Skin rash after general anesthesia

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Patient in 50 s male for out pat arthroscopy develops rash a few minutes after Lma General anesthesia with Versed and fentanyl premed, propofol, lidocaine, glycopyrollate and cefazolin. Patient has had surgery before and received all of the above meds except lido and glycopyrollate. Cefazolin stopped immediately and epinephrine was administered with diphenhydramine, dexamethasone , famotidine.

ventilation was assisted until patient reverted to spontaneous ventilation. The surgeon cancelled the case and sent the patient for allergy testing. Further questioning reveals that patients sister has similar rash with anesthesia? Allergy specialists does not do any skin testing and sends Pt back with advise to premeditate the patient

First question is this anaphylaxis or some other rash? If it is anaphylaxis which drug to avoid the next time. What is prophylaxis, Benadryl, .
prednisone? How much. Suggestions

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Was it a “rash”, or was it urticaria? Where was the cutaneous distribution?

If it was just an isolated rash, probably not anaphylaxis (usually >1 organ system involved, plus hemodynamic manifestations). Was there hypotension? Angioedema? Bronchospasm? Periorbital edema? While mild anaphylaxis is a thing, it’s unlikely to present as just an isolated rash. If none of the above happened, this was more likely some other sort of drug reaction. Personally I would have kept going with the case if that’s all it was (and probably skipped the epi until bronchospasm or hypotension reared their ugly heads). Premedication usually consists of Benadryl, methylpred, ranitidine.
 
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PS dexamethasone should not be your steroid of choice here. It is a pure glucocorticoid, and you’re going to need something with mineralocorticoid activity.
 
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Propofol can cause a cutaneous rash most commonly across the chest. It is not allergic in nature.
 
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PS dexamethasone should not be your steroid of choice here. It is a pure glucocorticoid, and you’re going to need something with mineralocorticoid activity.

You sure about that?
 
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PS dexamethasone should not be your steroid of choice here. It is a pure glucocorticoid, and you’re going to need something with mineralocorticoid activity.

I was taught hydrocortisone 1st due to more rapid onset of action then dexamethasone. Glucocorticoid effects are what you want for an IgE mediated reaction. Choice is probably irrelevant.
 
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That is what I remember being taught in residency, but it seems you are right. Or, more accurately, neither of us is right since there’s not evidence to support the use of any sort of steroids in anaphylaxis:

So you talk out of your ass and then accuse @SaltyDog of being wrong? Wtf?
 
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PS dexamethasone should not be your steroid of choice here. It is a pure glucocorticoid, and you’re going to need something with mineralocorticoid activity.

You sure about that?

I was taught hydrocortisone 1st due to more rapid onset of action then dexamethasone. Glucocorticoid effects are what you want for an IgE mediated reaction. Choice is probably irrelevant.

If you're trying to pre treat anaphylaxis reaction, glucocorticoids activity is all you need.

If you are trying to treat adrenal insufficiency, you need to consider mineralocorticoid.

I refused to believe one steroid works faster than the other when they all have to diffuse through lipid layers to stop DNA transcription as the mechanism of action.

If this is a true anaphylaxis reaction, the steroid is very much an afterthought. If the patient is unstable, use 100% of your energy to make the patient stable. If the patient is stable, oh well whatever you do probably won't matter much. The fastest way to stabilize mast cells is epi.

The most important lesson here is that @SaltyDog is right, always.
 
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Sorry, more to the case, there was a difficulty ventilating After I inserted the lma, and patient and it appeared as though it was laryngospasm and I gave muscle relaxant. To break the spasm. then I noticed the vesicular Red raised rash and sbp was 80-90 and heart rate was 110. Immediately gave the epi to prevent full borne anaphylaxis.
 
Patient in 50 s male for out pat arthroscopy develops rash a few minutes after Lma General anesthesia with Versed and fentanyl premed, propofol, lidocaine, glycopyrollate and cefazolin. Patient has had surgery before and received all of the above meds except lido and glycopyrollate. Cefazolin stopped immediately and epinephrine was administered with diphenhydramine, dexamethasone , famotidine.

ventilation was assisted until patient reverted to spontaneous ventilation. The surgeon cancelled the case and sent the patient for allergy testing. Further questioning reveals that patients sister has similar rash with anesthesia? Allergy specialists does not do any skin testing and sends Pt back with advise to premeditate the patient

First question is this anaphylaxis or some other rash? If it is anaphylaxis which drug to avoid the next time. What is prophylaxis, Benadryl, .
prednisone? How much. Suggestions

