Found it! Why no analgesia with intubation?

[Veneficus]

First things first,

I am not advocating not using analgesia, only pointing out something I found on the issue.

Please do not attack the messanger.

For those of you who don't know my current endevors, this month I am wrestling with the goal of making it through Miller's Anesthesia. (the whole book)

Anyway, neatly started on page 2284 of the Seventh edition, is the discussion on using analgesia in intubated trauma patients.

It discusses in about 4 paragraphs,using analgesia in hypotensive trauma patients needs to be done with great care do to the hypotension or cardiac insult that can occur resulting in sudden cardiac arrest.

It doesn't howver discuss in this chapter a specific number to measure hypoperfusion and I don't want to type all of it out anyway.

I can only deduce that they are referring to patients in whom hemorrhage is still an ongoing issue, and not yet surgically repaired or otherwise managed. (aka very sick people in the initial stages of hospital treatment)

It text takes shots at everything from etomidate to propofol, and even thiopenthal and ketamine were not spared.

It lists as the cause interruption of compensatory sympathetic outflow coupled with the sudden change to positive pressure ventilation. It reminds readers that there may not be a drop in BP in an otherwise healthy adult until 40% of the total blood volume is lost. (class III shock) That is a fancy way to imply that it is catecholamine surge that is maintaining perfusion in these patients.

Obviously analgesia would inhibit that.

Long story short, it recommends using only sedation doses of anesthetics or small quantities of bezodiazapines.

It does recommend the use of 0.2mg of scopolamine to assist in amnestic effect when analgesics are not used, but warns it may interfere with subsequent neuro checks.

In closes by saying that while certain recall in the ED and OR is not unusual, an analysis of intraoperative awareness lawsuits in the American Society of Anesthesia (ASA) database revealed no claims related to awareness in trauma patients requiring surgery.

(for thos who don't know, absense of awareness is one of the principles of anesthesia)

Now that we all know a bit more about it, let's put it to some EMS use?

in the CC or IFT world, before adding analgesia to an intubated and sedated trauma patient,(or any suffering from hypovolemia) perfusion, volume status, and compensatory levels of physiology should be closely assessed.

In the field, if you have a really bad patient who is still conscious and you choose to RSI, there is a caution that doses of 1/10 normal in the setting of hypovolemic shock can produce deep anesthesia. So you may want to go easy on those. Particularly if you are concerned about inducing cardiac arrest.

When dealing with other providers, give consideration that this is the recommendation they are working with. They may not be experienced enough, or have the skill or equipment required to make a clinical decision on the use of analgesics in severely injured/ill populations and are trying to err on the side of caution.

Be aware no legal claims have been made against any US provider doing this, which probably means it is an accepted practice and/or the patient is not caused significant grief from recall of any part of the event. (The latter being more important in my opinion than the former.)

As a discussion point, I am also willing to bet that most patients who undergo RSI for trauma either: are stabilized without the need of surgical/intensive intervention or didn't require this level of intervention for stabilization to begin with.

Just some food for thought really.

 

[zmedic]

One method I've heard about with trauma patients that I like is from Scott Weingartt (EMCrit). He says if the trauma patients have low MAP (like bellow 65) give blood. If their pressure is fine but their limbs are cool (ie poor peripheral perfusion) they are peripherally clamped down and you should give narcs, ideally fentanyl. The goal in MICU is not complete anesthesia. Now during transport you may aim to sedate a little deeper so they don't wake up in the back of the chopper and start flailing.

Going back to the initial point. If you use fentantyl, the half life is so short that if they get a little hypotensive you just turn down the drip or give a little blood and in 10 minutes you should be back where you want.

In a similar fashion, I would say that if your intubated patient is hypertensive and tachycardic they may need a narcotic. If they are agitated, coughing, or you are worried about recall that's what your sedative (versed, propofol) are for. The narcs aren't really for "sedation," but rather if you can control the patient's pain and irritation from the tube, you actually don't really need to have them that sedated. They should be able to chill with good pain control and minimal sedation.

So if you are worried about the pressure and can't give enough narcs, that's when having a drip of both is nice. With both a versed drip and a fentanyl drip you need less of each and have a better side effect profile.

I should mention that it is important to think about what your sedation goals are. In the ICU we are looking for a RASS of -2 to 0. You can look up what RASS is but basically we are aiming for someone who is lying quitely with their eyes closed but when you say their name they open their eyes for a short while.

 

[Veneficus]

In terms of early resuscitation and the physiology of it, there is evidence (considerable actually when you consider what is published about anesthetic hypovolemia in the OR) that early vasodilation preserves function of the gut and liver, which both are stipulated as either a cause or prognostic of MODS.

In an actively bleeding patient however, this must be balanced with the risk that opioids causing vasodilation in the external cardiac arteries and corresponding vasoconstiction of capilaries in endocardium, (I have seen literature which is not immediately handy describing this) creating the potential of Q wave infarctions from endocardial ischemia.

I think in the grand scheme of trying to manage sedation and volume (at whatever level your endpoint) should be determined by whether or not there is still active bleeding.
(defined as early resuscitation vs. late.)

