory rate at the end and adjuvants 10 minutes before wake-up.

This is what I currently do.

Is there any truth to central sensitization occurring in acute pain/injury? I thought this was more of a chronic pain phenomenon. My co residents used this as their argument as to why they "load up the receptors " and give boluses of dilaudid from induction through to emergence.

Though I must admit, preventing pain does sound better than treating it later .
 
I use opiates as part of my balanced anesthetic. Type, timing and dose depend on the patient and procedure. And you can work some more in at the end as well.
I'm not sure what you gain by leaving it out during the case.

Also, I think there are probably better ways to deal with hypotension than relying on pain to bump your BP back up to acceptable levels. No?
 
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All roads lead to Rome, my friend. Find what works best for you and the patients. Mine depends on type of surgery, surgeon, etc. I in general tend to avoid up front, give some short-acting ones at incision, and titrate the longer-acting stuff to respiratory rate at the end and adjuvants 10 minutes before wake-up.
That's also what I do nowadays, with outpatients and not so painful short procedures. I rarely use long-acting opiates in this setting. The approach I described above is for the type of case the OP mentioned: long and painful.
 
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Also, I think there are probably better ways to deal with hypotension than relying on pain to bump your BP back up to acceptable levels. No?
That part is debatable, because some people argue that there is no sensation of "pain" during general anesthesia, just sympathetic response, hence the entire movement for treating it with short-acting beta-blockers.

I personally don't agree with them, because if it's not "pain", why does it elicit a pain-type spinal reflex, such as withdrawal from noxius stimuli, even under general anesthesia? I might not need to block the cortical pain pathways, but I definitely need to block the spinal and peripheral ones. Unless it's a short and rare stimulus, I expect the same type of mediator release I would get if the person were conscious, and I treat the patients the same way I would treat them if conscious, after accounting for the analgesic effects of all the drugs on board, including inhaled anesthetics.
 
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This is what I currently do.

Is there any truth to central sensitization occurring in acute pain/injury? I thought this was more of a chronic pain phenomenon. My co residents used this as their argument as to why they "load up the receptors " and give boluses of dilaudid from induction through to emergence.

Though I must admit, preventing pain does sound better than treating it later .

Good question. Due to studies showing low dose Ketamine at induction reliably reduces pain scores by blocking NMDA receptors, I think there is something to it. I think we are just scratching the surface of pain receptor pathways and their interactions so it makes for good banter.

Personally, I have no problem giving a little ketamine, but I try to do what I think makes patients the most comfortable based on experience. Regional is my answer if feasible and if not I am not light-handed with narcotics. I like toradol and decadron as well, but Ofirmev is a sham in my opinion for most cases.
 
I frequently use toradol, mag, ketamine, IV clonidine, decadron (4),preop acetaminophen, and occ preop gabapentin. Anything to keep those narcs down

Never heard for mag for pain (I'm an EM guy). Could this have any application outside of the OR/peri-operative management?
 
What about getting the patient to breathe spontaneously and titrating narcotic to respiratory rate? Assuming you are using an inhaled anesthetic.
 
What about getting the patient to breathe spontaneously and titrating narcotic to respiratory rate? Assuming you are using an inhaled anesthetic.
That's the gold standard. However, too many people use NDNMB to cover up sloppy anesthesia. These are the same people who give everyone reversal and their patients are throwing up in pacu.
 
That's the gold standard. However, too many people use NDNMB to cover up sloppy anesthesia. These are the same people who give everyone reversal and their patients are throwing up in pacu.

really? there seems to be plenty of evidence that everybody SHOULD be reversed
 
really? there seems to be plenty of evidence that everybody SHOULD be reversed
So if you gave only a defasciculating dose of relaxant for a case that lasted hours, would you reverse even if they met all extubation criteria? I am eager to see the evidence you refer to. Please post.
 
I can't/won't do the study, but I suspect there is probably a direct correlation between the dose of intraop narcotic and the level of postop pain. More narcs means more hyperalgesia means more pain. Interesting study 5-10 years ago in lap choles randomized patients to morphine or esmolol (I think) intraop and the esmolol patients had less pain postop.

Anesthetized brains don't experience the psychological effect we call pain, but we treat their autonomic responses with opioids. Is it right? Probably to a degree in the name of balanced anesthesia. But going heavy handed on the narcs is probably not in the patient's best interest.

Personally I attempt to maximize non narcotics like po acetaminophen and iv toradol and ketamine and use the iv narcs to smooth out the intraop course a bit, but the biggest doses are for patients that are awake and capable of experiencing pain. I'd rather not overload their receptors while unconscious.
 
