Differentiating Thyroid Storm from Sepsis

[Melclin]

Epi on the other hand binds to beta receptors on mast cells, increasing the production of cAMP and reducing the production of all the inflammatory mediators as well as treating all aspects of the syndrome through alpha and beta stimulation. So basically, the opposite of your statement holds true.

That.

That very question was on my exam. "Explain the action of adrenaline in anaphylaxis".

The answer being:
"Adrenaline has positive inotropic and chronotropic actions through B1 receptors and casues vasoconstriction via Alpha receptors, addressing the problem of poor perfusion. Importantly, it also increases the intracellular production of cAMP which inhibits the influx of calcium (which is increased by the action of IgE) required for the exocytosis of inflammatory mediators namely histamine, kinis, prostaglandins and leukotrines."

I realise that benadryl is an anti-histamine (it is after all in just about every medicine cabinet com spring) but that is not in itself a reason we should carry it. But its only going to work on attenuating part of the inflammatory response, and its only an antagonist, it doesn't stop the production of histamine. If its competing against an unregulated massive histamine dump, its not going to win the battle for every receptor. Not to mention all the other mediators that it has no action on, granted histamine is probably the main one.

My understanding of diphen from my learnings on this forum was that it was for mild to moderate allergic reactions and to be considered as an ADJUNCT to adrenaline in anaphylaxis, but was not at all essential, and certainly not to be used alone - hence my question, "why should we carry it?"

 

[Smash]

There was also a small degree of humor to my post, since I was trying to connect anaphylaxis to sepsis after mycrofft pointed out our topic jump.

It's actually not such a big jump. Sepsis and anaphylaxis are essentially two manifestations of SIRS. In fact the definition of sepsis is SIRS in the setting of a know (or strongly suspected) pathogen. Sepsis gets really interesting, complicated and often fatal when SIRS is overcome by CARS. Anaphylaxis is essentially the ultimate expression of SIRS at it's most dramatic.

I'm curious as to which textbooks are stating that histamine receptor antagonists are the ultimate treatment for anaphylaxis as that is most definitely not the case. Histamine is but one small componenet in a deluge of inflammatory mediators like kinins, IL-4, TNF, NO and so on. Epi will decrease the release of these mediators as well as dealing with all the symptoms. Anti-histamine are merely going to control one or two symptoms and do nothing to the underlying problem.

The risks involved with epi are pretty much in proportion to how sick the patient is. Some IM epi (or even IV) in a 26 year old asthmatic is not dangerous given the downside of not giving it. Give it to a well 87 year old patient with heart disease and obviously you'll have trouble. Epi is not a drug to be scared of so long as one has a clear understanding of the risk/benefit profile. Witholding epi when it is required can be fatal.

As for DIC, I would be very, very uncomfortable with EMS
providers administering things like heparin in a patient with DIC. With epi, or norepinepherine in the field we are trying to correct physiological parameters that are deranged as a temporizing measure until we can get the to hospital, not necessarily trying to treat any underlying pathologies (which is what vene has already said, sorry) Treatment of DIC is complex and difficult and I can't see that us throwing more stuff into the mix than we need to.

 

[Veneficus]

That.

That very question was on my exam. "Explain the action of adrenaline in anaphylaxis".

The answer being:
"Adrenaline has positive inotropic and chronotropic actions through B1 receptors and casues vasoconstriction via Alpha receptors, addressing the problem of poor perfusion. Importantly, it also increases the intracellular production of cAMP which inhibits the influx of calcium (which is increased by the action of IgE) required for the exocytosis of inflammatory mediators namely histamine, kinis, prostaglandins and leukotrines."

I realise that benadryl is an anti-histamine (it is after all in just about every medicine cabinet com spring) but that is not in itself a reason we should carry it. But its only going to work on attenuating part of the inflammatory response, and its only an antagonist, it doesn't stop the production of histamine. If its competing against an unregulated massive histamine dump, its not going to win the battle for every receptor. Not to mention all the other mediators that it has no action on, granted histamine is probably the main one.

My understanding of diphen from my learnings on this forum was that it was for mild to moderate allergic reactions and to be considered as an ADJUNCT to adrenaline in anaphylaxis, but was not at all essential, and certainly not to be used alone - hence my question, "why should we carry it?"

In my experience in the US both north and south, during spring and especially travelers for some reason like to call EMS when they have allergic reactions that really are on the mild to moderate side.

When we would give them the benadryl iv it would speed the process through the ed or in many cases trigger a refusal.

Basically a bit less nuclear that epi by itself.

 

[MrBrown]

Adrenaline would be my first choice for an anaphylactic patient (IM or IV) as well as fluids and salbutamol (if they have laryngeal edema).

As has been previously stated, it has some antihistamine properties (although these arent high on the list).

We do not carry DPH but do carry steriods.

For DIC hmm, lots of transport. Why would you give heparin for DIC?