IM Atropine dose for peds emergency

MmacFN · May 23, 2006

Hey Mike

Im not suggesting standing by like Gomer Pyle :) Im suggesting using the drug correctly to reverse the parasympathetic vagal response, and that would be IV/IO.

While i understand that not all peds anesthesia cases need an IV, understanding the pharmacokinetics of atropine suggests that a bradycardic kiddie would be reversed quicker by taking the time to insert an IV and give the atropine than give it IM. Unless your suggesting giving it prior to every intubation, its pointless. If im wrong, please prove it with research not rhetoric. I can prove my point.

Is it better to give a drug to prevent or attenuate a bradycardic response or stand there like Gomer Pyle?
PPV is always the first like offense to break a laryngospasm
The first line defense is don't muck with the cords during stage II of anesthetic depth
I have not used lidocaine directly on the cords (nor have I had to use the DART) PPV has worked thus far... knock on wood...
I vaguely remember reading something somewhere about lidocaine on the cords to break a spasm but most texts discuss sux as the primary back up following PPV. M&M has a vignette about a pressure point behind the ear that can break a spasm but again I don't remember the details.
Mike

maturner · May 23, 2006

Hey Mike
Im not suggesting standing by like Gomer Pyle :) Im suggesting using the drug correctly to reverse the parasympathetic vagal response, and that would be IV/IO.
While i understand that not all peds anesthesia cases need an IV, understanding the pharmacokinetics of atropine suggests that a bradycardic kiddie would be reversed quicker by taking the time to insert an IV and give the atropine than give it IM. Unless your suggesting giving it prior to every intubation, its pointless. If im wrong, please prove it with research not rhetoric. I can prove my point.

Look MAN! I am not suggesting anyone to act on anything I have said.

Looking up every bit of research to determine how to act and respond is great. However, this is nothing more than a chat room and I am simply sharing my experience and not writing a thesis. I have a life outside of healthcare and have bigger fish to fry. I have absolutely NOTHING TO PROVE TO YOU.

I was simply stating what my experience has been thus far, what the practice is in my part of the country and what is in the texts. The people that I know who have used the dart have had good experience with it. There are Pros and cons to the administration of any medication by any route and each situation should be evaluated for the best course of action. If I encounter a laryngospasm that does not break with PPV and the patient has no IV I will administer a SUX/Atropine dart as is suggested by Morgan and Mickhail and what has been used successfully by people with whom I have practiced.

Being that you are the one that has nothing better to do than argue online and look up research, why don't you provide EBP guidelines or research regarding the negative implications following the coadministration of IM SUX/ATROPINE for the abatement of Larygospasm in the pediatric population prior to establishment of an intravenous line?

Mike

maturner · May 23, 2006

No where do I see an onset of 15 minutes! Interestingly the onset following deltoid injection falls right within the the onset of 3-5 minutes for Sux. Those darn pharmokinetics. So much for useless...

Anesth Analg. 1997 Jan;84(1):54-8.

Sullivan KJ, Berman LS, Koska J, Goodwin SR, Setzer N, White SE, Graves SA, Nall AV.

Department of Anesthesiology, University of Florida College of Medicine, Gainesville 32610-0254, USA.

In children undergoing inhaled induction of anesthesia with halothane who suffer bradycardia, submental glossal injection of atropine may result in more rapid onset of vagolysis than traditional intramuscular sites. We compared the intervals between injection and onset of heart rate acceleration (tHR increases) after intramuscular injection of atropine into the deltoid, vastus lateralis, and glossa in children between 1 mo and 10 yr of age scheduled for elective surgery. The tHR increases was determined by measuring the interval between atropine injection and the time point at which the slope of the heart rate curve initially became positive. To ensure that the drug had taken effect before surgical stimulation, heart rate observation was continued until it increased at least 5% above baseline with evidence of continuing acceleration. Anesthesia was induced in all subjects by mask with nitrous oxide and halothane. After tracheal intubation, constant inspired concentrations of the anesthetics were administered for 3 min. While heart rate was monitored, atropine (0.02 mg/kg) was injected into one of the three sites. Each patient's end-tidal anesthetic concentrations were recorded, and minimum alveolar anesthetic concentrations (MAC) were subsequently calculated and adjusted for age. The tHR increases was recorded and averaged for each group. The study groups did not differ by age, weight, end-tidal anesthetic concentrations, age-adjusted MAC, or heart rate at the time atropine was administered. After submental glossal injection (n = 11), tHR increases increase was fastest (3.0 +/- 1.1 min) and was significantly faster than that found with deltoid injection (n = 16; 4.4 +/- 1.1 min) or vastus lateralis injection (n = 8; 6.4 +/- 2.4 min) (P

