ER question for Smart Person

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Impressions

Membership Revoked
Removed
10+ Year Member
15+ Year Member
Joined
Mar 8, 2006
Messages
405
Reaction score
1
I was wondering if a smart person can help me with this question.

If a patient presents with acute adrenal insufficiency w/tachycardia, hypotension, and hyperkalemia. What is the 1st step in managment?

A) Steroids
B) Infusion of Normal Saline
C) Calcium Gluconate (for hyperkalemia)

Is there an algorithim for this? What do you do 1st than 2nd etc.

Thanks to the smart person

Members don't see this ad.
 
i can't say im the smartest person...but you always start with the abc's on evaluation. i havent had a person with adrenal insufficiency yet but i would always start and iv and give fluids before steroids. and i woulnt give calcium gluconate without getting an ekg. you dont know how dehydrated the person is or how high the K is either.
 
I was wondering if a smart person can help me with this question.

If a patient presents with acute adrenal insufficiency w/tachycardia, hypotension, and hyperkalemia. What is the 1st step in managment?

A) Steroids
B) Infusion of Normal Saline
C) Calcium Gluconate (for hyperkalemia)

Is there an algorithim for this? What do you do 1st than 2nd etc.

Thanks to the smart person


I'm not smart, but I'd get an EKG first. If there are no EKG changes, then you've got some time, and should start with fluids. If you start seeing QRS widening or peaked T-waves then you have to treat the hyperkalemia first.
 
Members don't see this ad :)
I was wondering if a smart person can help me with this question.

If a patient presents with acute adrenal insufficiency w/tachycardia, hypotension, and hyperkalemia. What is the 1st step in managment?

A) Steroids
B) Infusion of Normal Saline
C) Calcium Gluconate (for hyperkalemia)

Is there an algorithim for this? What do you do 1st than 2nd etc.

Thanks to the smart person

Sounds like a boards question. You want to take care of urgent things first - airway, breathing, circulation. assuming airway and breathing are ok you are worried about circulatory problems. How bad is the hyperkalemia? Are there EKG changes, peaked T waves etc. Then you would want to give Calcium.
After that you definetely want to give them fluids and if necessary pressors to keep their blood pressure up. Steroids dont work quickly so that would be the last step.
 
For boards purposes, volume replacement (hypotension is part of the "C" in "ABC") would come before electrolyte correction, which would come before the administration of steroids.
 
For boards purposes, volume replacement (hypotension is part of the "C" in "ABC") would come before electrolyte correction, which would come before the administration of steroids.

Totally right but just to make it clear "electrolyte correction" would mean in this case lowering the K+ (dialysis, kayexalate) while giving the calcium which is an electrolyte isnt electrolyte correction its cardioprotective.
 
Totally right but just to make it clear "electrolyte correction" would mean in this case lowering the K+ (dialysis, kayexalate) while giving the calcium which is an electrolyte isnt electrolyte correction its cardioprotective.

Yes, but this is where clinical experience can mess you up on board questions. The question didn't state that the hyperkalemia was clinically significant, so you shouldn't assume that it is. Don't read things into the question that aren't there. Stick to the basics.
 
Yes, but this is where clinical experience can mess you up on board questions. The question didn't state that the hyperkalemia was clinically significant, so you shouldn't assume that it is. Don't read things into the question that aren't there. Stick to the basics.

The hypotension can certainly be due to the arrhythmia that you would develop with the high K+, but if the question doesnt says thet the hyperkalemia is significant then of course you would want to correct the other cause of the hypotension, which you are assuming is hypovolemia.
 
The hypotension can certainly be due to the arrhythmia that you would develop with the high K+, but if the question doesnt says thet the hyperkalemia is significant then of course you would want to correct the other cause of the hypotension, which you are assuming is hypovolemia.

No, I'm not assuming anything. The question is about the management of adrenal crisis. In adrenal insufficiency, hypotension and tachycardia result from sodium and volume loss. The question isn't about the management of hyperkalemia. Again, don't get sidetracked.
 
