what's up here?

[Teillard]

Hold your fire, boys. I posted this on another forum and got over 60 views and exactly zero replies. Just looking for an attending consult if you get my drift. Here goes:

Seen this too many times to count now. O/W healty male or female for some kind of neck or lower back fusion. 30-60 yrs old, maybe smokes, normal hight and weight for the most part (the occasional fatso). Biggest item on their history is their chronic pain for which they are on at least two opiate analgesics (norco, oxycont. straight vicodin, whatever) and a muscle relaxant du jour. These for no less than three months, all day everyday. NO antidepressants on the patients I'm thinking of. Here's the deal. They get their pre-op versed and fentanyl which doesn't do anything, put them to sleep with completely stable vs and they absolutely hit the wall in that they are intolerant to even modest levels of vol. ax. for the entire case. Volume with modest gains on hemodynamics but what reaallly helps is neo and not ephedrine. The first couple of times I did this on a 3 or so level fusion I woke them up without any narcotic to speak of. Mistake. They'd go from supported blood pressure on 4% Des to no Des and coming off the table. Now I put 'em to sleep on appropriate vol. ax. (usually 6 or more of Des.) and give fentanyl on a per kg basis based on the surgical assault (3-4 lumbar levels start with 10-12 ug/kg fentanyl in the first half hour). I support their blood pressure with a neo infusion. 25-30 mins to the end of the case I get them breathing and titrate dilaudid to a RR of 12. Sometimes I'll give 8-10 mg of dilaudid on a case like the ones above and they open their eyes on the roll supine AND they say they're a little sore.

First thing I think is catecholamine depletion because ephedrine doesn't work and neo does. No steroids involved, no anti-depressants either. Making good urine too. What's up?

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[jetproppilot]

Hold your fire, boys. I posted this on another forum and got over 60 views and exactly zero replies. Just looking for an attending consult if you get my drift. Here goes:

Seen this too many times to count now. O/W healty male or female for some kind of neck or lower back fusion. 30-60 yrs old, maybe smokes, normal hight and weight for the most part (the occasional fatso). Biggest item on their history is their chronic pain for which they are on at least two opiate analgesics (norco, oxycont. straight vicodin, whatever) and a muscle relaxant du jour. These for no less than three months, all day everyday. NO antidepressants on the patients I'm thinking of. Here's the deal. They get their pre-op versed and fentanyl which doesn't do anything, put them to sleep with completely stable vs and they absolutely hit the wall in that they are intolerant to even modest levels of vol. ax. for the entire case. Volume with modest gains on hemodynamics but what reaallly helps is neo and not ephedrine. The first couple of times I did this on a 3 or so level fusion I woke them up without any narcotic to speak of. Mistake. They'd go from supported blood pressure on 4% Des to no Des and coming off the table. Now I put 'em to sleep on appropriate vol. ax. (usually 6 or more of Des.) and give fentanyl on a per kg basis based on the surgical assault (3-4 lumbar levels start with 10-12 ug/kg fentanyl in the first half hour). I support their blood pressure with a neo infusion. 25-30 mins to the end of the case I get them breathing and titrate dilaudid to a RR of 12. Sometimes I'll give 8-10 mg of dilaudid on a case like the ones above and they open their eyes on the roll supine AND they say they're a little sore.

First thing I think is catecholamine depletion because ephedrine doesn't work and neo does. No steroids involved, no anti-depressants either. Making good urine too. What's up?

Missing your drift.

What exactly is vol. ax. ???

 

[toughlife]

Missing your drift.

What exactly is vol. ax. ???

volatile anesthetics?

 

[Teillard]

volatile anesthetics?

Yeah, sorry. Volatile agent. Also a disclaimer. Blew this by both neurosurgeons and attendings.

 

[jetproppilot]

Yeah, sorry. Volatile agent. Also a disclaimer. Blew this by both neurosurgeons and attendings.

Nice post.

But I dont have an answer to your question of why you are seeing a hemodynamic drop from what you attribute to volatile anesthetics.

Your explanation of increased opiods makes sense....

but your question about a BP drop from gas....and it's response to neo and not ephedrine.....

not sure.

Maybe you are on to something that needs more investigation on this chronic-pain-type-of-patient that undergoes these procedures.

