Precedex

I'm not quite so sure about that ;)

Yeah, your going to have come with more than that, Narcan (used properly) is an incredibly safe drug, and hell used incorrectly is still safer than most drugs out there.

What makes you think it isn't safe?
 
I guess it depends on your definition of 'used correctly.' Narcan given in 40 mcg boluses q3 min titrated to a decent resp rate is probably very safe. Note, that is the 0.4 mg/ml diluted in 10 cc. A 0.4 mg bolus of narcan can off somebody.

When I was in paramedic school I was preached the doctrine of narcan's benign nature. Well, it's untrue. Narcan is a very potent antagonist and anytime you rapidly antagonize such a widespread system in the body, there are bound to be repercussions. You give a patient with valvular heart disease or coronary artery disease too much narcan, and you can put them into florid heart failure easily. There is a sympathetic discharge that comes with opiate reversal (especially rapid and potent antagpnism) that markedly increases myocardial oxygen demand and CO2 production and acutely increases afterload.

I was that medic. My protocols called for 0.4 mg narcan IVP for opiate reversal and I gave it like adenosine. I loved to teach the addicts a lesson. But that bolus has effects beyond what you may see in the prehospital world, I promise.

Slow and steady wins the race. And you don't need a patient awake enough to do calculus. You need them protecting their airway, nothing more.
 
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I guess it depends on your definition of 'used correctly.' Narcan given in 40 mcg boluses q3 min titrated to a decent resp rate is probably very safe. Note, that is the 0.4 mg/ml diluted in 10 cc. A 0.4 mg bolus of narcan can off somebody.

When I was in paramedic school I was preached the doctrine of narcan's benign nature. Well, it's untrue. Narcan is a very potent antagonist and anytime you rapidly antagonize such a widespread system in the body, there are bound to be repercussions. You give a patient with valvular heart disease or coronary artery disease too much narcan, and you can put them into florid heart failure easily. There is a sympathetic discharge that comes with opiate reversal (especially rapid and potent antagpnism) that markedly increases myocardial oxygen demand and CO2 production and acutely increases afterload.

I was that medic. My protocols called for 0.4 mg narcan IVP for opiate reversal and I gave it like adenosine. I loved to teach the addicts a lesson. But that bolus has effects beyond what you may see in the prehospital world, I promise.

Slow and steady wins the race. And you don't need a patient awake enough to do calculus. You need them protecting their airway, nothing more.

Care to cite any literature?

I agree with not slamming the patients back to full consciousness but narcan is fairly benign when used properly. I don't know if I'm buying all the later down the road consequences you're claiming.
 
I guess it depends on your definition of 'used correctly.' Narcan given in 40 mcg boluses q3 min titrated to a decent resp rate is probably very safe. Note, that is the 0.4 mg/ml diluted in 10 cc. A 0.4 mg bolus of narcan can off somebody.

When I was in paramedic school I was preached the doctrine of narcan's benign nature. Well, it's untrue. Narcan is a very potent antagonist and anytime you rapidly antagonize such a widespread system in the body, there are bound to be repercussions. You give a patient with valvular heart disease or coronary artery disease too much narcan, and you can put them into florid heart failure easily. There is a sympathetic discharge that comes with opiate reversal (especially rapid and potent antagpnism) that markedly increases myocardial oxygen demand and CO2 production and acutely increases afterload.

I was that medic. My protocols called for 0.4 mg narcan IVP for opiate reversal and I gave it like adenosine. I loved to teach the addicts a lesson. But that bolus has effects beyond what you may see in the prehospital world, I promise.

Slow and steady wins the race. And you don't need a patient awake enough to do calculus. You need them protecting their airway, nothing more.

Theoretical. Only a handful of cases in the literature and even those cases it is unclear if it was actually the Narcan that caused it. And I work in the in non-prehospital realm, so I am well aware of what goes on after the patient is transferred (both in the ED and beyond. . .)
 