At best, you will get a point of care K+ back in 5-10 minutes. So, in this particular clinical scenario, you should have 2 liters of NS hanging to treat the 82/47 that you see on arrival. To be devils advocate, in another patient, who has happened to miss his last 3 dialysis appointments, giving calcium to address the K+ would be the first step, rather than flooding someone who is already volume overloaded.
 
This thread is making me even more confused. According to Goljan's audio, in this USMLE situation you would give steroids 1st to correct the problem. Did he make a mistake? Also, in Washington Manual it states give steroids too.

I always thought that ABC should come first but I am not sure any more. As for the Calcium Gluconate (this is cardioprotective). You can work all you want with ABC's, however acute hyperkalemia can lead to immediate death via v. fib. Isn't this more important for the 1st step? Who knows? I heard the exact value of the hyperkalemia is beside the point because people with chronic hyperkalemia can survive for a long time. Acute hyperkalemia is dangerous for arrthymias because immediate changes in K+ is detrimental to the cardiac electrical system.

Man, I am totally confused now. Help!
 
This thread is making me even more confused. According to Goljan's audio, in this USMLE situation you would give steroids 1st to correct the problem. Did he make a mistake? Also, in Washington Manual it states give steroids too.

I always thought that ABC should come first but I am not sure any more. As for the Calcium Gluconate (this is cardioprotective). You can work all you want with ABC's, however acute hyperkalemia can lead to immediate death via v. fib. Isn't this more important for the 1st step? Who knows? I heard the exact value of the hyperkalemia is beside the point because people with chronic hyperkalemia can survive for a long time. Acute hyperkalemia is dangerous for arrthymias because immediate changes in K+ is detrimental to the cardiac electrical system.

Man, I am totally confused now.


The correct answer would be to start NS first. You can always do this while you're checking an EKG and getting steroids ready.
 
in practice you would place iv lines, start fluids and then immediately put the patient on a heart monitor. Then order an ekg, draw blood for a stat potassium level. Then if there are ekg/heart monitor changes you'd give calcium...

here's something from emedicine

* Administration of glucocorticoids in supraphysiologic or stress doses is the only definitive therapy.
*
o Dexamethasone does not interfere with serum cortisol assay and, thus, may be the initial drug of choice. However, because dexamethasone has little mineralocorticoid activity, fluid and electrolyte replacement is essential.

o A short ACTH stimulation test may be performed during resuscitation. Once complete, hydrocortisone 100 mg IV every 6 hours is the preferred treatment to provide mineralocorticoid support.

o Delaying glucocorticoid replacement therapy while awaiting the results of the ACTH stimulation test is inappropriate and dangerous.

* In addition to corticosteroid replacement, aggressive fluid replacement with 5 or 10% intravenous dextrose and saline solutions and treatment of hyperkalemia is mandatory. Fludrocortisone, a mineralocorticoid, may also be given.
*

* A thorough search for a precipitating cause and administration of empiric antibiotics is indicated. Reversal of coagulopathy should be attempted with fresh frozen plasma.

* Pressors (eg, dopamine, norepinephrine) may be necessary to combat hypotension.
 
Members don't see this ad :)
The correct answer would be to start NS first. You can always do this while you're checking an EKG and getting steroids ready.

Correct. Board questions are easy when you know the answer...they become hard when you have to think about them. ;)

On the boards, ABCs always come first.
 
I was wondering if a smart person can help me with this question.

If a patient presents with acute adrenal insufficiency w/tachycardia, hypotension, and hyperkalemia. What is the 1st step in managment?

A) Steroids
B) Infusion of Normal Saline
C) Calcium Gluconate (for hyperkalemia)

Is there an algorithim for this? What do you do 1st than 2nd etc.

Thanks to the smart person


This is a medicine question. The emergency doctor only knows the patient is hypotensive and tachycardic. He may suspect acute adrenal insufficiency based on history, and he may suspect hyperkalemia, again based on history or perhaps even an EKG done in triage, but for most of us that patient would get a liter of saline long before we knew he was hyperkalemic.