 

[stanleykristian]

Is it possible that these patients have an increased sympathetic outflow due to the chronic pain issues, possible they are relatively dry intravascularly due to increased vascular tone.

 

[Teillard]

I've thought about this. What might you see if you drew serum catechols pre and post induction, intra-op and post op? Cortisol levels, whatever? I guess I could ask the lab, but what would you draw them in, how would you treat the samples (ice, etc.) what kind of labs would they need to go to? How fast would they need to go?

 

[Teillard]

Is it possible that these patients have an increased sympathetic outflow due to the chronic pain issues, possible they are relatively dry intravascularly due to increased vascular tone.

They don't, in our experience, present hypertensive or treated for htn. At least not the ones referred to.

 

[stanleykristian]

chronic pain causes an increase in sympathetic outflow, a compensatory response by the body is diuresis. Thus intravascularly dry. They are not hypertensive due to the success of the compensatory measure. They do not have idiopathic htn. Read on chronic pain, it may have the answer you are looking for.

 

[stanleykristian]

You will never really know and it is ultimately irrelevant, try preloading with a liter of LR if they are asa 1 and 2 then they should tolerate this no problem. When I go to speak to the patient in preop to get their history and decide my plan I will open the IV and get as much fluid into them as possible.

 

[Teillard]

Read on chronic pain, it may have the answer you are looking for.

OK. I'll read more. But what if the the patient is still making urine with a supported BP swimming in narcotic and volatile agent? When I posted "moderate gains... with volume" I meant aggressive crystalloid resus. Sorry for the confusion. You're right, might never really know. But I might, too. Does it matter? Don't know that either, but if it is some kinda funky presentation in chronic pain for spine procedures, might could avoid some morbidity, don't ya think?

 

[Huktonfoniks]

Does the hypotension occur before or after turning them prone. If its after its likely decreased venous return due to the prone position. Therefore, phenylephrine would work better by increasing venous return/CO rather than ephedrine. If they go hypotensive after induction and prior to turning them its probably the loss of sympathetic drive as previously posted.

 

[armygas]

Hypertension is a comorbid condition associated with chronic pain issues / opioid use. I think that your point that phenylephrine works where ephedrine does not answers your question.

Chronic pain patients like this have a volume deficit (pretty much like every patient) which may or may not be related to a hypertension comorbidity and the inability of ephedrine to work (as it requires stored catecholamines to work as part of its actions) suggests a catecholamine deficit.

 

[Planktonmd]

Hold your fire, boys. I posted this on another forum and got over 60 views and exactly zero replies. Just looking for an attending consult if you get my drift. Here goes:

Seen this too many times to count now. O/W healty male or female for some kind of neck or lower back fusion. 30-60 yrs old, maybe smokes, normal hight and weight for the most part (the occasional fatso). Biggest item on their history is their chronic pain for which they are on at least two opiate analgesics (norco, oxycont. straight vicodin, whatever) and a muscle relaxant du jour. These for no less than three months, all day everyday. NO antidepressants on the patients I'm thinking of. Here's the deal. They get their pre-op versed and fentanyl which doesn't do anything, put them to sleep with completely stable vs and they absolutely hit the wall in that they are intolerant to even modest levels of vol. ax. for the entire case. Volume with modest gains on hemodynamics but what reaallly helps is neo and not ephedrine. The first couple of times I did this on a 3 or so level fusion I woke them up without any narcotic to speak of. Mistake. They'd go from supported blood pressure on 4% Des to no Des and coming off the table. Now I put 'em to sleep on appropriate vol. ax. (usually 6 or more of Des.) and give fentanyl on a per kg basis based on the surgical assault (3-4 lumbar levels start with 10-12 ug/kg fentanyl in the first half hour). I support their blood pressure with a neo infusion. 25-30 mins to the end of the case I get them breathing and titrate dilaudid to a RR of 12. Sometimes I'll give 8-10 mg of dilaudid on a case like the ones above and they open their eyes on the roll supine AND they say they're a little sore.

First thing I think is catecholamine depletion because ephedrine doesn't work and neo does. No steroids involved, no anti-depressants either. Making good urine too. What's up?

