# Anaphylaxis!



## J. Burdett (Apr 8, 2011)

Well, I had a great call last shift that IMO went very well despite some obstacles. Here is the break down-

-We receive a call for a 58 yo female pt c/c allergic reaction to peanuts. Upon arrival a FF greets us and states "Her lips and face are a little swollen but she seems ok. You want us to walk her out?". Negative. Upon entering the room I notice a elderly female pt seated in a chair tripoding. Upon physical assessment significant angioedema was noted to her face, tongue, and neck w/ urticaria popping up all over, it seemed, right before my eyes lol. Pt stated that she accidentally ingested a product that contained peanuts approx 10min PTA and stated that she felt dysphagia and SoB. FF gives baseline vitals they obtained while I hook the pt up to our monitor. My partner readies the SQ epi and I place the pt on 15lpm NR and listen to lung sounds. She sounded tight in all fields w/ expiratory wheezes bi-laterally, RR was around 24-28 slightly labored. A FF and I attempt IV access w/ the FF succeeding w/ a 20g L hand on what was a difficult stick (clutch!). Hx, meds, and allergies obtained w/ pt was currently taking carvedilol. 50mg Benadryl and 125mg Solu-Medrol given IV while my partner contacts med control from .3 SQ epi due to pt's cardiac hx (previous MI, angina, CHF, PCI, and sinus tach at 110 on monitor). 

 Epi approved and was given and pt was transferred to stretcher while I administered 1.25 neb Xopenex. Total on scene time 11 min, whew! I have done extensive research on Glucagon and understand it's effects on intracellular cAMP. I could tell the epi was incomplete due to the carvedilol and no improvement was noted to lung sounds or BP, which was 82/54. I then call for orders for .5 Glucagon (pt hx DM w/ a glucose of 186) and explain my reasoning. Orders approved w/ instructions to give a additional .3 SQ epi after Glucagon administration! While I prepare the glucagon I ask the FF to obtained another line for a potential fluid res or epi drip. He comes through (clutch!). 0.5 Glucagon given w/ improvement noted to RR, lung sounds, and BP. Upon arrival pt was given a additional .5 Glucagon by ED doc and pt recieved 2L fluid resuscitation plus a epi drip. 

I got to see her later that night and she seemed in great shape but was being transferred to the unit for observation. A full recovery is expected!

Pretty good call and I was very happy we didn't have to intubate.


----------



## J. Burdett (Apr 8, 2011)

Oh yeah, pt also received pepcid. Anybody know how that works? I had never heard of that...


----------



## medicstudent101 (Apr 8, 2011)

First and foremost, CONGRATS!!
Sounds like a balls to the wall sort of run that could've gone down hill very quickly. The crew and yourself need to give each other a pat on the back!

As far as the pepcid, it's a histamine-2 blocker. So more of a supplemntal type thing. Sounds like you guys did everything else for her, so the ED had to throw a little something on board too B)


----------



## MrBrown (Apr 8, 2011)

Brown is interested you used glucagon with adrenaline.


----------



## J. Burdett (Apr 8, 2011)

MrBrown said:


> Brown is interested you used glucagon with adrenaline.



Pretty neat huh? I'll try and keep it short and sweet. cAMP is a messenger inside the cell. When epi gets to the cell cAMP relays it's message to complete it's effects. Carvedilol is a noncardioselective type of beta-blocker which was blocking the epi message. Glucagon significantly raises the amount of cAMP by way of beta 2 agonist. This basically overrides alpha and beta receptors so that epi does not require those receptors to send it's message. 

This was my only true anaphylaxis pt ever. I have had many allergic reaction and adverse reaction pt's but never a true anaphylaxis, and she had to be taking a beta blocker. What luck...


----------



## MrBrown (Apr 8, 2011)

J. Burdett said:


> Pretty neat huh? I'll try and keep it short and sweet. cAMP is a messenger inside the cell. When epi gets to the cell cAMP relays it's message to complete it's effects. Carvedilol is a noncardioselective type of beta-blocker which was blocking the epi message. Glucagon significantly raises the amount of cAMP by way of beta 2 agonist. This basically overrides alpha and beta receptors so that epi does not require those receptors to send it's message.