How many of us have had a tachycardic, hypotensive patient that we made the diagnosis of hyperkalemia prior to getting the labs back? It doesn't happen very often. The EKG changes are pretty subtle until the hyperkalemia is severe.
 
This is a medicine question. The emergency doctor only knows the patient is hypotensive and tachycardic. He may suspect acute adrenal insufficiency based on history, and he may suspect hyperkalemia, again based on history or perhaps even an EKG done in triage, but for most of us that patient would get a liter of saline long before we knew he was hyperkalemic.

How many of us have had a tachycardic, hypotensive patient that we made the diagnosis of hyperkalemia prior to getting the labs back? It doesn't happen very often. The EKG changes are pretty subtle until the hyperkalemia is severe.

agree- I was waiting for someone else to be brave enough to state the obvious....
 
Didn't I do that about 12 posts back? ;)

yes -you did answer the priorities question but desparado actually made the point that you probably won't even recognize the lytes abnormalities until labs come back.
 
desparado actually made the point that you probably won't even recognize the lytes abnormalities until labs come back.

It's not really a "medicine question"...it's an emergency medicine question. You don't even have to know how to manage adrenal insufficiency in order to get the right answer...you just have to recognize the importance of the ABCs. These sort of questions pop up all the time on the boards. Don't overthink the obvious.
 
If ya'll will pardon my ignorance for a moment... what causes the hyperkalemia? Insufficient aldosterone leads to lowered output of the K-Na-Cl channel in the tubule?

(step 1 coming up for me :p )
 
It's not really a "medicine question"...it's an emergency medicine question. You don't even have to know how to manage adrenal insufficiency in order to get the right answer...you just have to recognize the importance of the ABCs. These sort of questions pop up all the time on the boards. Don't overthink the obvious.

The way the OP is worded it isn't a board question at all. On an EM exam, the stem would be something like:
Hypothetical board question said:
A patient presents to the ED with mental status change, BP 82/45, HR 129 RR 24 and Temp 38C. The son tells you the patient has been treated with prednisone for years for his rheumatoid arthritis but ran out 2 days ago. His EKG is below (figure 1 shows an EKG with normal QRS duration, slightly prominent vs peaked Twaves, normal QT interval, no acute ST changes, etc). Which of the following should you do first after establishing IV access and placing the patient on a cardiac monitor and oxygen?

You certainly wouldn't be given a diagnosis or a lab value before stablizing the patient. The history would make you think about adrenal insufficiency and perhaps sway you to give steroids; the EKG makes you think hyperkalemia in the setting of possible adrenal insufficiency and may sway you to give Calcium. But good test taking in an EM board test means you do ABCs first and give NS.
 
On an EM exam, the stem would be something like...

On the family med boards, it would probably look more like this:

Mr. Jones is an 18-year-old caucasian male who you have been taking care of since birth. He has done well in school, and is the quarterback for the local high school football team. His mother brings him to your office because he has not been feeling well for the past three weeks, complaining of generalized weakness and a 10-pound weight loss. Although it is early Spring, he seems to have developed a suntan. His blood pressure is 82/45, heart rate is 129, respiratory rate is 24, and temperature is 38C. His EKG is shown below (Figure 1 shows an EKG with normal QRS duration, slightly prominent vs peaked T waves, normal QT interval, no acute ST changes, etc). Which of the following should you do first?

A) Direct patient's mother to take him to the local ED for urgent evaluation to rule out acute adrenal insufficiency
B) Send off labs, including a CBC, CMP, TSH, and cortisol level
C) Refer to endocrinology
D) Prescribe a Z-Pack

(Kidding...we get the same lame-ass questions you guys get.) ;)
 
This reminds me of an actual patient a week or two ago. This is how the conversation went:

ER Doc: Hey BellKicker, we have this guy that probably needs to come in.