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Will you accept a textbook citation? I hope this is enough without making me go to pubmed, cuz I'm kinda tired. This is cut and paste from Barash "Clinical Anesthesia"




In clinical anesthesia practice, naloxone is administered to antagonize opioid-induced respiratory depression and sedation. Because opioid antagonists will reverse all opioid effects, including analgesia, naloxone should be carefully titrated to avoid producing sudden, severe pain in postoperative patients. Sudden, complete antagonism of opioid effects with naloxone has been reported to cause severe hypertension, tachycardia, ventricular dysrhythmias, and acute, sometimes fatal, pulmonary edema.288 Naloxone-induced pulmonary edema can occur even in healthy young patients who have received relatively small doses (80 to 500 μg) of naloxone.289,290 The mechanism for this phenomenon is thought to be centrally mediated catecholamine release, which causes acute pulmonary hypertension. Because most patients with opioid-induced respiratory depression will often breathe on command, it is important to stimulate them in addition to administering carefully titrated naloxone doses in the immediate postoperative period. It is also essential to monitor vital signs and oxygenation closely after naloxone is administered to detect occurrence of any of these potentially serious complications.
Naloxone will precipitate opioid withdrawal symptoms in opioid-dependent individuals. Clinicians tend to be aware of this risk when treating patients with known opioid addiction, but it is important to consider the potential for opioid withdrawal syndrome when treating nonaddicts who use opioids chronically, such as cancer patients and severe burn and trauma patients with protracted recovery courses.
Naloxone has a very fast onset of action, and thus is easily titrated. Peak effects occur within 1 to 2 minutes, and duration is dose-dependent, but total doses of 0.4 to 0.8 mg generally last 1 to 4 hours.1 Suggested incremental doses for IV titration are 20 to 40 μg given every few minutes until the patient's ventilation improves, but analgesia is not completely reversed. Because naloxone has a short duration of action, respiratory depression may recur if large doses and/or long-acting opioid agonists have been administered. When prolonged ventilatory depression is anticipated, an initial loading dose followed by a naloxone infusion can be used. Infusion rates between 3 and 10 μg/hr have been effective in antagonizing respiratory depression from systemic as well as epidural opioids.291


Not theoretical. I have watched a patient have an NSTEMI after a slug of narcan. Or you can just look in the PDR or epocrqtes under adverse reactions.
 
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Not theoretical. I have watched a patient have an NSTEMI after a slug of narcan. Or you can just look in the PDR or epocrqtes under adverse reactions.

Serious side effects from nalaxone are not theoretical, but they are also not common.

I do not have a lot of experience with nalaxone. I've given it a few times, watched it given a few more times, and read a fair amount about it. Aside from the common sense "if you give too much or give it too fast it can cause problems, especially in addicts", and "try to only give enough to get them breathing" warning, I've never thought of nalaxone as an especially hazardous drug.

Then, as of late, it seems there has been a lot of talk about nalaxone on the EMS sites and blogs, mostly by those saying we shouldn't use it, because it is so dangerous. However, no one has really given a good explanation or cited any new or damning literature, that I've seen.


Here's how I see it:

Serious side effects from any medication are possible, especially in large doses or rapid administration. I don't hear people saying that we should not use fentanyl or versed or propofol, even those meds are probably responsible for more problems than nalaxone.

The alternative to using nalaxone in a severely narcotized patient is intubation. Intubation will commonly require exposing the patient to other drugs that also have potentially serious side effects. Not to mention that prehospital intubation is probably associated with more problems than is nalaxone administration.


Anyway, because I was curious about this and because I was not able to find much info on the hazards of nalaxone, I spent about that past 60 minutes consulting the following textbooks:

Clinical Anesthesia (Barash)
Miller's Anesthesia
Clinical Anesthesiology (Morgan & Mikhail)
Essential Clinical Anesthesia (Vacanti)
Manual of Clinical Anesthesiology (Chu & Fuller)
Nurse Anesthesia (Nagelhout)
Pharmacology & Physiology in Anesthetic Practice (Stoelting)
Principles of Pharmacology (Golan)
Lippincott's Pharmacology Review's (Harvey)
Anesthetic Pharmacology (Evers)
Goodman & Gillman's Manual of Pharmacology & Therapeutics

Not one of those texts described nalaxone as especially hazardous. Every one of them did refer to problems that can potentially result from sudden sympathetic overstimulation secondary to opiate antagonism. Most of them state that side effects of nalaxone are dose-dependent.