I have so many questions and comments.
0) dude assuming you gave succinylcholine to break the "laryngospasm" that's literally all this is. Sux causes histamine release and sux rash is fairly common.
But also,
A) rash - where, and was it resolving?
B) intraop anaphylaxis is like BAM your systolic is 60 the HR is 140 and there is a full body rash and the pt needs epi for hours
C) the surgeon didn't cancel the case, you did - or didn't you? If the surgeon insisted on doing the case when you thought it was anaphylaxis you woulda been like "cool"?
D) I don't wanna hear about sisters unless they have freakin MH or PD. "WeLl mY mOm GoT a RasH wItH PenICiLin"
E) always send a tryptase
F) make it crystal clear if you are referring to allergy what the potential exposures were
G) ps it's "glycopyrrolate"
 
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I was taught hydrocortisone 1st due to more rapid onset of action then dexamethasone. Glucocorticoid effects are what you want for an IgE mediated reaction. Choice is probably irrelevant.
I thought solumedrol is preferred over hydrocortisone or at least thats what I was taught.
 
Is it? I really don’t know. I share some of the sentiment above. Usually give steroids as an afterthought, after everything else. A lot of my patients get 4 of dex anyway up front as an antiemetic.
Probably doesn’t matter anyways if steroids have questionable benefit.
 
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Steroids do not help with the acute anaphylactic reaction. They do help with the late recrudescence which can occur hours after the initial acute reaction and is the result of inflammatory mediator/cytokine/evil humor release
 
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Steroids do not help with the acute anaphylactic reaction. They do help with the late recrudescence which can occur hours after the initial acute reaction and is the result of inflammatory mediator/cytokine/evil humor release

Thats what I was taught many years ago. Up to Date however questions their benefit...

 
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Thats what I was taught many years ago. Up to Date however questions their benefit...


Great discussion and all, but ultimately a dumb one
A) most/ many patients already get dexamethasone for PONV ppx
B) when the systolic is 50-60 and the HR is 140 just give ****in everything and worry about intellectual wankery later
 
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Great discussion and all, but ultimately a dumb one
A) most/ many patients already get dexamethasone for PONV ppx
B) when the systolic is 50-60 and the HR is 140 just give ****in everything and worry about intellectual wankery later
A) no
B) yes
 
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PS dexamethasone should not be your steroid of choice here. It is a pure glucocorticoid, and you’re going to need something with mineralocorticoid activity.
Why do you need "mineraolcorticoid activity"? What you need is a potent glycocorticoid and Dexamethasone is an excellent choice.
 
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I am not sure giving Epinphrine for just a rash is a great idea! The difficulty ventilating that you assumed to be "laryngospasm" was probably the usual LMA not seated well combined with inadequate anesthesia, and the BP 80-90 is common after induction. A rash after induction of anesthesia is a fairly common thing and most of the time all you need is an antihistamine, maybe anti H1 and anti H2. Usually you never really find out what caused the reaction.
 
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Sorry, more to the case, there was a difficulty ventilating After I inserted the lma, and patient and it appeared as though it was laryngospasm and I gave muscle relaxant. To break the spasm. then I noticed the vesicular Red raised rash and sbp was 80-90 and heart rate was 110. Immediately gave the epi to prevent full borne anaphylaxis.
Hard to tell from the description of the rash. Vesicles are not a rash that just appears like that, hard to tell based on your description what the rash was, could be hives or a drug eruption like others have mentioned. Sux seems like the most likely.

as mentioned Above, anaphylaxis is cutaneous symptoms plus either hypotension, mucous membrain involvement, GI involvement, etc. Hard to tell if the hypotension was just induction. I don’t think anyone would fault giving epi and cancelling the case.

But you are unfortunately know in the situation where you have to do the case again since the allergist sent the patient right back. I would do a GA with minimal medications, induce with a stick of propofol, no muscle relaxant, wait until after induction to give any antibiotics and opioid.
 
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Randomly saw this. Dermatologist here (sorry to crash).
Not totally sure what this might be either - would definitely defer to you guys since you would be seeing this/in this particular clinical situation a lot more than me.

My thoughts:
- vesicular rashes aren't really common with anaphylaxis/angioedema, usually urticarial
- Agree with tryptase, r/o mastocytosis. Unlikely given described morphology of rash, but definitely need to consider given clinical situation
- Drug rash that quickly after administration would be unusual, usually a few days after since it's a type IV hypersensitivity reaction, even if there was prior exposure/sensitization, unless it was actually type I/IgE mediated
- Favor rash unrelated to other symptoms. Given described morphology as vesicular and presumed acute onset, would favor miliaria/heat rash. Propofol causes vasodilation right? Maybe combination of cutaneous vascular dilation and moisture - again, wouldn't account for the respiratory symptoms.
 
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