Me (thinking): Be a wall, be a wall....

ER DOC: So, he's been vomiting for a few days; probably that norovirus that's been going around. The thing is he is really orthostatic. We just can't get him up.

Me: No fever? He's not septic?

ER DOC: No

Me: He's not throwing up his prednisone or anything like that?

ER DOC: (while frantically clicking away on the computer)... Erm, no he's not on steroids.

As it turned out, he was on prednisone for PMR....:cool:

Lesson of the story is that fluids, labs, EKGs etc. are long done when the thought of (relative) adrenal insufficiency even comes up.

And in our ICU, we give roids to almost everyone so the finer points are often lost.

For the USMLE'ers out there, the reason we give dexamethasone over, say, solumedrol is not that dex doesn't suppress ACTH production (it does) but rather that it does not interfere with the cortisol assay (in the ACTH stim test).
 
For the USMLE'ers out there, the reason we give dexamethasone over, say, solumedrol is not that dex doesn't suppress ACTH production (it does) but rather that it does not interfere with the cortisol assay (in the ACTH stim test).

This would be an error. It is important to get mineralcocorticiod effect to treat the shock and the electrolyte problems. Dex won't do that and fludrocrotisone (the only mineralocorticoid available) is an oral med. Pt will not be able to keep it down.

The correct answer both from EM and the endocrine docs is to draw a stat cortisol and give hydrocortisone in doses high enough to attach to the aldosterone receptor in the kidney (100mg every 8 hours). After the taper in a few days, if the patient is still with us, you can worry about testing.:)
 
Correct me if I'm wrong, but I just read this chapter in tintinalli's.
typically the adrenal crisis that occurs with exogenous steroid withdrawal (ie prednisone patient who stops suddenly) is secondary Adrenal insufficiency and there is no hyperkalemia associated with this as aldosterone is NOT under the control of the hypothalamic/pituitary axis, but rather is controlled by the renin-angiotensin-aldolsterone system. Hyperkalemia in itself stimulates the kidneys directly to secrete aldosterone.

so unless you have primary Adrenal insufficiency (ex. addison's) then aldosterone isn't typically affected.

It seems as if everyone always assumes that if you have adrenal crisis you'll have hyperkalemia when in reality the most common cause of adrenal crisis is withdrawal of exogenous steroids and that doesn't affect aldosterone production/secretion.

However, you'll of course see hypoglycemia, hypotension, mental status changes etc....

just an observation.

later
 
Correct me if I'm wrong, but I just read this chapter in tintinalli's.
typically the adrenal crisis that occurs with exogenous steroid withdrawal (ie prednisone patient who stops suddenly) is secondary Adrenal insufficiency and there is no hyperkalemia associated with this as aldosterone is NOT under the control of the hypothalamic/pituitary axis, but rather is controlled by the renin-angiotensin-aldolsterone system. Hyperkalemia in itself stimulates the kidneys directly to secrete aldosterone.

so unless you have primary Adrenal insufficiency (ex. addison's) then aldosterone isn't typically affected.
later

Yes. I was just about to write the same thing.

In primary adrenal insufficiency (Addison's, bleeds, TB, histo), you need to worry about mineralocorticoid production. Of course this is very very rare. BKN certainly has a point in that not all glucocorticoids are created equal with regards to mineralocorticoid effect. Hydrocortisone is the most "mineralo" of the bunch but don't forget that is has 125 less potency than fludrocortisone.

As an aside, although cortisol (=hydrocortisone) does have mineralocorticoid effects in supra-physiologic doses, it has no sich effect in physiologic doses. There are exceptions to that rule. Two well-described conditions, apparent mineralocorticoid excess (AME) and licorice ingestion, lend the mineralocorticoid receptors more sensitive to cortisol. These are important for medicine boards but probably less so for EM boards.

Now, in secondary adrenal insufficiency, like steroid withdrawal or pituitary insult, you don't need to worry about mineralocorticoid effect. ACTH does have a slight, but important, permissive effect on aldosterone production so florinef can still be a consideration in very long-standing secondary adrenal insufficiency.

