# Differentiating Thyroid Storm from Sepsis



## Melclin (May 17, 2010)

So I understand that sepsis is a common woopsie on the way to a thyroid storm diagnosis. 

I'm getting the impression that the presentations don't _quite_ look the same, but I'm trying to nut out a nice clear description of the difference in presentations for exam prep, and I can't really seem to nail it down.

Is the heart rate likely to be a bit higher that you would expect if it were simply a reaction to hypotension in sepsis? 

History of hyperthyoidism is obviously a big one but people with a history thyroid conditions are not beyond presenting with sepsis as well, nor are they beyond being unresponsive such that they cannot tell us about their recent thyroid operation.


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## Aidey (May 17, 2010)

This is purely from experience, the one person I've seen in thyroid storm was much more manic/agitated/violent than anyone I have ever seen in sepsis. I've had plenty of septic patients that are confused and get combative, but this lady was 5 ft tall, 90lbs soaking wet and trying to take on 3 cops that were all twice her size. 

If I remember right, someone in thyroid storm will have high BP, while someone who is septic is likely to have low BP.

Beyond that, I think differentiating without lab tests is going to come from the history.


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## rescue99 (May 17, 2010)

Melclin said:


> So I understand that sepsis is a common woopsie on the way to a thyroid storm diagnosis.
> 
> I'm getting the impression that the presentations don't _quite_ look the same, but I'm trying to nut out a nice clear description of the difference in presentations for exam prep, and I can't really seem to nail it down.
> 
> ...



Isn't normal/hypertension the suspecting factor? Since DIC, fever, tachycardia, delerium and acidosis are common between the two, BP might be the only hint we'd get in the field. I would expect the blood pressure to be slightly high.


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## rescue99 (May 17, 2010)

Aidey said:


> This is purely from experience, the one person I've seen in thyroid storm was much more manic/agitated/violent than anyone I have ever seen in sepsis. I've had plenty of septic patients that are confused and get combative, but this lady was 5 ft tall, 90lbs soaking wet and trying to take on 3 cops that were all twice her size.
> 
> If I remember right, someone in thyroid storm will have high BP, while someone who is septic is likely to have low BP.
> 
> Beyond that, I think differentiating without lab tests is going to come from the history.



OOPS....Aidey beat me to it.


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## mycrofft (May 17, 2010)

*Saw one thyroid storm after blunt trauma and some sepses,*

including two "toxic shock syndromes" from snorting crank into staph infected noses. (Not that uncommon; one was male).
The TSS pt's _*felt*_ sick. The thyroid guy was _*alarmed*_ at his elevated pulse and somewhat excitable.

We had another guy who was septic and we didn't know it, being a delerious sociopath he became abusive and uncooperative but not truly "hyper" because he didn't have the energy. (He did have a "large" abscess hidden up in the dome of his diaphragm and TB meningitis..I wonder what his HIV status was on post-mortem?).

What's going on is dependent upon the stage of the respective processes, and what else is going on in their lives, such as drugs, psych., and nutritional status.

For an off the cuff answer: energy is shot in sepsis, not in thyroid, before they collapse. After: septic BP should drop and thyroid stay high, although each may have a rapid pulse (one thready, the other strong; you guess which).

Another differentiation: alcohol or benzo detox, far more common than thyroid. A third would be an adrenaline-pumping pheochromocytoma. Oh, and an overdose of levothyroxine. A fifth is an Elavil OD....


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## Melclin (May 17, 2010)

*AHH the BP.*



Aidey said:


> This is purely from experience, the one person I've seen in thyroid storm was much more manic/agitated/violent than anyone I have ever seen in sepsis. I've had plenty of septic patients that are confused and get combative, but this lady was 5 ft tall, 90lbs soaking wet and trying to take on 3 cops that were all twice her size.
> 
> If I remember right, someone in thyroid storm will have high BP, while someone who is septic is likely to have low BP.
> 
> Beyond that, I think differentiating without lab tests is going to come from the history.





rescue99 said:


> Isn't normal/hypertension the suspecting factor? Since DIC, fever, tachycardia, delerium and acidosis are common between the two, BP might be the only hint we'd get in the field. I would expect the blood pressure to be slightly high.