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I've seen the old studies that implicated reversal, and the ones refuting those. Anecdotally, I believe it is multifactorial and related to the NPO status (elevated glucagon levels, epi,stress), narcotics, AND reversal. I did recently see a study that showed the odds ratio of nausea/vomiting increased after reversal, and I will post when I can find it. Some of the established PO guidelines for certain surgeries are now being questioned, such as the enhanced recovery after surgery colorectal study where carbohydrate drinks are given up until surgery. Again, my 2 cents.
 
Good argument for early use of long acting opioids. Out of curiosity how often do you use low dose ketamine infusion as adjuvant? What dose are you running? Any benefit over using ketamine bolts precincts ion?
I use ketamine for almost every case with non-trivial pain expectations. I usually start with a 0.5 mg/kg bolus with induction, then give 10 mg every hour or so during the case. It's easier than messing with a pump and it works.

I think I'm going to start trying some magnesium too, maybe just added to the first bag of IV fluids. I give almost everyone ketorolac, preferably in preop holding if it's not a bloodletting kind of case or an ortho case with a surgeon who thinks NSAIDs are to blame for his nonunions. Dexamethasone 4 mg with almost every induction. I'm using more IV acetaminophen lately too.


What about getting the patient to breathe spontaneously and titrating narcotic to respiratory rate? Assuming you are using an inhaled anesthetic.

Most of the time, I leave patients on the vent to keep MV up to get gas off. I don't try to get them spontaneously breathing often, even with LMAs.

On those occasions when I do have a patient initating his own breaths, I'll titrate to an ETCO2 around 50. I think that's a better gauge of comfort and optimal amount of opiate than rate.
 
I use ketamine for almost every case with non-trivial pain expectations. I usually start with a 0.5 mg/kg bolus with induction, then give 10 mg every hour or so during the case. It's easier than messing with a pump and it works.

I think I'm going to start trying some magnesium too, maybe just added to the first bag of IV fluids. I give almost everyone ketorolac, preferably in preop holding if it's not a bloodletting kind of case or an ortho case with a surgeon who thinks NSAIDs are to blame for his nonunions. Dexamethasone 4 mg with almost every induction. I'm using more IV acetaminophen lately too.




Most of the time, I leave patients on the vent to keep MV up to get gas off. I don't try to get them spontaneously breathing often, even with LMAs.

On those occasions when I do have a patient initating his own breaths, I'll titrate to an ETCO2 around 50. I think that's a better gauge of comfort and optimal amount of opiate than rate.
So if you have a respiratory rate of 30 but an ETCO2 of 50, you assume you have a good level of narcotic on board??
 
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So if you have a respiratory rate of 30 but an ETCO2 of 50, you assume you have a good level of narcotic on board??
In a kid, maybe.

That's an odd combination of numbers for an adult and I'd suspect a problem, eg a badly seated LMA or slightly kinked tube that was causing some obstruction or limiting tidal volumes.

The point is that I think minute ventilation is a better gauge of comfort than rate.

Surely you'll acknowledge that a rate of 12 and ETCO2 of 30 suggests a different pain level than a rate of 12 and ETCO2 of 50?


The problem with titrating to RR (or ETCO2) is that volatile anesthetics have analgesic effects and respiratory effects (increasing rate and decreasing tidal volumes). And when that gas is gone they need more opiates. I just prefer to not have to give anything after wakeup.

I get comfortable wakeups, faster, if I just leave them on the vent until the gas is gone. I don't want them to breathe spontaneously at an ETCO2 of about 45. But when I do let them breathe, I'm more interested in ETCO2 than rate.
 
I use very little intra op narcotics; almost never at induction a little before incision and as needed during the case. If it's a very long case (rare in my practice) i'll set up an infusion of sufenta/ketamine at a low rate generally 6-7.5 mcg/h with 15mg K/h.
I titrate long acting narcotics iv at the end and maybe give some IM for longer coverage. I use regional as much as i can: a majority of uro or abdominal cases with TAP blocks will get no narcs.
I reserve magnesium for patient in the PACU with residual pain after all common meds have been given and it works well in that setting.
I always mix sufenta and ketamine (4mcg/10mg) so when i'm giving sufenta there's always a K kick to it.
 
Depending on case length, patient outpatient meds, case type and appropriateness of regional, I'm partial to adding Ofirmev and ketamine (sometimes bolus, sometimes bolus and drip) to the mix. Haven't run narcotic drips in a long time - not that I'm averse to narcotic drips. Only narcotic I typically consider front-loading is maintenance methadone. I prefer titrating narcotics intraop.
 
How do you titrate long acting opioids at the end of a case and not stack your doses and still leave the room in an efficient amount of time? 0.5 mg of dilaudid q2-3min to resp rate does not work as well for me as a 2mg load early (given 1mg at a time to assess response) and then fentanyl at the end, pull the ett deep (when approp) and out the door.