But.... then there's "relative adrenal insufficiency" and this is where the ACTH (cosyntropin) stim test comes in. If you have a septic patient, he may or may not be able to mount a proper cortisol response. Most recommendations go like this:

Start Dex on admission to the ICU

Do a Stim test

If your delta cortisol (change before and after 250 mcg cosyntropin) is less than 9, you treat.

If your delta is more than 9 some and your patient seems to be improving, you still treat. There is little evidence for this approach; in fact, a big study (CORTICUS) is coming out this summer to clarify this approach. Which agent to use? No one knows. Once your stim test is done, you can use whatever you want. Hydrocortisone is best studied (including in CORTICUS). Some studies include florinef, some don't.

If your delta is more than 9 and the cortisol does not seem to make the patient better, you stop. Although in real life lots of people will keep it going.

BKN brings up baseline cortisol. That's a nebulous concept in relative adrenal insufficiency. The problem is lab variability, physiologic variability. There is no censusus regarding interpretation. However, most people would say that a cortisol greater than 25 is sufficient. Less than 2 is diagnostic for adrenal insufficiency - but it's never less than two.

I should say that a baseline cortisol in primary or secondary adrenal insufficiency is clearly indicated and I believe that's what BKN was talking about.
 
Yes. I was just about to write the same thing.

In primary adrenal insufficiency (Addison's, bleeds, TB, histo), you need to worry about mineralocorticoid production. Of course this is very very rare. BKN certainly has a point in that not all glucocorticoids are created equal with regards to mineralocorticoid effect. Hydrocortisone is the most "mineralo" of the bunch but don't forget that is has 125 less potency than fludrocortisone.

As an aside, although cortisol (=hydrocortisone) does have mineralocorticoid effects in supra-physiologic doses, it has no sich effect in physiologic doses. There are exceptions to that rule. Two well-described conditions, apparent mineralocorticoid excess (AME) and licorice ingestion, lend the mineralocorticoid receptors more sensitive to cortisol. These are important for medicine boards but probably less so for EM boards.

Now, in secondary adrenal insufficiency, like steroid withdrawal or pituitary insult, you don't need to worry about mineralocorticoid effect. ACTH does have a slight, but important, permissive effect on aldosterone production so florinef can still be a consideration in very long-standing secondary adrenal insufficiency.

But.... then there's "relative adrenal insufficiency" and this is where the ACTH (cosyntropin) stim test comes in. If you have a septic patient, he may or may not be able to mount a proper cortisol response. Most recommendations go like this:

Start Dex on admission to the ICU

Do a Stim test

If your delta cortisol (change before and after 250 mcg cosyntropin) is less than 9, you treat.

If your delta is more than 9 some and your patient seems to be improving, you still treat. There is little evidence for this approach; in fact, a big study (CORTICUS) is coming out this summer to clarify this approach. Which agent to use? No one knows. Once your stim test is done, you can use whatever you want. Hydrocortisone is best studied (including in CORTICUS). Some studies include florinef, some don't.

If your delta is more than 9 and the cortisol does not seem to make the patient better, you stop. Although in real life lots of people will keep it going.

BKN brings up baseline cortisol. That's a nebulous concept in relative adrenal insufficiency. The problem is lab variability, physiologic variability. There is no censusus regarding interpretation. However, most people would say that a cortisol greater than 25 is sufficient. Less than 2 is diagnostic for adrenal insufficiency - but it's never less than two.

I should say that a baseline cortisol in primary or secondary adrenal insufficiency is clearly indicated and I believe that's what BKN was talking about.

I've written a big reply twice for this and the posts are getting submitted. Bah, I'm waiting till tonight.
 