The description that I found most helpful came from Nagelhout:

"The effects of naloxone use range from discomfort to pulmonary edema to sudden death. Pulmonary edema after naloxone administration has been observed in patients with a documented history of cardiovascular disease. Prough and co-workers reported two cases of acute onset of pulmonary edema in young male patients who received either 100 or 200 mcg of naloxone. The report discusses the ability of naloxone to inhibit endogenous pain suppression pathways and to allow unopposed noradrenergic transmission from medullary centers that can produce neurogenic pulmonary edema. Neurogenic pulmonary edema results from an increase in catecholamine levels in healthy patients, as well as in patients with a history of cardiovascular disease. Cautious titration of naloxone is of paramount importance in both cardiovascular patients and healthy patients."

Granted, these texts are all a few years old so maybe there's some newer info out there. But I have yet to see a compelling reason why nalaxone shouldn't be used when indicated - with caution, like any other medication.
 
Yes, that is certainly a balanced view. But keep this in mind-- with the availability and use of oral opiates these days, it is not just the addicts we are seeing anymore. A lot of my elderly patients are on chronic opiates and some on multiples from different doctors without realizing it. There is a big difference in the tachycardia and hypertension from narcan in a 28 yo addict vs. reversing grandma with aortic stenosis, cad, or pulmonary hypertension.

When you are reversing opiates, you should view narcan as a vasoactive substance and all of the implications thereof should be taken into account.


My point - it is not the benign drug I was led to believe it was in paramedic class. And I do my best to make sure my paramedic friends understand that too.

Sorry for the soapbox.
 
My point - it is not the benign drug I was led to believe it was in paramedic class. And I do my best to make sure my paramedic friends understand that too.

I think that is a good point.
 
When you are reversing opiates, you should view narcan as a vasoactive substance and all of the implications thereof should be taken into account.


My point - it is not the benign drug I was led to believe it was in paramedic class. And I do my best to make sure my paramedic friends understand that too.

Sorry for the soapbox.
Don't be sorry for the soapbox that you are on!

While I tend to think of Narcan as basically benign, I am also quite aware of the dangers of using it incorrectly - such as slamming the dose in. While the Narcan itself doesn't cause the effects, it allows an unchecked "stomping of the gas" on the patient, which the opiate was kindly keeping the brakes on. I might consider doing a 0.2-0.3mg IM injection and the balance of a 0.4mg dose would be given slow IVP. Why? Start the process of increasing their respiratory drive and allow the IM injection the time to slowly bring the patient up to consciousness.

Simply put though, I'm not going to, nor have I ever, slammed in the 0.4mg Narcan dose just because I can or I feel like punishing my opiate OD patient, nor am I going to give it right before delivery to the ED. Why? I much prefer a sedated patient that's not going to cause me problems that all I have to deal with is just keeping a close watch on their respiratory status. No sense in fighting someone that hates my guts completely because I wrecked their high.
 
I transported one patient on Precedex from a V.A Hospital and this was the first time that I had ever heard of it. It was a ventilated patient and it was being used for sedation. It wasn't doing the job very well and the doctor was insistent on leaving it run and not change to something else for transport. As usual, we got bolus dose order for Ativan.

Needless to say, soon as we got down to the unit the RN with us gave like 10mg of Ativan and the patient was great for the transfer.
 
I transported one patient on Precedex from a V.A Hospital and this was the first time that I had ever heard of it. It was a ventilated patient and it was being used for sedation. It wasn't doing the job very well and the doctor was insistent on leaving it run and not change to something else for transport. As usual, we got bolus dose order for Ativan.
Pretty much the issue for transport. Well, that and it's ungodly expensive compared to the standards (propofol or versed/fent).

Needless to say, soon as we got down to the unit the RN with us gave like 10mg of Ativan and the patient was great for the transfer.
All at once?:unsure: You know there's this thing called titration....

One of the common complaints among physicians is the patient's level of sedation is titrated to nurse comfort rather than what's appropriate for the patient. While I'll be the first to say physicians have at times hard time understanding the transport environment, this would seem to be exactly what they're complaining about.
 
Pretty much the issue for transport. Well, that and it's ungodly expensive compared to the standards (propofol or versed/fent).


All at once?:unsure: You know there's this thing called titration....