PMID: 8988999 [PubMed - indexed for MEDLINE]

susswood · May 23, 2006

I NEVER do a peds case without a sux/atropine dart. Not only that, but I carry it with me to the PACU, 'cause it sucks when they spasm on the way there and they show up hypoxic and bradycardic and the it takes the PACU nurses 3 minutes to open the crash cart and find atropine.

p.s. the patient did fine

susswood · May 23, 2006

Shouldn't some of you be in clinical right now?

Nurse Ratched, RN · May 23, 2006

Here's what I hate about stepping in to moderate the CRNA forum: clinically, I haven't the faintest notion what y'all are talking about most of the time. That said, when I wade through the stuff I can't read, I too often see it interspersed with rising tempers and personal attacks, which I can read. All I'm asking is that you JUST talk about things I _don't_ get. Link to clinical resources, debate current research versus anectdotal experience, but please don't "yell" at each other.

Thank you! :)

sjt9721, BSN, RN · May 23, 2006

Here's what I hate about stepping in to moderate the CRNA forum: clinically, I haven't the faintest notion what y'all are talking about most of the time. That said, when I wade through the stuff I can't read, I too often see it interspersed with rising tempers and personal attacks, which I can read. All I'm asking is that you JUST talk about things I _don't_ get. Link to clinical resources, debate current research versus anectdotal experience, but please don't "yell" at each other.
Thank you! :)

:roll

jwk · May 23, 2006

Here's what I hate about stepping in to moderate the CRNA forum: clinically, I haven't the faintest notion what y'all are talking about most of the time. That said, when I wade through the stuff I can't read, I too often see it interspersed with rising tempers and personal attacks, which I can read. All I'm asking is that you JUST talk about things I _don't_ get. Link to clinical resources, debate current research versus anectdotal experience, but please don't "yell" at each other.
Thank you! :)

:chuckle Actually, this is pretty sedate compared to a number of other threads.

MmacFN · May 23, 2006

Nice article, Mike

My assumption that it could take up to 15 minutes for absorbtion of IM atropine (depending on site of injection) is commonly taught in both medical school and nursing school. However, the reference is directly out of the Merek manual:

Aqueous solutions of drugs are usually absorbed from an IM injection site within 10-30 min, provided blood flow is unimpaired. Faster or slower absorption is possible, depending on the concentration and lipid solubility of the drug, vascularity of the site (there are differences between various muscle groups), the volume of injection, the osmolality of the solution, and other pharmaceutical factors. Substances with molecular weights >20,000 daltons are principally taken up into the lymphatics.

In anycase, I do not believe that there is a soul on this board (including yourself) who would suggest that IM anything acts as fast as IV. So, a peds pt who is all the sudden in extremis due to a HR of 30 may have a negative outcome if the IM route was chosen over the IV route. Those 3 minutes may be the difference between a coding kid or not and i doubt that M&M's ascertions will be much of a defense in court in the face of the AHA and >20 years of evidence indicating the correct choice would be to insert an IV or IO. If this was not the case then IV/IO medications for paediatric's would not be preferred as standard of care for bradycardia. The overwhelming evidence has resulted in the choice to bore a needle in a childs tibia (IO) over an IM injection (> 400 research articles on the superiority of IOs alone).

I know you dont actually believe that IM atropine is the appropriate treatment of the bradycardic paediatric child in extremis. Obviously, your not an idiot. I think we may be arguing two different points. Im suggesting it is inappropriate to give IM atropine to a child in extremis, your evidence (and post) only discusses giving atropine/Sux combination to combat larygospasm. There are no existing guidlines for giving IM atropine for symptomatic bradycardia.

seems we were just on two different pages of the same book.

