Time for some clinical discussion

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Noyac said:
I think you are right pgg. Both prednisone and Dexamethasone are glucocorticoid steroids. Therefore if this were an adisonian crisis Dexamethasone should work fine.

Anyone know how I knew this wasn't an adisonian crisis? This is important to know because both conditions, vasoplegia and adisonian crisis manifest similarly in the OR, but are treated differently.
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I would say based on the normal(ish) electrolytes, no hypoNa+, hyperK+, or hyperCa++.
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twoliter said:
I would say based on the normal(ish) electrolytes, no hypoNa+, hyperK+, or hyperCa++.
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Yes that's part of it. What I focused on was that this pt wasn't on exogenous steroid therapy which would rule out secondary adisonian disease. Also, more importantly he had worsening glucose control and significant HTN. ADisons disease is hypoglycemic and hypotensive, among other things.
 
Nice discussion. Not to hijack but do any of you ever cancel an elective case if patient takes an ace inhibitor or arb on the day of surgery?
 
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Re: methylene blue: I had a case of profound vasoplegia the other day in the heart room. It was barely responding to big doses of vaso (like 5 units a push q 5-10 minutes), norepi, epi, phenyl. We gave 0.5mg/kg x2 of methylene blue, and within about 20 minutes, the pressors were working much better. We had ruled out other causes of hypotension, no excessive bleeding, contractility was fair on echo, no new drugs to cause anaphylaxis, no hx of steroids, ventilatory parameters were unchanged, volume status on echo, CVP and PADP were adequate (yes, i realize the limitations of static measures for predicting volume responsiveness), so it must have been vasoplegia. I haven't used it more than a handful of times, but it works well when it does work.
 
Sonny Crocket said:
Nice discussion. Not to hijack but do any of you ever cancel an elective case if patient takes an ace inhibitor or arb on the day of surgery?
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No and our group through our PAC actually tells them to take all of their antihypertensives.

Pick your poison: a bunch of 210/110 bps prior to induction or the occasional (usually quite treatable) ACE/ARB induced hypotension.
 
I prefer the former, as long as it's not chronic.
 
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okayplayer said:
No and our group through our PAC actually tells them to take all of their antihypertensives.

Pick your poison: a bunch of 210/110 bps prior to induction or the occasional (usually quite treatable) ACE/ARB induced hypotension.
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Vasoplegia is not something I like playing with. I'd much rather 210/110.

But I haven't cancelled a case because they took their ACE/ARB.

On another note, I find the ARB's more troublesome. Anyone else?
 
geogil said:
Re: methylene blue: I had a case of profound vasoplegia the other day in the heart room. It was barely responding to big doses of vaso (like 5 units a push q 5-10 minutes), norepi, epi, phenyl. We gave 0.5mg/kg x2 of methylene blue, and within about 20 minutes, the pressors were working much better. We had ruled out other causes of hypotension, no excessive bleeding, contractility was fair on echo, no new drugs to cause anaphylaxis, no hx of steroids, ventilatory parameters were unchanged, volume status on echo, CVP and PADP were adequate (yes, i realize the limitations of static measures for predicting volume responsiveness), so it must have been vasoplegia. I haven't used it more than a handful of times, but it works well when it does work.
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What was the cause in your case?
 
Noyac said:
Vasoplegia is not something I like playing with. I'd much rather 210/110.

But I haven't cancelled a case because they took their ACE/ARB.

On another note, I find the ARB's more troublesome. Anyone else?
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I think it mostly has to do with the t1/2 of the drug. That's why sometimes even if they do hold it you can get burned on the ultra long acting ARBs/ACEs.
 
Noyac said:
On another note, I find the ARB's more troublesome. Anyone else?
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Uggh... losartan. I agree.

I told a story sometime back about a urologist who insisted that none of his patients receive a pressor - any pressor - during a case. And his patients would never have their ACE-I/ARB held preoperatively. It was a real nightmare trying to manage his patients intraoperatively. He would refer cases to peer-review if he found out you were even giving neo for hypotension and the case didn't go as he expected for any reason. The prototypical "it's anesthesia's fault" a-hole. Thought he knew more about anesthesia than the person giving it. Fortunately I don't work there anymore and have to interact with that jerk.

You know what they say? You play with dicks long enough eventually you turn into one.
 
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Libertas said:
I know of an attending who will induce every patient on an ace/arb with etomidate.
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The problem I see with this is that it would confuse the hypotension issue. I have seen adrenal suppression with a single dose of etomidate. I find this a bad idea.
 
oh I think its a bad idea too. Just interesting that some are so afraid of ace/arb. I think the true refractory hypotension caused by them is very uncommon, though
 
Etomidate is a drug that no one should use. There's just no reason. I haven't used it in over 5 years.

