Full disclosure I'm limited to what I read on the internets... but in layperson terms what we're concerned with here is phenergan (or any promethazine family drug) preventing epinephrine's vasosuppressor effect. In terms someone like me, average allergy mom, would understand that means promethazine would block epinephrine's ability to contract blood vessels walls.
Anaphylaxis can include the symptom of blood vessel walls becoming flabby, less effectively able to circulate blood, resulting in an acute drop in pressure. No contraction of vessel walls to narrow, no hope of counteracting the drop in blood pressure, no way to fight shock should it occur. That particular combination of epinephrine and promethazine actually synergizers for a greater drop in pressure.
All other epinephrine effects are unaffected but for vasosuppression by promethazine? And no other drug's vasosuppressor effect can work against promethazine?
Right-- the problem is that under even partial beta-blockade (which is what this class of drugs does), epinephrine effect is unpredictable at best-- though the reason I posted this is that
it is a secondary effect of the drug's MAJOR effect, which is H1-blockade... and THAT is the reason why most doctors (and even a few pharmacists) won't pick up on it as a red flag. They think of promethazine as an anti-emetic because of it being a "first-gen antihistamine." Sounds benign, right? The side effects are almost all related to that H-1 blockade, and not to the other back-door mechanism that results in beta-blockade... it's neever USED as a beta-blocker, so that isn't how doctors and pharmacists encounter it.
Okay, as an aside, here, understand that one of the mental tricks that docs and pharmacists use to remember all of the stuff about therapeutic effects of drugs has them "categorizing" different drug classes into a sort of outline by effect/mechanism. Which is fine until you get to a class which is 'dirty' in the pharmalogical sense, and has
more than one mechanism of activity. As long as that second mechanism/effect is mostly mild and benign, or impacts a receptor that isn't that important for the purposes of most patient care, it's not a big deal to not remember what that second thing is. This is definitely a special case.
Until pretty recently, the number of patients receiving vasopressors for "home" use (e.g. autoinjectors or anakits) was so small that this just didn't get much press... and the effect has been recognized since at least the late 1940's, but it was the sort of thing that was a concern for HOSPITALISTS only.
Hospitals have a lot more tools at their disposal for dealing with shock-- they can titrate to a dosage that can overcome blockade, and use continuous monitoring to make it safe, basically, in a way that in-office surgeons and patients in post-op recovery at home don't really have available. They can also use volume rescusitation in a pinch... but again, not something that is a DIY project. Also not something you're going to live to enjoy if you aren't IN the hospital already when you need that kind of intervention.
Most of us can't just start dopamine on a drip. KWIM?