I get the uber agitation part, but I was thinking later stage than that. On the topic of BPs, there was not actually any mention of the BP in the lecture, only that we might consider fluids for dehydration, so I figured a low BP maybe due to some kind hyper osmolar type kidney dysfunction... ++sympathetic outflow etc...I looking for a reason why ^symp outflow wasn't causing hypertension, but seeing as though it looks like it does..I spose problem solved. Which does make me wonder though why it can be mistaken for sepsis. Is there perhaps a late stage presentation.... around unconsciousness time, where the BP might drop? 

Also my pathophys text says that vasodilation occurs to dissipate the extra heat of all the metabolism, which also got me to figurin' hypotension. I guess the heart really does kick it up a notch. 

What would you expect a person's blood sugar to be? Is it elevated because of all this extra sympathetic and metabolic  -->  ^ gluconeogenesis and ^ glygenolysis, or is it depressed because all the metabolising that the body is busy doing chews it all up? Is there a pattern at all? 



mycrofft said:


> including two "toxic shock syndromes" from snorting crank into staph infected noses. (Not that uncommon; one was male).
> The TSS pt's _*felt*_ sick. The thyroid guy was _*alarmed*_ at his elevated pulse and somewhat excitable.
> 
> We had another guy who was septic and we didn't know it, being a delerious sociopath he became abusive and uncooperative but not truly "hyper" because he didn't have the energy. (He did have a "large" abscess hidden up in the dome of his diaphragm and TB meningitis..I wonder what his HIV status was on post-mortem?).
> ...



I don't think I fancy working in your area mate 

Pheochromocytoma was is on our list... too bloody obscure to be examinable I reckon...*grumble*. Thyroxine ODs we covered too. Alcohol and benzo detox I didn't think of, and I'll have to read more about. I had to look up Elavil, but we do cover TCA OD, although I've seen one myself and subsequently discussed it with an experienced medic, who said the presentation I saw was typical of the many he'd seen. None of which had the anticholinergic affects I'd expected or the ECG changes we'd learned about (just a altered conscious state, GCS 11, and a very mild tachycardia)...I spose maybe its something that takes a while to present.


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## MonkeySquasher (May 17, 2010)

Now, I'm not entirely sure of my own statement.  So if I'm wrong, please, just point it out and don't grind me into hamburger.   =D





Aidey said:


> This is purely from experience, the one person I've seen in thyroid storm was much more manic/agitated/violent than anyone I have ever seen in sepsis. I've had plenty of septic patients that are confused and get combative, but this lady was 5 ft tall, 90lbs soaking wet and trying to take on 3 cops that were all twice her size.
> 
> If I remember right, someone in thyroid storm will have high BP, while someone who is septic is likely to have low BP.






rescue99 said:


> Isn't normal/hypertension the suspecting factor? Since DIC, fever, tachycardia, delerium and acidosis are common between the two, BP might be the only hint we'd get in the field. I would expect the blood pressure to be slightly high.






mycrofft said:


> The TSS pt's _*felt*_ sick. The thyroid guy was _*alarmed*_ at his elevated pulse and somewhat excitable.
> 
> For an off the cuff answer: energy is shot in sepsis, not in thyroid, before they collapse. After: septic BP should drop and thyroid stay high, although each may have a rapid pulse (one thready, the other strong; you guess which).




I agree with the above.  Both will have elevated HR, N/V/D, fever.  Sepsis should have a lower BP and, at later stages, worse mentation.  However, the person in TS should, at the start, have a lot of energy, and be more generally hyperthermic than fever, as I understand it.  Also, as I understand it, TS onset and progression should be MUCH more rapid than sepsis.

http://www.medicinenet.com/script/main/art.asp?articlekey=77774


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## mycrofft (May 17, 2010)

*Suspend the Meatgrinder!*

Sounds good monkeyman.

Another differentiator: a hyper thyroid-oid mioght not let you keep EKG leads on him.

