Stress Dose?? steroids

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The other thread got me thinking about a topic that I hadn't thought about in a while....I want to see/hear what other's opinions are.

One of the many goals of anesthesia is to "blunt" the so-called "stress response" that surgery causes, because the "stress response" ultimately causes many of our perioperative complications: dvt, pe, mi, stroke, chf decompensation, dm decompensation, etc.

The origins of these complications can be partially traced back to the rise of the stress hormones (adh, renin, alds, fib, cortisol, epi, norepi, etc.)which has a time course that is well documented in certain types of surgery...and which peaks often times HOURS after the surgery is over.

Certain surgeries have little or no change in these hormones while others have dramatic changes...and the differences correlate with the likelihood of complications.

As anesthesiologists, we strive to provide an anesthetic where we most effectively blunt this sequential/serial rise in the stress hormones. Regional anesthetics have been taunted as being the best at blocking this response...high dose narcotics does it fairly well also.

So, I find in interesting that while on one hand we try our very best the "blunt" this stress response or provide a "stress free" anesthetic, that on the other hand, patients with "naturally" blunted responses (no adrenal glands or HPA suppression due to steroid use) we want to AUGMENT it?

Thoughts?

Maybe it seems overly simply to me, but if you have a patient who has a complete run-out of native adrenal function secondary to prolonged suppression of their primary stress organ, they are likely to crash if their bodies attempts to draw on that reserve (cortisol) to support their cardiovascular system. ACTH is released as part of the stress response, but it doesn't effectively have an organ to work upon. And, as such, the patient just sort of fails to do well peri-operatively.

In practice, I've only seen this once so far. We had a patient who just was not doing well post-operatively. BP was staying in the 80's and blood sugar was persistently low despite therapy. Patient was tubed in the SICU. (I was on an ICU month, not part of the case.) We tried everything. Changed sedation strategy. Gave sugar. Went back to make sure there wasn't an ACE-I given. Thought it was some sort of autonomic dysfunction. We knew the patient had been on longterm prednisone for a vasculitis, but they'd gotten a "stress dose" (250mg solucortef) perioperatively. It was until POD#2 that we re-instituted standing solumedrol, and they got better. It was a big belly case, and I actually went back and looked at the scans myself and you could barely see just slivers of adrenal glands.

So, who knows. The above was a n=1 scenario. A lot of times I've had patients in for minor surgeries who've been on steroids and they either get no steroids or just 4mg of decadron and do fine.

-copro

Originally Posted by militarymd

So, I find in interesting that while on one hand we try our very best the "blunt" this stress response or provide a "stress free" anesthetic, that on the other hand, patients with "naturally" blunted responses (no adrenal glands or HPA suppression due to steroid use) we want to AUGMENT it?

Thoughts?

I see it as two different patient populations here ... and two different goals.

One is the healthy patient undergoing some form of stress (e.g. trauma, surgery) and it's nice to be able to blunt the stress response for the reasons you've outlined (MI, DVT, PE, stroke, CHF, etc ...). Ergo, an anesthetic that blunts the stress response.

But there is a different patient population that becomes excessively vasodilated in response to stress, either in the form of trauma (e.g. surgery), general anesthesia, or sepsis. And these are patients who, interestingly enough, have inadequate stress hormone (cortisol) on board, whether endogenous or exogenous. In this patient population, steroids somehow magically make everything all right.

In other words, good anesthesia is necessary to blunt the stress response in those who are able to mount one. Steroids are necessary to ultimately provide vasomotor tone in those who are, for lack of a better word, weak.

The cortisol surge in response to stress is a physiological defense mechanism that among other mechanisms allow the body to shift gears and handle more demanding situations.
It allows more glucose to be available for increased energy demands, it enhances the effects of catecholamines on the cardiovascular system, it allows more water and sodium retention which contribute to higher cardiac output and more efficient oxygen delivery.....
Anesthesia is not about depriving the patient of the ability to handle increased demands, its about minimizing the triggering factors (pain, hypovolemia, hypoxia....) that initiate that stress response.
If you are doing a good anesthetic and providing good post op pain control you should see the HPA axis as your friend not your enemy.