So here is my take on it. Way back when I used to read I remember reading that the hypotension of Addisonian crisis was multifactorial. First, due to volume loss from the intractable N/V. Second you actually need glucocorticoids for your body to respond to endogenous or exogenous adrenergics, this was news to me at the time. Third, loss of mineralocorticoid effect. So, you treat one right away with NS. You treat two with Dex as soon as you can. I also recall reading that this was one of the weird steroid effects that didn't require the usuall 6 hour course of steroid binds to receptor which translocates to nucleus thus altering gene expression which eventually results in changes in protein expression which eventually results in a downstream effect. You worry about 3 after you've done your stim test.

To the question of EM vs IM diagnosis. I've diagnosed one classic primary Addison's disease and a handful of secondary Addisonian crises without the benefit of any labs. In none of those cases was the K high enough to do anything about. I did have the advantage in the Addison's disease case of the patient arriving with a note from the PCP (peds or FP I can't remember) that said, "Please rule out Addison's disease"
 
  • Like
Reactions: 1 user
Yes. I was just about to write the same thing.

In primary adrenal insufficiency (Addison's, bleeds, TB, histo), you need to worry about mineralocorticoid production. Of course this is very very rare. BKN certainly has a point in that not all glucocorticoids are created equal with regards to mineralocorticoid effect. Hydrocortisone is the most "mineralo" of the bunch but don't forget that is has 125 less potency than fludrocortisone.

As an aside, although cortisol (=hydrocortisone) does have mineralocorticoid effects in supra-physiologic doses, it has no sich effect in physiologic doses. There are exceptions to that rule. Two well-described conditions, apparent mineralocorticoid excess (AME) and licorice ingestion, lend the mineralocorticoid receptors more sensitive to cortisol. These are important for medicine boards but probably less so for EM boards.

Now, in secondary adrenal insufficiency, like steroid withdrawal or pituitary insult, you don't need to worry about mineralocorticoid effect. ACTH does have a slight, but important, permissive effect on aldosterone production so florinef can still be a consideration in very long-standing secondary adrenal insufficiency.

But.... then there's "relative adrenal insufficiency" and this is where the ACTH (cosyntropin) stim test comes in. If you have a septic patient, he may or may not be able to mount a proper cortisol response. Most recommendations go like this:

Start Dex on admission to the ICU

Do a Stim test

If your delta cortisol (change before and after 250 mcg cosyntropin) is less than 9, you treat.

If your delta is more than 9 some and your patient seems to be improving, you still treat. There is little evidence for this approach; in fact, a big study (CORTICUS) is coming out this summer to clarify this approach. Which agent to use? No one knows. Once your stim test is done, you can use whatever you want. Hydrocortisone is best studied (including in CORTICUS). Some studies include florinef, some don't.

If your delta is more than 9 and the cortisol does not seem to make the patient better, you stop. Although in real life lots of people will keep it going.

BKN brings up baseline cortisol. That's a nebulous concept in relative adrenal insufficiency. The problem is lab variability, physiologic variability. There is no censusus regarding interpretation. However, most people would say that a cortisol greater than 25 is sufficient. Less than 2 is diagnostic for adrenal insufficiency - but it's never less than two.

I should say that a baseline cortisol in primary or secondary adrenal insufficiency is clearly indicated and I believe that's what BKN was talking about.

OK I'm going to try this again. I claim no special expertise except experience and that I wrote the chapter on Pituitary and Adrenal emergencies for the Adam's EM test. The book hasn't been published yet, nor do I know when and if it will be.

1.The original question as posted is a case of acute primary adrenal insufficiency with hypotension, tachycardia and hyperkalemia. I agree with some of the other posters, that you would never know get all four facts simultaneously. If you did somehow, you would do all three treatments simultaneously. But for the board question (if that's what it was), shock gets treated first by crystalloids. And I still maintain that the program in my previous post is the correct one.

The comment that the cortisol level is always above 2 is untrue, I had a patient this week with a level of 1.6. The comment that primary crisis is "very, very rare" is overstating it a bit. I've diagnosed several including the patient this week. Maybe uncommon would be a better adjective.