Saw a pt once, was arrested holding a gun to his temple in the middle of a busy street, knocked down with a baton gun..took TWO rounds to do it. Was dx as manic with psychotic, but closer look revealed pheochromocytoma AND hyperthyroid due to a nodule. Knocked down the thyroid with meds, addressed hypertension with meds...then they released him. Never heard from him again.


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## 8jimi8 (May 17, 2010)

Everyone is forgetting that sepsis does not present with just one set of symptoms.

sepsis is a continuum.  

Early sepsis will present with a fever, and excellent perfusion. The endotoxins circulating can cause dead heart tissue to contract.  So these people will not present as your typical shock/sepsis, they have great pulse and b/p and often tachy in the 100s may have a fever >100.

It is late sepsis where you will see distributive shock and a low grade temps.


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## MonkeySquasher (May 17, 2010)

mycrofft said:


> Never heard from him again.




Yeah, now that he was more medically stable, he went and finished the job off.


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## mycrofft (May 18, 2010)

*Sepsis..*

"Have you been sick lately".
"Why, YES!!".


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## Veneficus (May 23, 2010)

*missed this in all the confusion*

Somehow in all the confusion of finals and being told what I don't know by some overzealous EMT Bs this post escaped me.

The most common cause of thyroid storm is infection in a person with a history of hyper thyroid. 

In older people, Goiter is grossly apparent sign but may not present in children with a history. 

Because of the nature, exothalmus is almost always present in all ages with long standing history. 

In the event of a thyroidectomy (partial or from an undiagnosed hot nodule lower in the thoracic cavity) you might also see the relocation incision and scar usually near the wrist of the parathyroid gland.

Differentiating from early sepsis. (late sepsis seems apparent so i don't want to type it out)

The hyperpyrexia may be more at a level closer to a malignant hypertension than "a mere fever" It may be uncontrolled by NSAIDs. 

The major mortality factor is arrythmia, that is what you must be on the alert for. What you have is a massive catecholamine release and of course the presentation you would expect to see from it, high BP, hyper alert/ activity/agitation, possibly seizure. Even jaundice without a history of liver disease.

If I was going to make a memory aid for early presentation: History/goiter, hyperactivity, High fever, high bp, arrythmia. (if not a lethal one, very fast, well above boarderline tachy) From lack of prefil, you may also consider similar symptoms from heart failure. (if they are not in secondary heart failure from the hyperthyroid history)

Hope this helps.


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## Veneficus (May 23, 2010)

*I meant*

Exophthalmos (also called exophthalmia or proptosis)

One day I will learn to spell and type or be able to afford a medical spell check program.

Today is not that day.


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## mycrofft (May 23, 2010)

*Ruling out sepsis might be easier.*

If not ruling out, then discovering and passing on that it's likelihood is low.

MANY hyperthyroid cases (slo-mo thyroid storm if you will) are missed because the initial s/s are often psych-like and masked with benzo's. A lot of these are people of advancing age, losing body mass, but thyroid Rx is not being regulated properly, either by the MD, or by the pt themselves. Over time, they may show mild signs of thyroid overload like exopthalmia, but that takes tie and never gets like the acute emergencies.
OD of levothyroxine due to intent or accident can also cause it, acutely, without the exopthalmia.


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## Veneficus (May 23, 2010)

mycrofft said:


> Over time, they may show mild signs of thyroid overload like exopthalmia, but that takes time



(hope you don't mind my adding the "m")

I understand the Exophthalmos is caused by a disorder of collegen synthesis because of the increased metabolism. 

Like I said 

_"Because of the nature, exophthalmos is almost always present in all ages with long standing history."_

(fixed my spelling too)



mycrofft said:


> OD of levothyroxine due to intent or accident can also cause it, acutely, without the exopthalmia.[/FONT]



That is a really good point.

OD is also the second leading cause of thyroid storm. 

Making it is important to consider a hx of hypothyroid (the most common cause being surgical removal of) as suspect as well.

I couldn't find anything about sudden thyroid storm that was not from an OD, undiagnosed/untreated thyrotoxicity or a neoplasm.

Because of potential anatomical deviation of or "extra" glands due to variations in embryo development, the thyroid or a hot nodule may be a palpable mass usually no lower than the clavical, near the midline. But as with all things in medicine, nothing is absolute and some patient will probably be happy to demonstrate their subclavical variation I'm sure.