Originally Posted by TIVA

I see it as two different patient populations here ... and two different goals.

One is the healthy patient undergoing some form of stress (e.g. trauma, surgery) and it's nice to be able to blunt the stress response for the reasons you've outlined (MI, DVT, PE, stroke, CHF, etc ...). Ergo, an anesthetic that blunts the stress response.

But there is a different patient population that becomes excessively vasodilated in response to stress, either in the form of trauma (e.g. surgery), general anesthesia, or sepsis. And these are patients who, interestingly enough, have inadequate stress hormone (cortisol) on board, whether endogenous or exogenous. In this patient population, steroids somehow magically make everything all right.

In other words, good anesthesia is necessary to blunt the stress response in those who are able to mount one. Steroids are necessary to ultimately provide vasomotor tone in those who are, for lack of a better word, weak.

So when you say "weak" you mean only the HPA, and not all the other organ systems?...

Originally Posted by militarymd

So when you say "weak" you mean only the HPA, and not all the other organ systems?...

Yes.

Originally Posted by Planktonmd

Anesthesia is not about depriving the patient of the ability to handle increased demands, its about minimizing the triggering factors (pain, hypovolemia, hypoxia....) that initiate that stress response.
If you are doing a good anesthetic and providing good post op pain control you should see the HPA axis as your friend not your enemy.

Well-stated ... certainly more eloquently than I did.

Originally Posted by Planktonmd

The ........
Anesthesia is not about depriving the patient of the ability to handle increased demands, its about minimizing the triggering factors (pain, hypovolemia, hypoxia....) that initiate that stress response.
If you are doing a good anesthetic and providing good post op pain control you should see the HPA axis as your friend not your enemy.

So are you saying that if surgery were pain free, without blood loss, without hypoxia, then there would be no "stress response" and the "HPAxis axis" would not be needed?

Originally Posted by militarymd

So are you saying that if surgery were pain free, without blood loss, without hypoxia, then there would be no "stress response" and the "HPAxis axis" would not be needed?

No, that's not what I said.
But if you can minimize these triggers you will minimize the stress response of the HPA axis and other systems, and that's what good anesthesia is about.
Surgery will still trigger a degree of systemic inflammatory response no matter how good your anesthetic is.
I am not sure what you mean by saying:"HPAxis axis would not be needed"
Are you suggesting that we only need the HPA system under stress?

Originally Posted by Planktonmd

No, that's not what I said.
But if you can minimize these triggers you will minimize the stress response of the HPA axis and other systems, and that's what good anesthesia is about.
Surgery will still trigger a degree of systemic inflammatory response no matter how good your anesthetic is.
I am not sure what you mean by saying:"HPAxis axis would not be needed"
Are you suggesting that we only need the HPA system under stress?

typo.

I 'm thinking outloud here....or typing out my thinking here....

A spinal anesthetic completely abolishes the neurally mediated component of the stress response, and we say this is desirable.

So how is a patient's stress response who has a suppressed HPA axis having a total knee arthroplasty (intermediate risk...moderately invasive surgery) different from that of a person having a normal HPA axis having the same surgery under a spinal.

Now Obviously the cytokine-mediated component of the stress response still exists but is delayed, and the cortisol response to that is not as high (i think).

so ......should supplement steroids become necessary, does the timing change just because you're using a different anesthetic technique....

Originally Posted by coprolalia

Maybe it seems overly simply to me, but if you have a patient who has a complete run-out of native adrenal function secondary to prolonged suppression of their primary stress organ, they are likely to crash if their bodies attempts to draw on that reserve (cortisol) to support their cardiovascular system. ACTH is released as part of the stress response, but it doesn't effectively have an organ to work upon. And, as such, the patient just sort of fails to do well peri-operatively.