Agree with lose dose ketamine (prefer if midaz on board) and other adjuncts like apap, ketorolac...regional if work flow permits.
 
How do you titrate long acting opioids at the end of a case and not stack your doses and still leave the room in an efficient amount of time? 0.5 mg of dilaudid q2-3min to resp rate does not work as well for me as a 2mg load early (given 1mg at a time to assess response) and then fentanyl at the end, pull the ett deep (when approp) and out the door.

Agree with lose dose ketamine (prefer if midaz on board) and other adjuncts like apap, ketorolac...regional if work flow permits.
Your right. Dilaudid takes a few minutes to fully kick in and therefore, I tend to load them in the course of the case when I use it. Usually, towards the end though. Then I give Fent at the end to titration RR to my goal, usually 12 in adults.
 
The point is that I think minute ventilation is a better gauge of comfort than rate.

Surely you'll acknowledge that a rate of 12 and ETCO2 of 30 suggests a different pain level than a rate of 12 and ETCO2 of 50?


The problem with titrating to RR (or ETCO2) is that volatile anesthetics have analgesic effects and respiratory effects (increasing rate and decreasing tidal volumes). And when that gas is gone they need more opiates. I just prefer to not have to give anything after wakeup.

I get comfortable wakeups, faster, if I just leave them on the vent until the gas is gone. I don't want them to breathe spontaneously at an ETCO2 of about 45. But when I do let them breathe, I'm more interested in ETCO2 than rate.
I don't disagree with your approach and we all know that there are many ways to skin a cat. But my thinking is more like this. Narcs cause us to breath slow and deep. Therefore as I titrate my narcs I'm using RR which I want in the 10-14 range in adults, I also pay attention to TV. I notice the breathes become larger and ETCO2 remains the same usually. This is ideal to me but I ve never used ETCO2 as a gauge. I guess I usually see ETCO2's in the 45-55 range.
 
I don't disagree with your approach and we all know that there are many ways to skin a cat. But my thinking is more like this. Narcs cause us to breath slow and deep. Therefore as I titrate my narcs I'm using RR which I want in the 10-14 range in adults, I also pay attention to TV. I notice the breathes become larger and ETCO2 remains the same usually. This is ideal to me but I ve never used ETCO2 as a gauge. I guess I usually see ETCO2's in the 45-55 range.

I tend to use ETCO2 and minute ventilation instead of RR because of how unreliable the size of TV can be when a patient is breathing spontaneously through an ETT or LMA. The respiratory "drive" is to get rid of CO2 in the blood stream via minute ventilation. Narcotics blunt that. If they have a RR of 24 but the ETCO2 is 50, I'm not so sure I'd want to give them even more narcotic and cause them to hypoventilate even more.
 
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If they have a RR of 24 but the ETCO2 is 50, I'm not so sure I'd want to give them even more narcotic and cause them to hypoventilate even more.
Slightly different style but same results.
In my experience though, if RR is 24 and ETCO2 50 like you describe I still give narcs. I seem to notice the ETCO either remains the same or improves because the TV actually increases. With that being said, a RR of 24 (adults)is pretty rare in my cases. So if I see that then something else is going on usually but not always.
 
Please post evidence that reversal causes PONV. I hear this sometimes but my gut feeling is that it is dogma.

This recent study seems to be decent, but not ideal. It's the largest I can see, but isn't an RCT, and has some issues but I think has some good points.

http://www.ncbi.nlm.nih.gov/pubmed/24296853
Retrospective investigation of postoperative outcome after reversal of residual neuromuscular blockade: sugammadex, neostigmine or no reversal.

RESULTS:
Data from 1444 patients (722 sugammadex, 212 neostigmine and 510 no-reversal) were analysed. The incidence of postoperative nausea and vomiting (PONV) in PACU was higher in neostigmine-reversed than sugammadex-reversed patients (21.5 vs. 13.6%; P <0.05).

On avg they used 2 mg Neo @ ~0.05 mg/kg. ~60+% of folks got antiemetics prophylactically, with 74% in the Neo group. Supposedly there was no difference between Sug reversal and No-reversal for PONV, but they don't explicitly state that Neo reversal was sig diff from No reversal.
 
40 kg (90 lb) patients???
Skewed distribution. Exact mean of 2.4 with a range of (0.8 - 3.8). Avg BMI ~ 28 though.

Australians aren't as obese as some, at least not yet.
 
really? there seems to be plenty of evidence that everybody SHOULD be reversed
I hear that a lot. I'm just not sure if that is a relic from when we didn't use TOF monitoring well and had less experience with paralytics.

http://www.ncbi.nlm.nih.gov/pubmed/15681938
The big study is based on data from 1995-1997. They show that reversal of muscle relaxants decreased mortality. They also show that reversal of opioids and muscle relaxants reduces mortality. Should everyone get Narcan? No, that's just silly.

http://www.ncbi.nlm.nih.gov/pubmed/25225821
This recent one is neat. No where as big, lots of caveats, but some interesting findings.