The definitive dx is circulating a t4/t3 test, which isn't going to happen prehospital. 

Based on the disease process, I would be more worried about an occult case of an undiagnosed child rather than an undiagnosed adult though. (which will probably add a little stress to the provider)

Another good point mycroft mentioned was misdiagnosing as psych. Like all patients with an altered mental status, be careful on your working dx. The potential seizure activity could also appear as a neurological cause or the jaundice might be mistaken for liver problems. 

Hyperthyroid is a very good example of why it is important to be really careful with dismissing somebody as simply "drunk." As I am constantly reminded, "drunk people get sick too."

That creates the question of: " Are you going to put every intoxicated person on a heart monitor to rule out an arrythmia as it is primarily responsible for the mortality?"

How are you going to explain calling for a higher level of care in a tiered response?


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## Melclin (May 23, 2010)

Golly, in my exam related brain haze I forgot about this thread. But thank you all, I had a much better understanding.

Just had my medical management exam. A big :censored::censored::censored::censored::censored::censored::censored: of an exam, predicatable short answer, so pleased with one of them: "explain the difference in presentation, pathophysiology and affected demographic of DKA and non ketotic hyperosmolar state - 10 marks" - had just the previous day drew a big flow chart on my whiteboard describing the differences.

Only a few non diabetes endo questions...presentation of addison's crisis and something about thyroid hormomes. 

Anyways cheers guys, I'm sure this will come in handy on the road someday.


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## mycrofft (May 24, 2010)

*Back to...The Storm*

As I hope I mentioned a few days ago, we had a minor case when a guy was running full tilt, slipped and fell head first into a trough urinal, slamming his anterior throat on the edge. His initial worry was he thought he was going to asphyxiate, but ice and oxygen helped. He was in C spine then cleared by local ER, who noted in their chem panel elevated thyroid (not elevated TSH). Over next three days he had an upswing in bp/pulse and affect was a little accelerated (not drunk-like), but after day three he returned to baseline with an interesting bruise. They were talking about propylthyrourocil (PTU) but he never became emergently hyper and recovered pretty fast. Good thing it did not cause a similar effect on the parathgyroids!


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## mycrofft (May 24, 2010)

*Congrats Melclin!*

Good on you!


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## Aidey (May 24, 2010)

Veneficus said:


> Hyperthyroid is a very good example of why it is important to be really careful with dismissing somebody as simply "drunk." As I am constantly reminded, "drunk people get sick too."
> 
> That creates the question of: " Are you going to put every intoxicated person on a heart monitor to rule out an arrythmia as it is primarily responsible for the mortality?"



Slightly off topic, but the first thing you said is one of the reasons all drunks/intoxicated people get a CBG in my amb. It has saved my butt at least 5-6 times. 

I do attempt to put the majority of my more intoxicated pts on the monitor and at least get a quick strip. Partially to make sure they are in an acceptable rhythm, and also because many of them aren't in good enough shape to give me a decent history, so it can give me a tad more info on the pt.


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## Melclin (May 25, 2010)

Aidey said:


> Slightly off topic, but the first thing you said is one of the reasons all drunks/intoxicated people get a CBG in my amb. It has saved my butt at least 5-6 times.
> 
> I do attempt to put the majority of my more intoxicated pts on the monitor and at least get a quick strip. Partially to make sure they are in an acceptable rhythm, and also because many of them aren't in good enough shape to give me a decent history, so it can give me a tad more info on the pt.



Definitely....any altered conscious state gets a BGL in my book...seeing as though my book has yet to be published (being a student....extending the metaphor to far?) I'd prefer to be sure. 



mycrofft said:


> Good on you!



Haha, cheers, but I haven't passed yet. Had my practical exam today, I didn't pass, but didn't fail, it has to go to the subject head for approval. So while I have a thread commandeered, I'll pose the question and lay my fate humbly at the feet of the collective wisdom of the participants of this thread (no sycophany though  ).  