In practice, I've only seen this once so far. We had a patient who just was not doing well post-operatively. BP was staying in the 80's and blood sugar was persistently low despite therapy. Patient was tubed in the SICU. (I was on an ICU month, not part of the case.) We tried everything. Changed sedation strategy. Gave sugar. Went back to make sure there wasn't an ACE-I given. Thought it was some sort of autonomic dysfunction. We knew the patient had been on longterm prednisone for a vasculitis, but they'd gotten a "stress dose" (250mg solucortef) perioperatively. It was until POD#2 that we re-instituted standing solumedrol, and they got better. It was a big belly case, and I actually went back and looked at the scans myself and you could barely see just slivers of adrenal glands.

So, who knows. The above was a n=1 scenario. A lot of times I've had patients in for minor surgeries who've been on steroids and they either get no steroids or just 4mg of decadron and do fine.

-copro

I've seen this only once also (from 1993 to 2008)...at Washington Hospital Center in the ICU as a resident.

Almost exactly same scenario from what I remember...steroid hx...big abdominal case ...in OR for hours.....except the patient never got supplemental steroids....did fine until POD2 when he/she got transferred to the ICU with intractable hypotension....100 mg of hydrocortisone (that's what I used then as a resident) fixed the problem...patient was transferred out before the 2nd dose.

Originally Posted by militarymd

typo.

I 'm thinking outloud here....or typing out my thinking here....

A spinal anesthetic completely abolishes the neurally mediated component of the stress response, and we say this is desirable.

So how is a patient's stress response who has a suppressed HPA axis having a total knee arthroplasty (intermediate risk...moderately invasive surgery) different from that of a person having a normal HPA axis having the same surgery under a spinal.

Now Obviously the cytokine-mediated component of the stress response still exists but is delayed, and the cortisol response to that is not as high (i think).

so ......should supplement steroids become necessary, does the timing change just because you're using a different anesthetic technique....

In most cases if the patient with chronic adrenal insufficiency is receiving proper Glucocorticoid and Mineralocorticoid replacement and had a good anesthetic they will probably tolerate the intraoperative phase without any steroid supplement , but what about the post operative phase and what if things don't go as planned intraoperatively?
Do I really want to wait and see? or just go ahead and add some steroids initially?
I think this remains debatable and should be decided on a case by case basis.

HPA suppression is a common consequence of glucocorticoid therapy,
whereas overt secondary adrenal insufficiency is a rare but life-threatening
condition. Prolonged hypotension and a response to adequate doses of a
glucocorticoid agent are not reliable ways to assess adrenocortical func-
tion. One must also demonstrate plasma cortisol levels that are inappropri-
ately low for the clinical situation. 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 miner-
alocorticoid deficiency. Recurrent problems of study design and interpre-
tation have plagued this area of investigation. Any patient who has received
a glucocorticoid in doses equivalent to at least 20 mg a day of predni-
sone for more than 5 days is at risk for HPA suppression. If the doses
are closer to but above the physiologic range, 1 month is probably the
minimal interval. Recovery from prolonged exposure to high doses of
glucocorticoids may take up to 1 year. Pituitary function returns before
adrenocortical function. Recovery from short courses of treatment (eg, 5
days) occurs more rapidly, in about 5 days. Recovery is time-dependent and
spontaneous. The rate of recovery is a function of the dose and duration of
therapy before tapering is started and while the dose is being reduced.
ACTH therapy does not cause adrenocortical suppression but offers no
advantage over glucocorticoids, has several disadvantages, and should no
longer be used. Patients on alternate day glucocorticoid therapy have some
suppression of basal cortisol levels but have normal or nearly normal
responses to provocative tests of adrenocortical function. The standard
short ACTH stimulation test is a reliable means of assessing adrenocortical
function preoperatively. The low dose (1 lg) short ACTH test is promising

but has not been sufficiently well characterized, requires serial dilutions and
cannot be recommended at this time. Studies of the physiologic adreno-
cortical response to surgical stress provide a basis for revised dose
recommendations for perioperative coverage in the patient with known or
suspected HPA suppression. Recommendations of a multidisciplinary group
are presented.