2. It is true that secondary insufficency does not generally require mineralocorticoid effect. On the other hand, if the disease is secondary to steroid withdrawal, you already know what the problem is, and don't need the stim test.

3. The diagnosis of "relative adrenal insufficency" in a seriously ill patient is both controversial and confusing. The ICU docs seem to have an easier time believing in this entity than do the endocrine guys. These patients generally have very high cortisols before the test due to an "internal" stress test from their illness. The question seems to be how much is enough. Some have proposed a level of 19, others of 29. An additional problem is that the higher the cortisol level, that higher the mortality. From this came the short stim test with a change of less than 9 being used to justify the treatment. I believe that the value was chosen to find the maximum the difference in mortality in those studied. but as Kicker has said, that doesn't translate to a clinical trial. Perhaps the people who don't respond as well to the stim test are simply closer to dying, and the addition of steroids won't help them as much it would the others.

I can remember when we got in trouble with the Internists and the ID guys if we gave antibiotics before cultures were obtained ( meningitis and pneumonia). But we were right, now it's the standard of care to get those bug killers in as soon as we can. Using the same logic, this is what I suggest for patients in noncardiogenic shock who have not responded to fluids followed by pressors:
1. draw a cortisol level
2. give them hydrocortisone 100 mg iv q 8 hours
3. call the unit and let themm worry about a stim test after the patient survives the disaster. :)


p.s. I'll post my bibliography on Wendesday when I'm in the office.
 
  • Like
Reactions: 1 user
BKN,

Great post:thumbup:

Only on SDN can you slug out cortisol levels with a PD - who wrote the book:eek: . At least I am not applying to your program; that would make it really weird.

I think we agree on this issue, except for a few things.

1) I think there is value in a stim test. I agree with the theoretical bonus of getting a (slight) mineralocorticoid effect from hydrocortisone over dexmathasone but I don't think that effect beats the information you get from a stim test.

This is my vantage point: I'm a medicine resident ; I admit to an open ICU every call night and we always get stims on the non-cardiogenic shock patients. Like you say, it tells us about how sick a patient is. If someone stims from 5 to 8, you know you have to push the steroids. Maybe you think Xigris, too, if the patient meets criteria. If someone stims from 18 to 35, we might still keep the steroids going but it's still usefull information.

I don't think I have ever stimmed someone after they got better. First of all, the hydrocortisone would ruin the test and I don't know what I would do with the information. Of course this is all about "relative" adrenal insufficiency. In primary adrenal insufficiency, you're probably right; I don't claim to know too much about those folk.

2) According to eMedicine, primary adrenal insufficiency is rare, whatever that means. In my view, such a patient represents a super-cool work-up. I have only seen one and that was on my endo month. So in my mind Addison's is almost a zebra. Maybe I have missed a few of them without knowing; that's certainly possible. Wait a minute, it does seem like I have had a lot of hyperpigmented people die from hypotension and hyperkalemia lately.:(......

I am switching to EM next year, so maybe I'll be shocked by the number of Addison's I'll see coming in. Maybe they are mostly kids?
 
I was wondering if a smart person can help me with this question.

If a patient presents with acute adrenal insufficiency w/tachycardia, hypotension, and hyperkalemia. What is the 1st step in managment?

A) Steroids
B) Infusion of Normal Saline
C) Calcium Gluconate (for hyperkalemia)

Is there an algorithim for this? What do you do 1st than 2nd etc.

Thanks to the smart person
I was wondering if a smart person can help me with this question.

If a patient presents with acute adrenal insufficiency w/tachycardia, hypotension, and hyperkalemia. What is the 1st step in managment?

A) Steroids
B) Infusion of Normal Saline
C) Calcium Gluconate (for hyperkalemia)

Is there an algorithim for this? What do you do 1st than 2nd etc.

Thanks to the smart person


i have adrenal insufficiency and have been in crisis several times. Steroids and fluids are first. You must get patient out of crisis with steroids and get the blood pressure up with fluids. Just never forget the importance of steroids when in crisis. Y'all are making it way too hard. If you don't start steroids, then the other problems won't matter to a dead patient.
 