I had an anaphylaxis pt:

54 female, volunteered that she thought she was having a reaction to a new antibiotic she had taken shortly before calling. I briefly asked her a few more questions to clear up what exactly had happened, she had abdominal cramps and had just had diarrhoea. Severely short of breath, obvious erythema on the neck, face. Extremely anxious, BP was 90/I forget, Pulse 110, RespRar - 12 (I took that to mean that she was in such profound resp distress that her RR was trending down), speaking only in single words, Sinus Tach, Loud expiratory wheeze, GCS 15. Tried some 100% through the closed circuit, wouldn't tolerate it, so back to simple face mask. I called for intensive care early, and had my partner draw up adrenaline while I did the vitals after I saw the erythema and SOB. There was a pause after obs for my explanation of the situation to the examiner (exam technique), I got nebulised Salbutamol and Ipratropium setup took another pressure and took HR off the monitor, no change in BP, HR now 120. Got the adrenaline on board. Partner to get the bed. Took meds and hx, spoke with intensive care, decided it would be quicker to go to the nearest ED and went, obs 5 minutely. 

I got canned for giving the adrenaline too early and not eliciting a proper history first. I replied that I thought the threat to her airway was paramount and that no information I elicited would change my management in anyway. He didn't agree, saying that I hadn't taken enough of an event history to show that it was anaphylaxis, and other information like a temp could have been helpful...."what if she had a chest infection and the wheeze was from that?" At that point I didn't argue further because I didn't want him in a bad mood when he referred it to the subject head, but that seemed like a :censored::censored::censored::censored: reason to me. Looking back on it now, I feel like I could have got the adrenaline on board earlier.

What do you think? This thread should be titled, "Help Melclin as he stresses through exam period".


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## Veneficus (May 25, 2010)

Melclin said:


> 54 female, volunteered that she thought she was having a reaction to a new antibiotic she had taken shortly before calling. I briefly asked her a few more questions to clear up what exactly had happened, she had abdominal cramps and had just had diarrhoea.



This is indicative of the side effects of clindamycin and an resultant overgrowth of _C. Difficile_ not anaphylaxis.

It also commonly causes UTIs in females.



Melclin said:


> Severely short of breath, obvious erythema on the neck, face. Extremely anxious, BP was 90/I forget, Pulse 110, RespRar - 12 (I took that to mean that she was in such profound resp distress that her RR was trending down), speaking only in single words, Sinus Tach, Loud expiratory wheeze, GCS 15. Tried some 100% through the closed circuit, wouldn't tolerate it, so back to simple face mask..



All of this respiratory difficulty would be helped by epinephrine. The pulse could go either way, depending on beta stimulation vs. response to increased perfusion. Depending on history, this might be normal for a 54 y/o female.  



Melclin said:


> I called for intensive care early, and had my partner draw up adrenaline while I did the vitals after I saw the erythema and SOB. There was a pause after obs for my explanation of the situation to the examiner (exam technique), I got nebulised Salbutamol and Ipratropium setup took another pressure and took HR off the monitor, no change in BP, HR now 120. Got the adrenaline on board. Partner to get the bed. Took meds and hx, spoke with intensive care, decided it would be quicker to go to the nearest ED and went, obs 5 minutely.



Sounds like you were really worried about the airway and breathing and went for the nuclear option. About the only way to further crush the inflammatory response would be some steroids and some malox. 

In my best arm chair quarterbacking, I think I would have tried either the nebs first with some Diphenhydramine or went with the Epi and saw how that worked out.



Melclin said:


> I got canned for giving the adrenaline too early and not eliciting a proper history first..



That sounds like BS to me. It was an aggresive approach, certainly not improper by any measure I have ever been held to. 



Melclin said:


> I replied that I thought the threat to her airway was paramount and that no information I elicited would change my management in anyway. He didn't agree, saying that I hadn't taken enough of an event history to show that it was anaphylaxis, and other information like a temp could have been helpful...."what if she had a chest infection and the wheeze was from that?" At that point I didn't argue further because I didn't want him in a bad mood when he referred it to the subject head, but that seemed like a :censored::censored::censored::censored: reason to me. Looking back on it now, I feel like I could have got the adrenaline on board earlier.