Thank you for the explanation, Brown was more interested in the fact you knew that and the medical control physician seemed to trust you enough to agree on your proposed course of treatment.

Brown will keep an eye on this one, perhaps you are not a barely homeostasasing loser cookbook medic?


----------



## J. Burdett (Apr 8, 2011)

:lol:

Thanks Mr. Brown. According to people close to me I seem to have a very unhealthy obsession w/ A&P, patho, and pharmacology. I have built a pretty good working relationship w/ some of the docs here which is a good thing I would think lol.


----------



## katgrl2003 (Apr 8, 2011)

MrBrown said:


> Brown will keep an eye on this one, perhaps you are not a barely homeostasasing loser cookbook medic?



Gasp! What a compliment!


----------



## MrBrown (Apr 9, 2011)

J. Burdett said:


> :lol:
> 
> Thanks Mr. Brown



"Mr" Brown sounds sooo formal, Your Excellency will suffice 



katgrl2003 said:


> Gasp! What a compliment!



Oh hush Kate


----------



## Veneficus (Apr 9, 2011)

Extraordinary work!!!

Especially the background study in both cellular physiology, pharmacology and how it can be applied clinically.

We can only hope that providers en mass take note of your abilities and success and seek to emulate them.

Your efforts inspire hope that EMS providers are truly cpable of being recognized as knowledgable and capable professionals. If I had the ability to give you an award, you would get it.


----------



## 18G (Apr 9, 2011)

Sounds like a very cool call (from provider point of view ha) and one that went really well! Great job.


----------



## skivail (Apr 9, 2011)

I am more than impressed.


----------



## usafmedic45 (Apr 9, 2011)

> Oh yeah, pt also received pepcid. Anybody know how that works?



Like someone said before, it's a histamine-2 blocking agent.  It actually also is a good adjunctive medication (as is Tagamet) for mild allergic reactions involving pruritus (itching) and hives.  It lasts longer than diphenhydramine and helps to minimize the change of a recurrence.  This is at least my experience as apatient with a long history of dermatographism.


----------



## medicstudent101 (Apr 9, 2011)

usafmedic45 said:


> Like someone said before, it's a histamine-2 blocking agent.  It actually also is a good adjunctive medication (as is Tagamet) for mild allergic reactions involving pruritus (itching) and hives.  It lasts longer than diphenhydramine and helps to minimize the change of a recurrence.  This is at least my experience as apatient with a long history of dermatographism.



I actually had to google dermatographism. Seems like a very interesting condition. I'm curious if you don't mind me asking, is it painful? Does the use of anti-histamine agents help either control or completely make the dermatographism subside for a period of time?


----------



## usafmedic45 (Apr 9, 2011)

It's not painful, however the itching associated with it can be quite severe when it flares up.  If I just scratch myself, I get painless little linear urticaria at the site that itch a little.   The non-sedating antihistamines tend to work well as a preventative measure, especially Zyrtec.  

When there's a severe flare (which luckily I have not had in a couple of years) there are large plaque-like urticaria (sometimes the size of dinner plates) that form, although this is almost always limited to my thighs. Normally when this happens, it takes a hefty dose of diphenhydramine (or Phenergan or Atarax), Zantac (or Pepcid) and maybe some steroids to get it under control.  The other common issue I get is that my fingers will swell up a little and itch.  Normally, that can be broken simply by putting them under cold running water.


----------



## firetender (Apr 10, 2011)

*Self-treatment of anyphlaxis: Run, Forest, Run!!*

I was on a solo motorcycle tour in Florida. I hit some gravel about midday and me and the bike went down, mashing both my glasses and its headlight out of shape, roadrashing my leg and tweaking the handlebars.

Sun comes down and I'm in the Ocala Nat'l forest, off-season, no one camping. Nearest ambulance, Vollies, 20 miles away. I set my tent up and nurse my wounds. Going to sleep I'm awakened by an itch. It persists. I scratch here and then I'm over there. Something's happening!

I get out my flashlight to look and see a small field of urticaria on my belly SPREADING upward to my chest into a Marching Carpet! And then, the tightness in my chest started. I jumped up and ran to the phone about 50 yards up the campsite. By the time I put my money in, dialed the number of the Gainesville hospital ER, about 30 miles away, my tongue was so swollen in my mouth I could not be understood!

