Anaphylaxis!

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J. Burdett

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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.
 
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Oh yeah, pt also received pepcid. Anybody know how that works? I had never heard of that...
 
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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)
 
Brown is interested you used glucagon with adrenaline.
 
MrBrown said:
Brown is interested you used glucagon with adrenaline.
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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...
 
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.
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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? :D
 
: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.
 
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.
 
Sounds like a very cool call (from provider point of view ha) and one that went really well! Great job.
 
Oh yeah, pt also received pepcid. Anybody know how that works?
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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.
 
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.
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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?
 
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.
 
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!
 
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.
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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.
 
sdadam said:
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.
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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.
 
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
 
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!
 
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