What if it was Feb 29th during the full moon, low tide, and a comet was visible in the sky?

I really can't find fault in the Epi. Not treating conservatively is not wrong, it is just another way. Appeal to a doctor. 



Melclin said:


> What do you think? This thread should be titled, "Help Melclin as he stresses through exam period".



No worries, I know exactly how you feel.


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## Aidey (May 25, 2010)

Veneficus said:


> This is indicative of the side effects of clindamycin and an resultant overgrowth of _C. Difficile_ not anaphylaxis.
> 
> It also commonly causes UTIs in females.



Wouldn't the likelihood of this depend on the time line of symptoms? Diarrhea and upset stomach within 15-30 minutes of taking the antibiotic would make me more suspicious of a systemic allergic reaction. Diarrhea 3 days into a course of the antibiotic makes me more suspicious that it's a side effect and not an allergic reaction.


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## Veneficus (May 25, 2010)

Aidey said:


> Wouldn't the likelihood of this depend on the time line of symptoms? Diarrhea and upset stomach within 15-30 minutes of taking the antibiotic would make me more suspicious of a systemic allergic reaction. Diarrhea 3 days into a course of the antibiotic makes me more suspicious that it's a side effect and not an allergic reaction.



The post says shortly before, it doesn't really specify how many times it was taken before, there would have had to be a prior sensitization. 

But you are right, if she had the same or similar ab before, she could have prior sensitization and it would point more towards an allegric rxn. 

The information is just not given.


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## MrBrown (May 25, 2010)

A helicopter doctor swanning down in his orange suit would have fixed it up for ya 

As we talked about, I dont find fault in your logic but  I could not resist plugging my beloved orange jumpsuit


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## Melclin (May 25, 2010)

Veneficus said:


> This is indicative of the side effects of clindamycin and an resultant overgrowth of _C. Difficile_ not anaphylaxis.
> 
> It also commonly causes UTIs in females.
> 
> ...





Aidey said:


> Wouldn't the likelihood of this depend on the time line of symptoms? Diarrhea and upset stomach within 15-30 minutes of taking the antibiotic would make me more suspicious of a systemic allergic reaction. Diarrhea 3 days into a course of the antibiotic makes me more suspicious that it's a side effect and not an allergic reaction.



She had taken the antibiotic "last night" and she was presenting about an hour after taking a morning dose, having experienced the symptoms for about 20mins.


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## MonkeySquasher (May 25, 2010)

Melclin said:


> We don't carry Diphen, in fact I don't think anyone does here in Aus. Steroids are a MICA issue.



You don't...  carry...  diphenhydramine.... ??  :wacko:


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## Aidey (May 25, 2010)

Melclin said:


> She had taken the antibiotic "last night" and she was presenting about an hour after taking a morning dose, having experienced the symptoms for about 20mins.



So it's plausible that dose 1 sensitized her, and dose 2 set off the reaction. 



MonkeySquasher said:


> You don't...  carry...  diphenhydramine.... ??  :wacko:



This x 2!


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## Melclin (May 26, 2010)

No service that I'm aware of in Australia carries diphenhydramine. 

I know Queensland, Victoria and New South Wales state ambulance services don't. The others I can't check but I suspect not. NSW and QLD carry Promethazine, mostly for nausea, but indicated for mild localised allergic reactions and absolutely contraindicated in moderate to severe allergic reactions/anaphylaxis.

I suppose the idea is that if its serious enough to warrant ambulance intervention  then its adrenaline (and we are fairly liberal with handing out the adrenaline), if not then it can wait until hospital. It seems sort of overly simplistic to me, but like I said, I'm not really read in on the subject and I haven't the time at the moment (I've had my med exam, now its time for the nearly dead, the newly bred and those off their head- obstets, geri and psych). Can someone explain why we should carry diphen? That'll give me something else to complain loudly about in tutes


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## MrBrown (May 26, 2010)

DPH is benadryl, an anti histamine.

We (like you) carry steroids.


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## Aidey (May 26, 2010)

Melclin said:


> I suppose the idea is that if its serious enough to warrant ambulance intervention  then its adrenaline (and we are fairly liberal with handing out the adrenaline), if not then it can wait until hospital.