Vasopressin on the other hand gets used frequently in refractory hypotension for ACE-I/ARB patients. Works quite nicely.
 
pgg said:
Yes it is. It's always a bad idea to use etomidate.

Unless you're an ER doc who needs some procedural "sedation" ... :)
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It's been proven again and again that one dose of etomidate does not produce clinically significant adrenal suppression and all the other BS. Not even in ICU patients. I never use it anymore, but then I never feel like I need it.

I try not to label medications as unusable, like it's Animal Farm: four feet good, two feet bad! There are very few truly bad drugs. In the right hands, almost every medication can be put to good use, otherwise it would have never made it to market. And usually, the older a medication the more well-known and safer.

When I started work as an attending, there were a few old timers who used to reverse muscle relaxants with physostigmine. It felt so archaic, but it worked perfectly for them every time. So who am I to judge them?
 
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FFP said:
It's been proven again and again that one dose of etomidate does not produce clinically significant adrenal suppression and all the other BS. Not even in ICU patients. I never use it anymore, but then I never feel like I need it.

I try not to label medications as unusable, like it's Animal Farm: four feet good, two feet bad! There are very few truly bad drugs. In the right hands, almost every medication can be put to good use, otherwise it would have never made it to market. And usually, the older a medication the more well-known and safer.

When I started work as an attending, there were a few old timers who used to reverse muscle relaxants with physostigmine. It felt so archaic, but it worked perfectly for them every time. So who am I to judge them?
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You do know that there are numerous medications that have been pulled off the market after they were originally approved by the FDA due to post-marketing surveillance? Just look at the majority of the meds in the COX-2 class as one example.

And I don't agree with you that etomidate has "been proven again and again" not to be a problem, especially in sickies.

http://www.ncbi.nlm.nih.gov/pubmed/22971586

http://www.ncbi.nlm.nih.gov/pubmed/21373823

http://www.ncbi.nlm.nih.gov/pubmed/20530707

And this limited meta-analysis published recently in Chest, which many accept as "proof" that a single dose isn't an issue, admits its own limitations and calls into question its own conclusion:

http://www.ncbi.nlm.nih.gov/pubmed/25255427

Want an alternative in this patient population? Consider ketamine.

http://www.ncbi.nlm.nih.gov/pubmed/19573904
 
FFP said:
It's been proven again and again that one dose of etomidate does not produce clinically significant adrenal suppression and all the other BS. Not even in ICU patients. I never use it anymore, but then I never feel like I need it.
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This is wrong. I have seen it. Years ago when I was a younger bull I had a late 30's man for emergent abdominal surgery. I don't recall all the particulars of the case but if I used etomidate then this guy was a bit sick. The case went well and this guy had a strong heart. But I just couldn't get his BP to a respectable level and stay there. So we decided to admit him to the ICU. The next day when I went to see him he was sitting up looking like a peach. The ICU doc gave him steroids and his BP nearly instantly improved and the pressers were discontinued. I don't think I ever used it again. I am very sure it can cause adrenal suppression with one dose.

It's very possible people don't see it since we give so much decadron in surgery. Answer give it early.
 
I just hate the way medications are labeled bad in the US, and then just thrown away. COX-2 inhibitors were an example. Mivacurium hits close to to home. We seldom use droperidol anymore because of, OMG, long QT! If we were thinking the same way about surgical procedures, we shouldn't do many of them, even elective ones, because, heck, some people even die intra-/postop. OMG!

As I said, I rarely think about etomidate. Also, I had the pleasure of an etomidate shortage years ago, so I learned to replace it (with low-dose propofol or ketamine). But I don't think it's such a bad drug that I want to forget it (plus, as Noyac said, one can give a steroid dose if one sees signs of adrenal suppression - which lasts up to 24 hours, and one can avoid giving it to septic patients). I have used it countless times during residency, and I can't remember one bad outcome (but I also give decadron to every non-TIVA patient). Would I use it in the sickest ICU patients? Will report back next year. :)
 
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Just curious, in the original case when you were using vaso did you run it via central access? And if so, when did you obtain central line?
 
Shimmy8 said:
Just curious, in the original case when you were using vaso did you run it via central access? And if so, when did you obtain central line?
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We are Anesthesia...

We are pretty good at getting a well-flowing IV, making sure an existing IV is not infiltrated, and checking on it periodically, so we can run (even bolus) certain pressors on a peripheral IV, without harming the patient.

The same way we can muscle relax patients with just an LMA in place, or we can put in A-lines with regular gloves, without the entire sterile show (they are not CVCs, for Pete's sake!), or we can put IVs even in anatomic locations that would require quasi-CEO approval for other people, or we can run ketamine on the floor etc.

We are Anesthesia, pam-param-pa-pam-pam-pam!
 
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Appreciate the responses.