Now, fairly bloated about the belly and chest getting tighter, I ran to my steed, cranked her up and hauled *** to the hospital. Problem was, I couldn't even do that very well because the headlight of the bike was pointed up to the trees to the right and my SUNGLASSES were tweaked down to the left (or something)!

First on back roads and then on the highway, I jammed to the hospital in fits and starts according to what I could see and not see. My heart was POUNDING in my chest and breathing was constricted and then I started to panic!

But at the very peak of my panic, everything leveled off and then started to recede!

By the time I got to the Gainesville Hospital, I was cured. I didn't even go in to get checked, just got a Motel Room for the night. I knew what had happened; I auto-transfused and shot myself up so full of adrenaline, I saved my own butt.

I'm curious; how could we write that up as a protocol? I mean, it REALLY works!


----------



## sdadam (Apr 14, 2011)

*Glucagon is not work "by way of beta 2 agonis(m)"*



J. Burdett said:


> Pretty neat huh? I'll try and keep it short and sweet. cAMP is a messenger inside the cell. When epi gets to the cell cAMP relays it's message to complete it's effects. Carvedilol is a noncardioselective type of beta-blocker which was blocking the epi message. Glucagon significantly raises the amount of cAMP by way of beta 2 agonist. This basically overrides alpha and beta receptors so that epi does not require those receptors to send it's message.



Almost but not quite.

Glucagon does increase the second messenger cAMP through stimulatory g-protein action on adenylate cyclase. 

However it is not by way of beta 2 agonism as stated. 

It is through activation of specific glucagon receptors which, although have similar intracellular effects to adrenergic receptors, cause different systemic responses mainly based on there varied expression.

This means that even in a hypothetical complete, irreversible and non-selective beta blockade glucagon is capable of causing an adrenergic type response. Describing it's effects as being "by way of beta 2 agonis(m)" is incorrect and could confuse people.


----------



## 8jimi8 (Apr 14, 2011)

sdadam said:


> Almost but not quite.
> 
> Glucagon does increase the second messenger cAMP through stimulatory g-protein action on adenylate cyclase.
> 
> ...



important clarification.   That is how I took it after quickly reading.

Does anyone have any references, or links?  I'd really like to take a slow look at this, so that i can tie up some loose ends in the physiology department.


----------



## systemet (Apr 15, 2011)

Take a look at any introductory university cell biology text, and look for "second messenger systems" or "G protein coupled receptor signalling".  An ok book is "Molecular Biology of the Cell" by Lodish.  If you pm me with an email address, I might be able to point you in the right direction.

This webpage talks a little bit about G protein coupled signalling, and mentions that glucagon and epinephrine are both Gs coupled.

http://watcut.uwaterloo.ca/webnotes/Metabolism/page-13.2.html

This might help (not sure if you can access it)

http://www.ncbi.nlm.nih.gov/books/NBK26912/#A2794

There seem to be some lectures on G proteins here as well:

http://www.folksemantic.com/visits/52770

I'd try mon 4/9 G protein coupled receptors

Mon 4/9 	G Protein Coupled Receptors


----------



## CTBryan11 (May 6, 2011)

This is extremely interesting!!!! I'm going to do some more research on all of this, and bring it up to my instructors in class to see if they have ever used an application like this in the field... Great job and way to study more in depth than just what they teach you in class!


----------



## phideux (May 7, 2011)

So in a nutshell, someone on a beta blocker having an anaphalactic reaction, and the Epi just ain't hitting it, Glucagon will help the Epi to do its job?


----------



## mycrofft (May 7, 2011)

*Cool!*

As an atrial fib person, I'd appreciate anything other than epi! Even the epi in dental local anesthesia gives me even more tachy and palpitations, I can imagine an "Epipen" on board:wacko:.


----------



## vamike (Jun 3, 2011)

I love this site!  I am constantly looking up def's of words.  I had to look up urticaria.  I feel so dumb:unsure:


----------



## rhan101277 (Jun 3, 2011)

phideux said:


> So in a nutshell, someone on a beta blocker having an anaphalactic reaction, and the Epi just ain't hitting it, Glucagon will help the Epi to do its job?