Uhhh...negative. 

Someone correct me if I'm wrong. An allergic reaction sets off a cascade in the body. An antihistamine can short circuit that cascade preventing the reaction from progressing. As far as I'm aware, the epi just treats the side effects of the reaction, it doesn't actually do anything to stop the reaction itself. Thus, prompt administration of an antihistamine can reduce the severity of the reaction and how much treatment and misery your patient has to go through. 

I personally am not a huge fan of being liberal with epi. In a healthy young adult it isn't likely to cause an adverse reaction. But in older people or people with medical conditions the epi can be quite the strain and cause some problems.


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## Smash (May 26, 2010)

Aidey said:


> Uhhh...negative.
> 
> Someone correct me if I'm wrong. An allergic reaction sets off a cascade in the body. An antihistamine can short circuit that cascade preventing the reaction from progressing. As far as I'm aware, the epi just treats the side effects of the reaction, it doesn't actually do anything to stop the reaction itself. Thus, prompt administration of an antihistamine can reduce the severity of the reaction and how much treatment and misery your patient has to go through.
> 
> I personally am not a huge fan of being liberal with epi. In a healthy young adult it isn't likely to cause an adverse reaction. But in older people or people with medical conditions the epi can be quite the strain and cause some problems.



Ok, I will. 

Anaphylaxis does indeed trigger a cascade. Mast cell degranulation releases a very wide range of inflammatory mediators: histamine is only one of them, there are leukotrienes, bradykinins, all sorts of bits and pieces.
Diphenhydramine competitively antagonizes Histamine receptors, essentially knocking the histamine off and minimizing the adverse effects of the histamine. Think of it as naloxone but for histamine receptors instead of opiod receptors. What it doesn't do is reduce in any way the production of histamine, nor any of the other inflammatory mediators. 

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. 

Diphenhydramine may still be an appropriate drug to carry both as an adjunct to the cornerstones of epi, fluid and steroids for anaphylaxis and for allergic reactions as opposed to anaphylaxis. However I can see the logic of the 'wait until hospital' idea (not that I necessarily agree with it).


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## mycrofft (May 26, 2010)

*I'm not good with epi.*

Even the epi in local anesthetics would give me chest tightness and SOB. I went on to develop atrial fibrillation. Epi would have, and might still, cause me to go into a worse arrrythmia.
Nothing to do with thyroid and sepsis though.


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## MonkeySquasher (May 26, 2010)

That's the thing, I've always been taught that diphen- was more to halt the reaction, where as Epi- was more to act on Beta to bronchodilate.

What about someone with a cardiac Hx, or someone on a Beta blocker?  Those would both cause a problem where diphen- wouldn't, right?  But then again, if the person is on a sedative, it'd mix poorly with the diphen-, so it's a double-edged sword.

Also, what about Mag Sulfate as a smooth muscle relaxer to ease the respiratory distress?  Would that work?


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## Aidey (May 26, 2010)

MonkeySquasher said:


> That's the thing, I've always been taught that diphen- was more to halt the reaction, where as Epi- was more to act on Beta to bronchodilate.
> 
> What about someone with a cardiac Hx, or someone on a Beta blocker?  Those would both cause a problem where diphen- wouldn't, right?  But then again, if the person is on a sedative, it'd mix poorly with the diphen-, so it's a double-edged sword.
> 
> Also, what about Mag Sulfate as a smooth muscle relaxer to ease the respiratory distress?  Would that work?



^^^ That has been what I was always taught too. It may just be that the  common paramedic texts don't go into the pathophys in that much detail. 

The gist of what I know about what epi does in anaphylaxis is that it decreases vascular permeability, causes vasoconstriction, causes increased contractility, and also causes bronchodilation. I double checked my book and it doesn't mention anything about cAMP.




mycrofft said:


> Even the epi in local anesthetics would give me chest tightness and SOB. I went on to develop atrial fibrillation. Epi would have, and might still, cause me to go into a worse arrrythmia.
> Nothing to do with thyroid and sepsis though.