L. Axelrod / Endocrinol Metab Clin N Am 32 (2003) 367–383

so, i think it's not so much about mounting a stress response. it's about preventing hypotension secondary to an impaired ability to vasoconstrict in the face of vasodilating anesthetics.

Originally Posted by Jeff05

HPA suppression is a common consequence of glucocorticoid therapy,
whereas overt secondary adrenal insufficiency is a rare but life-threatening
condition. Prolonged hypotension and a response to adequate doses of a
glucocorticoid agent are not reliable ways to assess adrenocortical func-
tion. One must also demonstrate plasma cortisol levels that are inappropri-
ately low for the clinical situation. 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 miner-
alocorticoid deficiency. Recurrent problems of study design and interpre-
tation have plagued this area of investigation. Any patient who has received
a glucocorticoid in doses equivalent to at least 20 mg a day of predni-
sone for more than 5 days is at risk for HPA suppression. If the doses
are closer to but above the physiologic range, 1 month is probably the
minimal interval. Recovery from prolonged exposure to high doses of
glucocorticoids may take up to 1 year. Pituitary function returns before
adrenocortical function. Recovery from short courses of treatment (eg, 5
days) occurs more rapidly, in about 5 days. Recovery is time-dependent and
spontaneous. The rate of recovery is a function of the dose and duration of
therapy before tapering is started and while the dose is being reduced.
ACTH therapy does not cause adrenocortical suppression but offers no
advantage over glucocorticoids, has several disadvantages, and should no
longer be used. Patients on alternate day glucocorticoid therapy have some
suppression of basal cortisol levels but have normal or nearly normal
responses to provocative tests of adrenocortical function. The standard
short ACTH stimulation test is a reliable means of assessing adrenocortical
function preoperatively. The low dose (1 lg) short ACTH test is promising

but has not been sufficiently well characterized, requires serial dilutions and
cannot be recommended at this time. Studies of the physiologic adreno-
cortical response to surgical stress provide a basis for revised dose
recommendations for perioperative coverage in the patient with known or
suspected HPA suppression. Recommendations of a multidisciplinary group
are presented.

L. Axelrod / Endocrinol Metab Clin N Am 32 (2003) 367–383

so, i think it's not so much about mounting a stress response. it's about preventing hypotension secondary to an impaired ability to vasoconstrict in the face of vasodilating anesthetics.

marik and zaloga

Originally Posted by Planktonmd

In most cases if the patient with chronic adrenal insufficiency is receiving proper Glucocorticoid and Mineralocorticoid replacement and had a good anesthetic they will probably tolerate the intraoperative phase without any steroid supplement , but what about the post operative phase and what if things don't go as planned intraoperatively?
Do I really want to wait and see? or just go ahead and add some steroids initially?
I think this remains debatable and should be decided on a case by case basis.

Pretty much covered by the 10 mg of dex that we use for ponv...but what about my scenario with the TKA patient

Originally Posted by militarymd

Pretty much covered by the 10 mg of dex that we use for ponv...but what about my scenario with the TKA patient

I am not sure that 10 mg of Dexamethasone has enough mineralocorticoid activity but could be.
The TKA under spinal really depends on the circumstances of the specific patient, most likely he will be fine inra-op and the post-op course would depend on how well his pain is managed, if he has any complications, and on how well his baseline exogenous steroid intake was compensating for his physiologic cortisol.

vent, should we sticky this thread?

Originally Posted by Planktonmd

I am not sure that 10 mg of Dexamethasone has enough mineralocorticoid activity but could be.
The TKA under spinal really depends on the circumstances of the specific patient, most likely he will be fine inra-op and the post-op course would depend on how well his pain is managed, if he has any complications, and on how well his baseline exogenous steroid intake was compensating for his physiologic cortisol.

the problems with HPA suppression and post op problems are not mineralocortoid related.

Originally Posted by militarymd

the problems with HPA suppression and post op problems are not mineralocortoid related.

Agree, it appears that it's more a glucocorticoid problem but you would think that if you want to replace cortisol you want both.