Unless I am making an erroneous assumption, the information presented was a recommendation for patients who are or may be actively hemorrhaging, not for resuscitation after hemorrhage is controled.

I will try to get the opinion of one of the anesthesiologists tomorrow, but unless I am mistaken, once hemostasis is achieved, the MICU treatment you mentioned is similar to the elective surgical patient, where induced vasodilation is routine.

 

[bstone]

zmedic, are you a critical care doc?

 

[zmedic]

Emergency Medicine Resident. We spend a fair amount of time doing critical care in the ER and MICU.

 

[Commonsavage]

Emergency Medicine Resident. We spend a fair amount of time doing critical care in the ER and MICU.

Thanks for the input Z, glad your here.

 

[Brandon O]

In terms of early resuscitation and the physiology of it, there is evidence (considerable actually when you consider what is published about anesthetic hypovolemia in the OR) that early vasodilation preserves function of the gut and liver, which both are stipulated as either a cause or prognostic of MODS.

In an actively bleeding patient however, this must be balanced with the risk that opioids causing vasodilation in the external cardiac arteries and corresponding vasoconstiction of capilaries in endocardium, (I have seen literature which is not immediately handy describing this) creating the potential of Q wave infarctions from endocardial ischemia.

If you have any of this literature handy, I'd love to see it. As far as I had been aware, the practice of adding intentional vasodilation via sedation to volume resuscitation is -- although practiced in a few places since its development at Shock Trauma -- still mostly without evidence. But maybe that's changed.

 

[KellyBracket]

That intestinal vasodilitation idea sounds a lot like the old "renal dose" of dopamine concept...

Just one note of caution, with the sedation and narcs and all, from my meager experience. The only times that I have really screwed up sedating people was in the patients whose physiology was "catecholamine-dependent." One was in cardiogenic shock, the other was a critical blunt trauma. They had acceptable BPs until I gave my "non-cardioactive" etomidate. Bad idea.

With regards to Zmedic - I believe I had the pleasure of his company in the ED when he was a wee' med student. He knows his stuff!

 

[Brandon O]

That intestinal vasodilitation idea sounds a lot like the old "renal dose" of dopamine concept...

Just one note of caution, with the sedation and narcs and all, from my meager experience. The only times that I have really screwed up sedating people was in the patients whose physiology was "catecholamine-dependent." One was in cardiogenic shock, the other was a critical blunt trauma. They had acceptable BPs until I gave my "non-cardioactive" etomidate. Bad idea.

With regards to Zmedic - I believe I had the pleasure of his company in the ED when he was a wee' med student. He knows his stuff!

As I understand it, the idea is that you titrate sedation alongside volume (drop 'em a little, fill 'em back up, repeat until normovolemic), maintaining a reasonable -- although probably permissive -- pressure the whole way. Preferably your fluid is blood products. In the end you have the same pressure you began with, but now it's a truly normal volume without vasoconstriction to vital organs (and without any issues caused by inducing relative hypertension) with improved afterload. "Low pressure, high flow."

As the good Dr. Z mentioned, Emcrit had some really good stuff on this -- see here. Dutton was the big name but I do know that at least some other centers have adopted this.

 

[Veneficus]

If you have any of this literature handy, I'd love to see it. As far as I had been aware, the practice of adding intentional vasodilation via sedation to volume resuscitation is -- although practiced in a few places since its development at Shock Trauma -- still mostly without evidence. But maybe that's changed.

I think there is some confusion on what I was trying to say.

I was not saying that intentional vasodilation was suggested during active hemorrhage.

I was trying to say that once hemorrhage is controlled and the patient was in late resuscitation, that theraputic vasodilation, as pointed out by zmedic in regards to lowering peripheral resistance with cool extremities in patients with acceptable blood pressure, was the same as what is done in the resuscitation of elective surgical patients.

The point being that his source for adding fent to relieve a patient who was "clamped down" was not an original idea from EMCrit. (well it may have been independantly thought of by said Dr. but it is in published text as well.)

In the OR, it is accomplished as part of the effects of sevoflurane.

Also with most sincere respects,

In the same chapter, of the same book, in the same paragraph, it specifically describes that the use of etomidate, despite "frequently espoused alternative because of its cadiovascular stability in comparison to other hypnotic drugs in trauma populations" (3 sources cited) "its inhibition of catecholamine release may still produce profound hypotension."

 

[bstone]

Emergency Medicine Resident. We spend a fair amount of time doing critical care in the ER and MICU.

Excellent. Lots of med students and an actual MD here. Not bad.

 

[STXmedic]

Excellent. Lots of med students and an actual MD here. Not bad.

jwk is an anesthesiologist if I remember correctly. We've got some knowledgeable people here that are kind enough to share some of their smarts with us

 

[zmedic]

With regards to Zmedic - I believe I had the pleasure of his company in the ED when he was a wee' med student. He knows his stuff!

Thanks. I'm just a lowly intern but getting there slowly. Removed my first roach from an ear last night. Ah, New York.