Nobody is interested in digging deeper, for obvious reasons. It’s name is on her chart and in my phone.
Garbled info would be better than none. She’s excessively fond of her pivacy.
Something else is going on–that broken foot. The bits and pieces are all pointed in the right direction, so they probably won’t cut, but she cannot put any weight on it, ruling out a walking cast. Then there’s her high blood sugar
No sulfites in Tylenol 3. If you are allergic to them when taken with food, mainlining them is contraindicated. Kill you dead.
She was succeeding. She could barely gasp, “Help me! I’m dying!”
Not intelligent. Observant. Once she was properly medicated she recovered in minutes. And the nurse giving her CPR was majorly hot, though her facial expression was more vacuous than vivacious. I’m going to Hell.
She, ex-Medical, claims that childrens chewable Benadryl absorbs faster than liquid, even, and is much more portable. She treated my bee sting with it and a bottle of ammonia passed under my nose like smelling salts (cheaper than an epi-pen and OTC). I stopped fainting/dying (we disagree about where one ends and the other begins), but I also had to stop observing the process of dying, which was disappointing.
Bolding mine
The one time that I’ve used my Epi, it was more like a reset than a pause. Everything went back to normal for about 20 minutes, which was long enough to make it to the hospital. The symptoms started up again just I finished checking in. That’s when they gave me the Benadryl.
I hope everything is ok with your wife. I have no knowledge of what the proper protocol is, but I know at school, the first response if a child has known allergies and goes into shock is the epi pen.
So, would it have been good for Wolf333 to take some benadryl along with the epi at home? And if you don’t have an epi, but someone is having a severe reaction, would crushing the pills before swallowing them help get them into the system faster? And should you give a higher dose of benadryl? (I understand the LD 50 of benadryl is pretty lenient, or is that wrong?)
I’m just sort of filing this discussion away for future reference.
I don’t have any allergies. I produce too many mast cells. Because of this, I already take three different antihistamines (Zantac, Zyrtec and doxepin).
I have had adverse reactions to Benadryl on at least one occasion (tachycardia), so I prefer to take it under medical supervision.
I was taught in First Aid training that the rule of thumb is benadryl for milder cases, epinephrine for more severe ones. But the real rule is that any one of our kids with an anaphylactic allergy will bring in meds, as well as paperwork that gives the proper protocol for that specific person (which we have to read over and sign when the kid shows up). Protocols I’ve seen have included just bena, just epi, bena then monitor and epi if needed, bena for mild and epi for serious, etc.
I think you made a slight misstep here. Benadryl’s target is the H1 receptor, which is on smooth muscles and capillaries. It blocks the effect of the histamine that the mast cell has released, not stabilizing the the mast cell preventing its degranulation … that’s things like cromolyn.
The other bit of Mama Zappa’s post that deserves comment is the 15 minutes bit. The point of EpiPen “in the wild” is that it controls/reverses/prevents the reaction long enough for the individual to get to the ED without panic, and to be there when the med wears off.
Wife would disagree, as noted above. And the kid pills are easier to lug around the bush.
Thanks for the tip, Doc. Duly noted. There are other preservatives that aren’t liable to kill the patient. Why use sulfites? That’s another product I’m cut off from, like wine, instant mashed potatos, and pepperoncini. A quick way to tell if giardiniera is sulfited is by looking at the cauliflower. If it looks edible it’s probably safe. If it’s the ghastly white of a science experiment, it’s sulfited.
Though chewable Benadryl is probably slightly quicker than liquid, both are fine, and epi is still needed for severe reactions. All ambulance crews have epinephrine.
If she recovered quickly after getting epi, anaphylaxis is more likely but I’d want to see an ECG, lactate, white count, vitals and glucose level.
Every source I can find says that even those with sulfite allergies should use Epi if it’s needed. I mean, after all, you’re getting Epi with the thing you’re allergic to…
Actually checking on myself not quite so. Or at least incomplete.
Yes in terms of the basic model but your original statement turns out to be right too; there appears to be a self-amplification mechanism as well (“released histamine then stimulates the adjacent mast cells or give positive feedbacks to further stimulate its host mast cells through H1 receptor.” - see fig. 2)
And I missed stating the important histamine receptors on various leukocytes, neurons, heart muscle, and of course the usual H2 antagonist target, gastric parietal cells. It’s part of a freakishly complex network of cellular events and feedbacks both positive and negative, with redundant and interacting messengers and signals. Trying to wade through that last article I have flashbacks of trying to diagram these things out in med school … it is not a pleasant flashback! Stuff like how “leukocyte rolling” is blocked by an H1 antagonist, not by an H2 antagonist, but most potently by both at the same time … [shivers] …
Regarding sulfite sensitivity - a good review article here and of note to this discussion is this line reinforcing WhyNot’s statement:
It is also “interesting” (those who suffer may read that word as “frustrating”) that the mechanism of sulfite sensitivity is so unclear. It does not seem to usually be an IgE or histamine primary allergic reaction itself, possibly more cholinergic mediated bronchoconstriction or prostaglandin and/or leukotriene mediated.
ETA: it is also interesting that the spelling in the same article switches between sulphite and sulfite!
I look for the -ite in ingredient lists. The metas are worse, but they all make me sick. And there probably ain’t much in a dose or two. Not like half a jar of giardiniera in vinegar.
Actually, at least some makers of acetominophen with codeine DO use sulfites. Cite..
Have you ever had a doctor say the “kill you dead” thing? I’ve asked numerous doctors - including my former allergist (who also worked at the FDA) and basically get a shrug and a faint “I dunno” from them. One said that the mechanism was thought to be related to the compounds becoming airborne and inhaled but he definitely wasn’t sure of it.
I avoid 'em on principle under the assumption that “might kill you dead” is an unnecessary risk.
No, but I know what they do if I ingest them, then projected the effect if sulfites were injected directly into my bloodstream. But it is very much dose-related.
It makes absolute sense to me that it’s a different pathway. The handful of times I’ve had a sulfite reaction were stunning in how quickly they developed - as in, one minute I was fine, the next minute, starting to feel tight, and the third minute starting to panic. This was back before inhalers were all that common - 1981 or so was the last time it happened - so of course I had no rescue meds with me.
But for me, a “routine” asthma attack has never, EVER developed that quickly, even when precipitated by something as sudden as exposure to very cold air. Nor does a routine attack self-resolve like that - both times I can recall (eating salad at different restaurants), I was fine by the end of the meal.
Whatever it is, it’s THOROUGHLY unpleasant*, and I’m glad sulfiting agents are used much less (banned entirely from restaurants, perhaps?).