Glucagon doesn't help epi do its job, it just works in a different way.  It is able to accomplish these effects without using the beta-adrenergic receptor site.


----------



## rhan101277 (Jun 3, 2011)

I had one of these which I posted about, mine was not as bad as yours.  I did not think they required epi, but they got benadryl and solumedrol.  Dr. gave .3mg Epi IM when we got there.  9y/o male.


----------



## jroyster06 (Jun 4, 2011)

sdadam said:


> Almost but not quite.
> 
> Glucagon does increase the second messenger cAMP through stimulatory g-protein action on adenylate cyclase.
> 
> ...




HE BEAT ME TO IT!!:sad::unsure:

Thats ok, he said it better than i could have lol.


----------



## jroyster06 (Jun 4, 2011)

This website should help some people. I found it useful! I never thought about it in an asthmatic. Ive had 2 pts I've had to drop and tube and despite me throwing the book at both of them, ventilations with bvm & ett were tough. Neither one ever opened up during transport. I wonder if Glucagon would have made a difference. After reading this, I really wish my service carried more than the 1mg we do.


----------



## NREMTB12 (Sep 19, 2011)

cAMP is this adenosine monophosphate??


----------



## Sasha (Sep 19, 2011)

Holy necromancy batman.

Sent from LuLu using Tapatalk


----------



## systemet (Sep 21, 2011)

NREMTB12 said:


> cAMP is this adenosine monophosphate??









Technically it's cyclic adenosine monophoshphate, with a diester linkage (middle image).  Read more here:

http://en.wikipedia.org/wiki/Cyclic_adenosine_monophosphate


----------



## NREMTB12 (Sep 23, 2011)

systemet said:


> Technically it's cyclic adenosine monophoshphate, with a diester linkage (middle image).  Read more here:
> 
> http://en.wikipedia.org/wiki/Cyclic_adenosine_monophosphate


Thank you system, very interesting i thought i was on the right track, and you clearified it for me with the link.


----------



## octoparrot (Sep 29, 2011)

Only non-cardioselective beta-blockers?


----------



## KellyBracket (Oct 1, 2011)

Are most people's protocols still describing SQ epinephrine? 

The standard of care, reflected in national guidelines, call for 0.01 mg/kg (max 0.5mg) intramuscular. The research showing that the IM route is preferable is pretty compelling. Google around for the "Second symposium on the definition and management of anaphylaxis:"

Around my neck of the woods, the ALS protocols dictate the IM route - got changed a number of years ago.


----------



## rhan101277 (Oct 2, 2011)

KellyBracket said:


> Are most people's protocols still describing SQ epinephrine?
> 
> The standard of care, reflected in national guidelines, call for 0.01 mg/kg (max 0.5mg) intramuscular. The research showing that the IM route is preferable is pretty compelling. Google around for the "Second symposium on the definition and management of anaphylaxis:"
> 
> Around my neck of the woods, the ALS protocols dictate the IM route - got changed a number of years ago.



Ours changed to IM a couple of days ago.


----------



## 18G (Oct 2, 2011)

Ours has been IM for years now.


----------



## J. Burdett (Nov 20, 2011)

KellyBracket said:


> Are most people's protocols still describing SQ epinephrine?
> 
> The standard of care, reflected in national guidelines, call for 0.01 mg/kg (max 0.5mg) intramuscular. The research showing that the IM route is preferable is pretty compelling. Google around for the "Second symposium on the definition and management of anaphylaxis:"
> 
> Around my neck of the woods, the ALS protocols dictate the IM route - got changed a number of years ago.



Still SQ :wacko:


----------



## usafmedic45 (Nov 20, 2011)

18G said:


> Ours has been IM for years now.



Likewise, I can't say I have ever seen it given subcutaneously.  It sometimes get charted that way because medical professionals are often rather dense...


----------



## Akulahawk (Nov 20, 2011)

In my county we can only give epinephrine subcutaneously or IV.  Deep IM is not authorized yet.  I do not know if it is going to be authorized at all.