Masui. 1994 Dec;43(12):1861-5. Related Articles, Links

[Effects of intravenous and intramuscular atropine on bradycardia during spinal anesthesia]

[Article in Japanese]

Hirabayashi Y, Saitoh K, Fukuda H, Saitoh J, Mitsuhata H, Shimizu R.

Department of Anesthesiology, Jichi Medical School, Tochigi.

The effects of intravenous and intramuscular atropine on pulse rate have been studied in 40 patients undergoing gynecological surgery. Intramuscular atropine 0.5 mg was administered 30 min before induction of spinal anesthesia in 20 patients (i.m. group). Intravenous atropine 0.5 mg was administered immediately after induction of spinal anesthesia in 20 patients (i.v. group). Decrease in heart rate after spinal block was significantly less in i.v. group than in i.m. group. Although no one in i.v. group was given an additional atropine, 10% of the patients in i.m. group was given an additional atropine for bradycardia. Authors conclude that intravenous atropine has more significant effect on prevention of bradycardia during spinal anesthesia compared with intramuscular atropine.

No where do I see an onset of 15 minutes! Interestingly the onset following deltoid injection falls right within the the onset of 3-5 minutes for Sux. Those darn pharmokinetics. So much for useless...
Anesth Analg. 1997 Jan;84(1):54-8.
Sullivan KJ, Berman LS, Koska J, Goodwin SR, Setzer N, White SE, Graves SA, Nall AV.
Department of Anesthesiology, University of Florida College of Medicine, Gainesville 32610-0254, USA.
In children undergoing inhaled induction of anesthesia with halothane who suffer bradycardia, submental glossal injection of atropine may result in more rapid onset of vagolysis than traditional intramuscular sites. We compared the intervals between injection and onset of heart rate acceleration (tHR increases) after intramuscular injection of atropine into the deltoid, vastus lateralis, and glossa in children between 1 mo and 10 yr of age scheduled for elective surgery. The tHR increases was determined by measuring the interval between atropine injection and the time point at which the slope of the heart rate curve initially became positive. To ensure that the drug had taken effect before surgical stimulation, heart rate observation was continued until it increased at least 5% above baseline with evidence of continuing acceleration. Anesthesia was induced in all subjects by mask with nitrous oxide and halothane. After tracheal intubation, constant inspired concentrations of the anesthetics were administered for 3 min. While heart rate was monitored, atropine (0.02 mg/kg) was injected into one of the three sites. Each patient's end-tidal anesthetic concentrations were recorded, and minimum alveolar anesthetic concentrations (MAC) were subsequently calculated and adjusted for age. The tHR increases was recorded and averaged for each group. The study groups did not differ by age, weight, end-tidal anesthetic concentrations, age-adjusted MAC, or heart rate at the time atropine was administered. After submental glossal injection (n = 11), tHR increases increase was fastest (3.0 +/- 1.1 min) and was significantly faster than that found with deltoid injection (n = 16; 4.4 +/- 1.1 min) or vastus lateralis injection (n = 8; 6.4 +/- 2.4 min) (P
PMID: 8988999 [PubMed - indexed for MEDLINE]

sandman1 · May 23, 2006

Thank you everyone for your well thought out and researched responses. Just to clarify,(as the title of this thread is "IM ATropine dose for peds emergency") I, nor anyone else on this board thinks that IM ATropine is a PRIMARY route for emergency for anyone. As I indicated, earlier in the thread, I am only asking in the case of the emergency of laryngospasm, or an emergency with No IV. I know IO proves better, etc but you better believe that if I have an IM dose of Atropine ready with no IV and I need it that I will give it a split second BEFORE I try to start an IV or IO, regardless of the unpredictible onset, etc. With that being said, I was wondering what an appropriate IM dose of ATropine might be if I had to give it. Thank you for the Nagelhout reference of .03mg/kg. I'll look for that one. Anyone see anything else besides .02 and .03? Many people in the clinical area still tell me .04 and even .05!

Home Health Columnist / Guide · May 24, 2006

Since focus strayed from content to individual poster, sandbox closed.