I was just imagining this playing out at my institution. Unexplained hypotension requiring large amounts of pressors probably would have bought this patient a central line after the procedure, of course, as always, depends on the attending.

Plus the ICU would be much appreciative.
 
Nice case Noyac. We were overdue for a good case. My $0.02...

50-90mcg/min phenylephrine, and 4+ units/hr vasopressin, is an outrageous dose. This is not vasodilation due to anesthesia. If you are running those doses you are masking a problem.

Vasoplegia happens. In a year in the ICU we saw this all the time. Often, ESRD patients, some end stage liver, some hepatorenal but most not. They get septic and they just NEVER clear their "evil humors." They sit there eating lunch while on 4mcg/min norepi and 2.4 units/hr vaso. You check a cortisol, it's normal, eventually you uptitrate the midodrine and the fludrocortisone and they get off pressors and gtfo. It happens.

Yeah for the record guys, decadron is NOT a good drug for adrenal insufficiency.

+1 for a bedside TTE to help you in the original scenario. Anesthesiology residents, if you are not being taught how to do bedside echo, bug your cardiac attendings until they teach you. This is your new stethoscope. Learn it.
 
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FFP said:
Probably the lack of mineralocorticoid effect.
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That's the point though; you don't need it or want it for secondary adrenal insufficiency due to steroid use.

Perioperative management of patients treated with glucocorticoids

p14 said:
As explained earlier, patients with glucocorticoid-induced secondary adrenal insufficiency do not have mineralocorticoid (aldosterone) deficiency. The mineralocorticoid activity of hydrocortisone may produce undesirable side effects including fluid retention, edema, and hypokalemia. Thus, it is preferable to use a glucocorticoid without mineralocorticoid activity when treating patients with this condition, especially when the total dose of hydrocortisone exceeds 100 mg per day.

...

Hypotension in patients previously treated with glucocorticoids is caused by loss of the permissive effect of glucocorticoids on vascular tone, which may be related in turn to enhanced PGI2 production in the absence of glucocorticoids. It is not caused by mineralocorticoid deficiency.
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Great educational post. I would add that the worse two intra-op cases of vasoplegia I have ever seen involved atypical anti-psychotics. One (an ENT procedure) necessitated a cancellation - which I rarely do. The other was VATs on a young schizophrenic patient that I limped along with various pressers. Both resolved at case conclusion but both stuck with me
 
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risnwb said:
From the following paper it appears that there are multiple mechanisms by which BOTH glucocorticoids and mineralocortacoids effect vascular tone.

http://m.cardiovascres.oxfordjournals.org/content/41/1/55.full
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That may be, but a measurable effect isn't necessarily clinically significant, and in any case a patient who's been getting prednisone, methylprednisolone, prednisolone, or dexamethasone won't have a mineralocorticoid deficiency that needs to be corrected.

Even if we have an adrenalectomized rat (or a legendarily etomidate-induced total adrenally suppressed patient?) where all endogenous corticosteroid production is gone, the concluding paragraph of that paper states:

The predominance of the evidence suggests that glucocorticoids and glucocorticoid receptors are more important than mineralocorticoids and their receptors in enhancing vascular tone. Yagil and Krakoff demonstrated that, in adrenalectomized rats, replacement with dexamethasone restored pressor responses to angiotensin II to normal, whereas replacement with aldosterone did not. Despite the fact that mineralocorticoids can bind to both mineralocorticoid receptors and glucocorticoid receptors and that glucocorticoids can bind to both glucocorticoid receptors and mineralocorticoid receptors, the receptor density of glucocorticoid receptors appears to be 20–30-fold greater than that of mineralocorticoid receptors in vascular tissue.
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Dexamethasone still appears to be the best correct answer to me.
 
pgg said:
Can you elaborate? What's wrong with it?
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a) It has no mineralocorticoid activity
b) It lasts longer than you really want it to
c) There's no evidence for its benefit in any condition pertinent to cardiovascular function
d) It's not the drug you mean to give -- (you actually mean to give hydrocortisone but are too lazy)

I acknowledge that the glucocorticoid effect is probably the dominant one in increasing catecholamine responsiveness in shock states, not the mineralocorticoid one...but the whole reason you're having this discussion is because the patient has a RELATIVE or ABSOLUTE hydrocortisone deficiency. Any argument that dexamethasone is better stems from the fact it's easily accessible in the drug drawer.
 
While we're on the topic of vasoplegia and shock folks, some more evidence for vasopressin being all killer, no filler.