----------



## mycrofft (Nov 20, 2011)

*We gave it SQ.*

I can see where IM has some benefits, just don't get the bolus too near a nerve. I've seen sloughs where it was intra and not sub dermal, or into fat.

Is Susphrine still used?


----------



## KellyBracket (Nov 20, 2011)

I uploaded the document I mentioned above to Scribd. Print out this article "Second Symposium on the definition and management of anaphylaxis" and hand it to medical control. There are still some people who didn't catch the memo about the change in route.


----------



## Trevor (Nov 23, 2011)

akulahawk- You can give Epi IV (I assume for Allergic reactions, since thats what the convo is about) But you cant give it IM?!?!?!?!?!? That doesnt make a whole lotta since to me...

I know some places give it IV for Allergic Reactions, but they (your system) thinks that is safer then IM?!?!?!?!?!


----------



## Handsome Robb (Nov 23, 2011)

Trevor said:


> akulahawk- You can give Epi IV (I assume for Allergic reactions, since thats what the convo is about) But you cant give it IM?!?!?!?!?!? That doesnt make a whole lotta since to me...
> 
> I know some places give it IV for Allergic Reactions, but they (your system) thinks that is safer then IM?!?!?!?!?!



We give IM first IV second. I don't see how IV would be more 'dangerous' provided your giving at the correct concentration. If you're at the point of giving it IV the patient is in a bad state.


----------



## systemet (Nov 24, 2011)

NVRob said:


> We give IM first IV second. I don't see how IV would be more 'dangerous' provided your giving at the correct concentration. If you're at the point of giving it IV the patient is in a bad state.



There's a difference in absorption and peak plasma levels.  If we give 300 ug (0.3mg) IM, it has to diffuse through the connective tissue, into a capillary, into the venous circulation, etc.  and it takes a while for it to get into the circulation.  Case in point, slower onset and longer duration of pain relief with IM morphine.

If I give an IV dose of epinephrine, e.g. 100ug (0.1mg) of 1:10,000 IV, I get instant absorption, by definition, and I'm giving a huge pressor dose of epinephrine in one go (consider a normal epinephrine drip is 0.5 - 10 ug/min  -- This is the dopamine equivalent of giving 200ug / kg in one minute, if you want to think about it another way).

So the coronaries, the heart, and the cerebral circulation are going to get exposed to much higher concentrations of epinephrine than they'll see if you give even a much larger amount IM.

This means you now have a hugely elevated risk for coronary vasospasm, cardiac arrhythmia, and a very sudden hypertension.  The bonus is that the plasma concentrations will fall very rapidly, so this will probably be short-lived.  But there's definitely associated risks.

* Anecdote.  I had a near-death anaphylaxis patient, profoundly desaturated, SpO2 reading 68% (for whatever that's worth - we all know the accuracy is questionable at that level), with no palpable radials, ST @ 180 with multifocal PVCs, and intermittent hypoxic seizures.  Horrible compliance.  Two doses of 0.1 mg epinephrine 1:10,000 IVP later, and I've still got  a train wreck, but I now have improved compliance, an SpO2 of 82%, radial pulses and a pressure of 190 / 120.  [End result an ETT, another 0.8 mg of epinephrine IM, some benadryl, sedation, analgesia, MDI ventolin, etc.]. 

IV administration is there for the near death patient where there's minimal perfusion to the muscular tissues, and we can't wait for the effects of IM epinephrine to take place.  I've heard of people giving very high doses of epinephrine IV, e.g. 0.3-0.5 mg doses to people in moderate distress, because "I have the IV, so why not?".  This isn't smart, it's exposing the patient to a very unnecessary risk.


----------



## InkaHootz (Nov 25, 2011)

Glucagon 0.5mg IVP, IM?

Is this standard protocol anywhere that anyone knows of?

Nice call.


----------



## Akulahawk (Nov 25, 2011)

Trevor said:


> akulahawk- You can give Epi IV (I assume for Allergic reactions, since thats what the convo is about) But you cant give it IM?!?!?!?!?!? That doesnt make a whole lotta since to me...
> 
> I know some places give it IV for Allergic Reactions, but they (your system) thinks that is safer then IM?!?!?!?!?!