One of the common complaints among physicians is the patient's level of sedation is titrated to nurse comfort rather than what's appropriate for the patient. While I'll be the first to say physicians have at times hard time understanding the transport environment, this would seem to be exactly what they're complaining about.

I pushed for propofol for transport and made my case but physician wouldn't budge.

I wouldn't have given the 10mg all at once personally as I think titration is best practice but the resp effect was irrelevant given the pt. was intubated. And pt. was on the hypertensive side to start. So I was like eh. It's all good.
 
the resp effect was irrelevant given the pt. was intubated.
Easy to think that, but one of the pluses of dex is the lack of effect on the respiratory drive. Meaning while you may not of seen it as a big deal, without knowing where they were in the weaning cycle this might have been a significant setback. Depending on the patient benzos can hang around a long time.
 
Easy to think that, but one of the pluses of dex is the lack of effect on the respiratory drive. Meaning while you may not of seen it as a big deal, without knowing where they were in the weaning cycle this might have been a significant setback. Depending on the patient benzos can hang around a long time.

I understand. Our patient was having issues with delirium as well and just needed sedated for safe transport and to blunt the sympathetic response and do well on the vent. Trust me, with an Autovent 4000, you need an out cold patient.
 
I've looked into Precedex a little more since this thread was originally active. Most of the studies I've seen reveal it as a decent drug in the quiet ICU for moderate sedation and not too bad of side effects. But the data pretty much says it doesn't offer any real advantages over a Versed drip or a propofol drip (those were being compared in the studies). Precedex cost a lot more too.
 
I hate the phrase "just give them enough to keep them breathing."

No, you're stupid. Give them just enough to keep them breathing AND protecting their own airway,

Does me no good to have to sit there and hold manual airway maneuvers, suction place adjuncts, whatever it may be when I can give another 100-200 mcg and bring them around enough that they'll breathe, not aspirated and stay super sleepy.
 
I've looked into Precedex a little more since this thread was originally active. Most of the studies I've seen reveal it as a decent drug in the quiet ICU for moderate sedation and not too bad of side effects. But the data pretty much says it doesn't offer any real advantages over a Versed drip or a propofol drip (those were being compared in the studies). Precedex cost a lot more too.

Benzodiazepines are now known to cause delirium in critically ill patients. Propofol will as well, though to a lesser degree. Delirium markedly increases both morbidity and mortality in ICU patients. Neither benzos nor propofol offer any analgesia. Precedex does have modest analgesic properties.

You are probably looking at what are termed the ProDex and the MiDex studies. These looked at time on the vent, hospital length of stay and ability to communicate pain scores. Patients on precedex got off the vent faster and were better able to communicate pain scores. This study did not look at mortality.

I sound like a precedex salesman, but in the critically ill population I think it is a great drug. Even in the CCT truck, most patients don't need to be unconscious. They need to be comfortable.
 
One of the neat and maybe bad things about naloxone is its ability to antagonize endogenous opioid binding. There are probably users on this forum who wouldn't get the same rush from posting if they were on a narcan drip...
 
Benzodiazepines are now known to cause delirium in critically ill patients. Propofol will as well, though to a lesser degree. Delirium markedly increases both morbidity and mortality in ICU patients. Neither benzos nor propofol offer any analgesia. Precedex does have modest analgesic properties.

You are probably looking at what are termed the ProDex and the MiDex studies. These looked at time on the vent, hospital length of stay and ability to communicate pain scores. Patients on precedex got off the vent faster and were better able to communicate pain scores. This study did not look at mortality.

I sound like a precedex salesman, but in the critically ill population I think it is a great drug. Even in the CCT truck, most patients don't need to be unconscious. They need to be comfortable.

I have heard about the benzos causing delirium as discussed on Emcrit.org. For IFT, our established goal in our acutely ill patients is to maintain a RASS score of at least -4 or -5. A paralytic is highly encouraged and our medical director is said to be implementing protocol for paralytic on our vent patients for transport. I personally like fentanyl followed by a low infusion dose of propofol in most patients.

Precedex was not shown to be superior overall at least from what I have seen. I've only encountered the drug once in clinical practice and wasn't impressed but maybe further use will change my mind.
 
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