Anesthesiology. 2014 Nov;121(5):930-6. doi: 10.1097/ALN.0000000000000430.
Vasoconstrictor responses to vasopressor agents in human pulmonary and radial arteries: an in vitro study.
Currigan DA1, Hughes RJ, Wright CE, Angus JA, Soeding PF.
Author information

Abstract
BACKGROUND:
Vasopressor drugs, commonly used to treat systemic hypotension and maintain organ perfusion, may also induce regional vasoconstriction in specialized vascular beds such as the lung. An increase in pulmonary vascular tone may adversely affect patients withpulmonary hypertension or right heart failure. While sympathomimetics constrict pulmonary vessels, and vasopressin does not, a direct comparison between these drugs has not been made. This study investigated the effects of clinically used vasopressor agents on human isolated pulmonary andradial arteries.

METHODS:
Isolated pulmonary and radial artery ring segments, mounted in organ baths, were used to study the contractile responses of each vasopressor agent. Concentration-response curves to norepinephrine, phenylephrine, metaraminol, and vasopressin were constructed.

RESULTS:
The sympathomimetics norepinephrine, phenylephrine, and metaraminol caused concentration-dependent vasoconstriction in the radial(pEC50: 6.99 ± 0.06, 6.14 ± 0.09, and 5.56 ± 0.07, respectively, n = 4 to 5) and pulmonary arteries (pEC50: 6.86 ± 0.11, 5.94 ± 0.05 and 5.56 ± 0.09, respectively, n = 3 to 4). Vasopressin was a potent vasoconstrictor of the radial artery (pEC50 9.13 ± 0.20, n = 3), whereas in the pulmonary artery, it had no significant effect.

CONCLUSIONS:
Sympathomimetic-based vasopressor agents constrict both human radial and pulmonary arteries with similar potency in each. In contrast, vasopressin, although a potent vasoconstrictor of radial vessels, had no effect on pulmonary vascular tone. These findings provide some support for the use of vasopressin in patients with pulmonary hypertension.
 
fakin' the funk said:
a) It has no mineralocorticoid activity
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Again, I feel like there's some kind of echo in here, but if you don't need the mineralocorticoid activity, who cares?

fakin' the funk said:
b) It lasts longer than you really want it to
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If a person is symptomatic from withdrawal of chronic steroid therapy, or if a rat has its adrenal glands whacked out, why is it preferable to use a short acting drug (hydrocortisone 1/2 life 8 hrs) rather than a longer acting drug (dexamethasone 36 hrs)? Why is it better to dose 100 mg q8h instead of 4 mg once? What's the downside to the longer acting drug?

fakin' the funk said:
c) There's no evidence for its benefit in any condition pertinent to cardiovascular function
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Do you disagree with the conclusions of the paper risnwb posted, particularly the part where it said dexamethasone restored pressor responses to normal?

fakin' the funk said:
d) It's not the drug you mean to give -- (you actually mean to give hydrocortisone but are too lazy)
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No reason to get condescending with accusations of laziness. I give the drugs I intend to give, even if they aren't the ones the surgeon helpfully staples to the chart.

Thus far in this thread I have read exactly zero reasons why dexamethasone is insufficient. Some perserverating on (irrelevant?) mineralocorticoid activity, but no good reasons.

fakin' the funk said:
I acknowledge that the glucocorticoid effect is probably the dominant one in increasing catecholamine responsiveness in shock states, not the mineralocorticoid one...but the whole reason you're having this discussion is because the patient has a RELATIVE or ABSOLUTE hydrocortisone deficiency. Any argument that dexamethasone is better stems from the fact it's easily accessible in the drug drawer.
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I think you're missing the forest for the trees here.

Set aside the question of whether or not dexamethasone is BETTER than hydrocortisone.

The question I'm interested in is whether dexamethasone is SUFFICIENT to treat the problem of secondary adrenal insufficiency causing hypotension refractory to vasopressors. And based on everything I've read, I think the answer is yes.


(edit to fix broken formatting)
 
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I can't disagree with you pgg. I was previously misinformed regarding the mechanism behind the cardiovascular response following stress dose steroids, and I really can't find any evidence against giving decadron instead of hydrocortisone...
 
I think some of the confusion has to do with time of onset of the relative glucocorticoids.

Hydrocortisone, being the analogue of human cortisol, is the fastest. This is what should be used in immediate shock states (like anaphylaxis). Decadron is clearly the most potent anti-inflammatory within the glucocorticoid family and has the longest duration of action. It is also the slowest onset.

That being said most of their ultimate effects are generally interchangeable with dosing, re-dosing, and withdrawal being the biggest issues. It just depends on how quickly and how long you want to see the effect.
 
risnwb said:
I can't disagree with you pgg. I was previously misinformed regarding the mechanism behind the cardiovascular response following stress dose steroids, and I really can't find any evidence against giving decadron instead of hydrocortisone...
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The main "evidence" AFAIK is based on two things: 1. endogenous cortisol is basically hydrocortisone 2. all important studies for steroid replacement have been done using hydrocortisone.
 
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