Late response, I know... but yes, IV epi is base order only. That's 0.1mg epi slow IVP, only for stridor and hypotension. They want us to manage those patients with Subcut. Epi, Benadryl IM, 2.5mg albuterol and saline... unless you're doing an IFT and your patient presents with anaphylaxis with stridor and hypotension. You can then simply do the 0.3mg subcut, 50mg Benadryl IM, start a line, and begin 0.1mg epi slow IVP as soon as you think it's clinically indicated. IFT is treated differently in the protocols.


----------



## jjesusfreak01 (Nov 26, 2011)

I'm with systemet on this one. IM use of Epi is a compromise between SQ and IV. You get faster action than SQ, but a drawn out administration that reduces cardiac risk. We are permitted to give IV only for FTD patients.


----------



## Medic Tim (Nov 30, 2011)

InkaHootz said:


> Glucagon 0.5mg IVP, IM?
> 
> Is this standard protocol anywhere that anyone knows of?
> 
> Nice call.



it is in our protocols.  1mg glucagon IVP q5 if they are on b-blockers.


----------



## jjesusfreak01 (Dec 9, 2011)

Medic Tim said:


> it is in our protocols.  1mg glucagon IVP q5 if they are on b-blockers.



I believe i've been told it will take a bit more Glucagon than that to reverse a beta blocker overdose. Its more like 3+ milligrams as a first  dose and then keep pushing til you get a good response. I'm finishing up my intermediate, and Glucagon is in my scope, so the question gets brought up a lot in class.


----------



## systemet (Dec 10, 2011)

jjesusfreak01 said:


> I believe i've been told it will take a bit more Glucagon than that to reverse a beta blocker overdose. Its more like 3+ milligrams as a first  dose and then keep pushing til you get a good response. I'm finishing up my intermediate, and Glucagon is in my scope, so the question gets brought up a lot in class.



I think you're probably right, and the dosing is going to be limited in most ambulances by the amount of glucagon on the ambulance, which is probably going to be < 5 mg total.  But you're going to need less to reverse the effects of the patient's prescription beta-blocker compared to an overdose with a much larger quantity of beta blocker on board.  There's also the question of whether a small improvement with glucagon might allow you to avoid using a more dangerous drug / therapy.


----------



## J. Burdett (Dec 12, 2011)

Thank you for this! We are currently gathering info for some protocol changes and I believe this will help!



KellyBracket said:


> I uploaded the document I mentioned above to Scribd. Print out this article "Second Symposium on the definition and management of anaphylaxis" and hand it to medical control. There are still some people who didn't catch the memo about the change in route.


----------



## 18G (Dec 12, 2011)

We only carry 1mg of glucagon.


----------



## MedicPatriot (Dec 18, 2011)

I never would have though about the Glucagon. 

I know it can be used in beta-blocker OD's but I have just one question of clarification. 

So in a patient taking betablockers in which epi isn't working you should consider Glucagon? Or is there more to it?


----------



## usalsfyre (Dec 18, 2011)

MedicPatriot said:


> So in a patient taking betablockers in which epi isn't working you should consider Glucagon? Or is there more to it?



Yes and yes.


----------



## Handsome Robb (Dec 18, 2011)

MedicPatriot said:


> I never would have though about the Glucagon.
> 
> I know it can be used in beta-blocker OD's but I have just one question of clarification.
> 
> So in a patient taking betablockers in which epi isn't working you should consider Glucagon? Or is there more to it?



The way it was explained to me and it may have even been in this thread, I don't remember, is that glucagon opens a "back door" so to speak. It bypasses the second messenger system of the cells which bypasses the beta blockade and allows for the desired effects of the beta stimulating meds.

Someone please correct me if I'm wrong.


----------



## systemet (Dec 18, 2011)

NVRob said:


> The way it was explained to me and it may have even been in this thread, I don't remember, is that glucagon opens a "back door" so to speak. It bypasses the second messenger system of the cells which bypasses the beta blockade and allows for the desired effects of the beta stimulating meds.
> 
> Someone please correct me if I'm wrong.



This is the essence of it.  Strictly, it would be more correct to say that glucagon activates a separate non-beta receptor (the glucagon receptor), that's coupled to the same second messenger system, and results in similar downstream responses.


----------