Correct. Board questions are easy when you know the answer...they become hard when you have to think about them. ;)

On the boards, ABCs always come first.
That's the trouble with board questions. They are questions..not real people. A patient with acute adrenal insufficiency needs steroids first.
 
This thread is making me even more confused. According to Goljan's audio, in this USMLE situation you would give steroids 1st to correct the problem. Did he make a mistake? Also, in Washington Manual it states give steroids too.

I always thought that ABC should come first but I am not sure any more. As for the Calcium Gluconate (this is cardioprotective). You can work all you want with ABC's, however acute hyperkalemia can lead to immediate death via v. fib. Isn't this more important for the 1st step? Who knows? I heard the exact value of the hyperkalemia is beside the point because people with chronic hyperkalemia can survive for a long time. Acute hyperkalemia is dangerous for arrthymias because immediate changes in K+ is detrimental to the cardiac electrical system.

Man, I am totally confused now. Help!
I've been through this several times as a patient in adrenal crisis. You must get steroids first!
 
I've been through this several times as a patient in adrenal crisis. You must get steroids first!
The problem is that these patients often don't come in with a sign around their neck saying "adrenal crisis."
 
  • Like
Reactions: 1 user
I've been through this several times as a patient in adrenal crisis. You must get steroids first!

Plus technically you could hang fluids in about 30 seconds versus several minutes to give steroids. Therefore fluids would come first just based on ease of delivery.
 
I've been through this several times as a patient in adrenal crisis. You must get steroids first!
So if you get IV fluids first you die?
 
  • Like
Reactions: 1 user
For God's sake, hold the fluids on that hypotensive pt! I'm having a hard time picturing that one.

Man, talk about the lazarus effect. 2006 thread?
 
  • Like
Reactions: 1 user
It's my FAVORITE when patients come on the forum and resurrect 10 year old threads to "inform" medical professionals based on their well-intentioned but largely incomplete understanding of their disease. *Sarcasm Alarm going bananas* At least I guess this is a real disease and not part of the chronic panc/end-stage fibro/chronic fatigue/chronic lyme/supratentorial total body dolor spectrum
 
  • Like
Reactions: 1 users
It's my FAVORITE when patients come on the forum and resurrect 10 year old threads to "inform" medical professionals based on their well-intentioned but largely incomplete understanding of their disease. *Sarcasm Alarm going bananas* At least I guess this is a real disease and not part of the chronic panc/end-stage fibro/chronic fatigue/chronic lyme/supratentorial total body dolor spectrum

Especially when the discussion is centered about a boards question rather than real life. Heck, for boards purposes, even the 'complete' understanding of an experience professional may be wrong. ABEM General is a special place.
 
Especially when the discussion is centered about a boards question rather than real life. Heck, for boards purposes, even the 'complete' understanding of an experience professional may be wrong. ABEM General is a special place.

Your statement demonstrates the absurdities of many of our certifying exams. If many practicing, board-certified EM physicians can get the question "wrong", then does the question/test have any validity?
 
  • Like
Reactions: 1 user
Your statement demonstrates the absurdities of many of our certifying exams. If many practicing, board-certified EM physicians can get the question "wrong", then does the question/test have any validity?

Sometimes. I can think of a couple of situations:

1) Topics that we've sort of agreed as a specialty (or at least the leaders of our organizations have) we should know about, but don't really have a bearing on our daily practice: bioterrorism agents, disaster related stuff, at least awareness of tox stuff, etc.

2) Topics that have emerged recently recently but have become super important yet older physicians might not be as up on it if it wasn't for requiring recertification: ARDSnet/lung protective ventilation, BiPAP, etc.

But I agree with you. Unfortunately most 'weird' board exam questions (ones you would never answer based on real life knowledge) do not fall into those categories, but are rather topics that are just easy to write exam questions about. HepB serologies, I am looking at you!
 
Top