Anesthesiology. 2014 Sep 15. [Epub ahead of print]
Effects of Neostigmine Reversal of Nondepolarizing Neuromuscular Blocking Agents on Postoperative Respiratory Outcomes: A Prospective Study.
RESULTS:
Neostigmine reversal did not improve S/F at postanesthesia care unit admission (164 [95% CI, 162 to 164] vs. 164 [161 to 164]) and was associated with an increased incidence of atelectasis (8.8% vs. 4.5%; odds ratio, 1.67 [1.07 to 2.59]). High-dose neostigmine was associated with longer time to postanesthesia care unit discharge readiness (176 min [165 to 188] vs. 157 min [153 to 160]) and longer postoperative hospital length of stay (2.9 days [2.7 to 3.2] vs. 2.8 days [2.8 to 2.9]). Unwarranted use of neostigmine (n = 492) was an independent predictor of pulmonary edema (odds ratio, 1.91 [1.21 to 3.00]) and reintubation (odds ratio, 3.68 [1.10 to 12.4]).

Again, lots of caveats to this. They seem to suggest high dose neostigmine (> 0.06 mg/kg) usage makes folks stay in PACU longer. If usage of Neo is unwarranted, as in you aren't using a TOF monitor or are dosing it before you have one twitch, patient is twice as likely to develop pulmonary edema and 4x more likely to get reintubated.
 
Don't misinterpret the studies. There are pts that should be reversed every time and others that can breath well enough with some fade on TOF. So the data isn't perfect in my opinion.
Here is my approach. If the pt is a young strongish pt with no pulmonary comorbidities, of which obesity falls into this category, the I will forgo reversal if the pt has 4/4 twitches for a decent amount of time. These pts can breath ell enough and if they can't then I reverse them at that point. If I extubate and they aren't breathing well enough then I give 2-3 cc propofol and some reversal. Also on a side note, I don't paralyze nearly like I did in the past. For example, I barely paralyze lap choles. I just make them weak.
If the pt has pulm comorbidities and I've given paralytics throughout the case then I reverse every time.
So obviously, I don't believe the ASA's statement that everyone should be reversed. But if I have any airways concerns then they get reversal.
 
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Really? If the patient has fade that you can detect, they are extremely weak. Are you using an accelerometer? if not respiratory complications, what about the discomfort/distress to the patient (the weakness, the blurry vision, etc)
 
http://journals.lww.com/anesthesia-...ased_Management_of_Neuromuscular_Block.1.aspx
Evidence-Based Management of Neuromuscular Block
Viby-Mogensen, Jørgen MD, DMSc, FRCA*; Claudius, Casper MD, PhD†

http://journals.lww.com/anesthesiol..._Assessment_of_the_Pharynx_at_Rest_and.5.aspx
Functional Assessment of the Pharynx at Rest and during Swallowing in Partially Paralyzed Humans: Simultaneous Videomanometry and Mechanomyography of Awake Human Volunteers
Eriksson, Lars I. MD, PhD; Sundman, Eva MD; Olsson, Rolf MD, PhD; Nilsson, Lena MD; Witt, Hanne MD, PhD; Ekberg, Olle MD, PhD; Kuylenstierna, Richard MD, PhD
(How did they recruit for this one)

 
I'm a huge fan of running a remifenta infusion intraop. Good smooth wake ups.

Also, I've worked with one attending who absolutely loves sufenta instead of fenta for induction.

But, yeah Toradol is a miracle drug.
 
I'm really surprised when people don't run intraop lidocaine infusions. The data is very solid. It is very easy and safe and no downside.

Also, there is a TON of literature that has already shown very clearly that intraop opioid amount STRONGLY correlates with increased post op pain and increased opioid use. The more you use, the more they will need.

Given that fact, coupled with the increased rate of post surgical infection with increased opioids and also the retrospective data on cancer and immune function, I absolutely think it is a wise goal to avoid opioids as much as possible.

Plus, it is very hard to predict how people respond. On call last week, a guy had an open chole...I told the resident to wave off on the TAP blocks. He had very little fentanyl for the case. He woke up pain free and needed very little pca. You just don't know... Better to wait and see for so many reasons.

I really believe nociception causing sympathetic outflow is not pain. Treat the symptom (sympathetic outflow).

To the person who doesn't believe any benefit of peri operative Tylenol....do the study to prove it. Because all studies so far on the subject totally disagree with you. I am anxious to see it.
 
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Oh and by the way codeblu, remi is the absolute worst in causing increased need and increased pain post operatively.

But you do get a nice wake up.
 
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