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Things not taught in Medic School: The Steroid edition

I have to credit Jace Mullen as he was the first to make mention of this on Twitter.

Thanks to my fellow FOAMFratter Jace I have a new outlook on the use of steroids in the emergency setting: Steroids like Decadron or Solumedrol do more for our patients than just “reduce inflammation”. These steroids are undoubtedly part of our cocktail we reach for in patients presenting with acute asthma, allergic reactions or anaphylaxis - and traditional clinical logic has taught us these drugs work to reduce inflammation in the airways and reduce bronchial mucus production.

It has long been held that steroids take longer to activate and as a result, administration of steroids tends to take a “back seat” and fall down the algorithm for many providers. I do not agree with this…

Let me be clear when I say, steroid administration should not take precedence over agents like epinephrine or direct beta-agonists in the management of acute asthmatics or anaphylactic patients. BUT….

What I do want to reiterate is that steroids have an otherwise unknown, immediate benefit for these patients. In fact, in the acute phases of steroid administration, they actually upregulate beta receptors - as Jace mentioned. Essentially meaning, they allow for more beta receptors to “show up” and be engaged for drugs to bind to them – say like our epinephrine and albuterol.

The mechanism by which steroids induce beta regulation has been studied since the 1980’s, surprisingly. There are two mechanisms by which steroids can augment beta receptors and catecholamine responses:*

Steroids increase the number of available adrenergic receptors on cell surfaces.

The exact mechanism by which this occurs is rather complex but to be brief: glucocorticoids increase the genes responsible for the transcription factors that produce the adrenergic receptors themselves on cell surfaces. Bear in mind, patients with chronic asthma or even COPD may be on long-acting beta agonists and at baseline, their beta receptors have become de-sensitized to beta agonists. Steroids can help to upregulate these receptors when acute on chronic exacerbations occur.

Steroids help create a “high affinity” state of these available receptors for beta agonist drugs

Our adrenergic receptors are part of a larger class of molecules known as G-coupled protein receptors. When a naturally occurring catecholamine (like epi or norepinephrine) bind to our adrenergic receptor it activates this G-coupled protein and causes a cascade of events within the cell known as a second messenger system and it results in the response we understand – alpha 1 for vasoconstriction, beta 1 for increased contractility and chronotropy, etc. However, these catecholamines don’t just sit and stay on the receptor. They eventually release… glucocorticoids help here in this gap by helping the receptor to “recover” to its previously sensitized state faster so it is ready to receive its next catecholamine.

How is this “practice changing”??

All of the science is cool (to me, at least) but the question I always seek to answer is: how does this affect my everyday practice? Here’s the scoop:

I found myself reaching for the steroids a little earlier in the treatment algorithm than I had before. Epi and albuterol are still my mainstay pharmacological treatments in severe asthma and anaphylaxis but steroids are the next drug I reach for.

If steroids upregulate the number of available adrenergic receptors (our alpha and beta’s) then theoretically it would have a synergistic effect with our first line agents of Epi and Albuterol as it makes available more sites for these agents to attach to. Once attached, steroids secondarily put these receptors in a high affinity state ready to receive the drugs in the acute setting.

*Taylor, D. R. (2000). Interactions between corticosteroids and beta agonists. Thorax, 55(7), 595–602.


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