It does have to do with sepsis in a remote way....epi is sometimes used to treat sepsis induced DIC isn't it? ^_^ 

I discussed using Epi with one of the ER docs the other day after I used it on a 26 year old status asthmaticus patient. I had followed my protocols so he didn't blame me, but he was quite surprised that it was still in the protocol. His opinion of epi was pretty low because of the number of people that ended up having reactions to the epi because of the stress it puts on the heart.


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## got_shoes (May 26, 2010)

Okay, I am a bit confused by the statement epi is used to treat DIC sometimes. wouldn't the treatment of DIC induced by sepsis, be treating the underlying condition? and if some one is septic, why would epi be used? wouldn't epi potentially cause some unwanted side effects?

please excuse my ignorance


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## Veneficus (May 26, 2010)

got_shoes said:


> Okay, I am a bit confused by the statement epi is used to treat DIC sometimes. wouldn't the treatment of DIC induced by sepsis, be treating the underlying condition? and if some one is septic, why would epi be used? wouldn't epi potentially cause some unwanted side effects?
> 
> please excuse my ignorance



I think (don't want to speak for them) they are refering to using an epi drip as the vasoconstrictor of choice in the later stage of DIC after the clotting factors are exhausted. 

Many pathologies can result in DIC, you do have to try to treat the underlying cause if possible, but the condition itself is lethal, so you must also do something to support the body too.


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## got_shoes (May 26, 2010)

Vene 

thanks for the info. I realize that DIC is a fatal condition, I was under the impression that vasopressin was indicated rather then epi. and i thought that epi was maybe useful in DIC, further more I thought that activated protein C was indicated in sepsis induced DIC. I realize the apC is not available in EMS and is potentially very dangerous.


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## Veneficus (May 26, 2010)

got_shoes said:


> Vene
> 
> thanks for the info. I realize that DIC is a fatal condition, I was under the impression that vasopressin was indicated rather then epi. and i thought that epi was maybe useful in DIC, further more I thought that activated protein C was indicated in sepsis induced DIC. I realize the apC is not available in EMS and is potentially very dangerous.



APC is for the Coag Phase.

http://emedicine.medscape.com/article/786058-treatment

here, norepi is the first line, but every doc has their favorite flavour of pressor and reasons why.


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## Aidey (May 26, 2010)

got_shoes said:


> Okay, I am a bit confused by the statement epi is used to treat DIC sometimes. wouldn't the treatment of DIC induced by sepsis, be treating the underlying condition? and if some one is septic, why would epi be used? wouldn't epi potentially cause some unwanted side effects?
> 
> please excuse my ignorance





Veneficus said:


> I think (don't want to speak for them) they are refering to using an epi drip as the vasoconstrictor of choice in the later stage of DIC after the clotting factors are exhausted.
> 
> Many pathologies can result in DIC, you do have to try to treat the underlying cause if possible, but the condition itself is lethal, so you must also do something to support the body too.



Yup, exactly. Also, once DIC has developed the treatment for the underlying condition may not work fast enough to help the patient much. 



got_shoes said:


> Vene
> 
> thanks for the info. I realize that DIC is a fatal condition, I was under the impression that vasopressin was indicated rather then epi. and i thought that epi was maybe useful in DIC, further more I thought that activated protein C was indicated in sepsis induced DIC. I realize the apC is not available in EMS and is potentially very dangerous.



Pre-hospital it is very very very unlikely that we would use any meds to treat DIC. Like Ven said, every doc has their favorite meds to use, and in late stage DIC there are a lot of medications that can be used to try and control the DIC. The last DIC pt I had I believe they used norepi on him, but I'm not 100% sure. 

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.


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## 8jimi8 (May 26, 2010)

Aidey said:


> Yup, exactly. Also, once DIC has developed the treatment for the underlying condition may not work fast enough to help the patient much.
> 
> 
> 
> ...




Sometimes the treatment is heparin and then FFPs.  Don't some agencies carry heparin drips?


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## Melclin (May 26, 2010)

Smash said:


> 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?"


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## Smash (May 26, 2010)

Aidey said:
			
		

> 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.


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## Veneficus (May 27, 2010)

Melclin said:


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



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.


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## MrBrown (May 27, 2010)

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?


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