You are talking about cases done in the prone position which causes a certain degree of decreased blood return to the heart, so if the patient is volume depleted, as most these people are, and you give them a vaso dilator like an inhaled agent, they get hypotensive.
Ephedrine works primarily by increasing cardiac output, so it's not going to help because you need to improve the preload first, and that's why you need a vasoconstrictor like phenylephrine to use the volume efficiently.
Easy isn't it?

 

[SexPanther]

chronic pain causes an increase in sympathetic outflow, a compensatory response by the body is diuresis. Thus intravascularly dry. They are not hypertensive due to the success of the compensatory measure. They do not have idiopathic htn. Read on chronic pain, it may have the answer you are looking for.

I've heard this repeated often, but what is the physiological basis of this statement? It's been a while since physio, but there are receptors (beta-1, if I remember correctly) on the juxtoglomerular apparatus which would be stimulated with an increase in sympathetic outflow leading to increased renin -- angiotensin -- aldosterone and an increase in intravascular volume (via increased reabsorption of sodium and actions of ADH to regulate osmolality). Moreover, sympathetic stimulation of alpha-1 receptors located on the afferent arteriole causes vasoconstriction and decreased GFR which leads to the same cascade as above.

Without getting into compensatory functions of ANP etc, what am I missing? Are these pts. suffering from catecholamine depletion (as suggested in earlier posts) which leads to decreased renin release and subsequent volume depletion?

 

[Teillard]

You are talking about cases done in the prone position which causes a certain degree of decreased blood return to the heart, so if the patient is volume depleted, as most these people are, and you give them a vaso dilator like an inhaled agent, they get hypotensive.
Ephedrine works primarily by increasing cardiac output, so it's not going to help because you need to improve the preload first, and that's why you need a vasoconstrictor like phenylephrine to use the volume efficiently.
Easy isn't it?

That all makes sense. It's just that when I see what I describe above, it is only with those patients who have been on potent narcotics for at least a couple of months (i.e. bad enough pain to need them. There are those pts who just gut it out on motrin). Others who do get hypotensive on the turn respond well to volume, a little lighter on the gas and a little sqeeze. They're different patients in my experience. They make urine fine. If they are more volume depleted than the "usual" patient presenting for these procedures, why don't they show it with oliguria and HR changes, which I don't see for the most part?

 

[Noyac]

chronic pain causes an increase in sympathetic outflow, a compensatory response by the body is diuresis. Thus intravascularly dry. They are not hypertensive due to the success of the compensatory measure. They do not have idiopathic htn. Read on chronic pain, it may have the answer you are looking for.

Please explain to everyone how chronic pain causes an increase in sympathetic outflow. Then how it causes diuresis.

Then tell us how long someone with chronic pain may actually have an increased sympathetic discharge.

 

[stanleykristian]

I will have to find the text, However the increased sympathetic outflow can go on indefinitley leading to RSD.

 

[rn29306]

Teillard.....Whenever we have someone who is an obvious meth user, I have found the exact description of what you have written. Totally oblivious to even 10 mg of IV versed in preop and enourmous amounts of fentanyl, but TOTALLY intolerant of volatile anesthetic. I have found these guys often require a dopamine gtt, but certainly my p value for these situations is quite low.

Good ole patient variability.....makes life interesting.

 

[Noyac]

Teillard.....Whenever we have someone who is an obvious meth user, I have found the exact description of what you have written. Totally oblivious to even 10 mg of IV versed in preop and enourmous amounts of fentanyl, but TOTALLY intolerant of volatile anesthetic. I have found these guys often require a dopamine gtt, but certainly my p value for these situations is quite low.

Good ole patient variability.....makes life interesting.

Meth causes a down regulation of the Dopamine receptors over time due to its 36 fold increase in dopamine release during its use (if I remember correctly). Also a meth high can last up to 12 hrs unlike the relatively short high of cocaine. This is why the users keep chasing the high. The receptors are constantly bombarded with dopamine which cause the down-regulation of receptors. Then we take them to the OR and induce them with a vasodilator and cardiac depressant. Not the typical qualities of versed and fentanyl. They cannot mount a very effective response to the insult due to the lack of dopa receptors (and neurotransmitter as well) and therefore, require augmentation with a vasoconstrictor, phenylephrine if your lucky, dopamine if your not.

Now chronic pain is different. The excitatory neurotransmitters released in chronic pain are Substance P, Calcitonin related peptide, Glutamate, and aspartate. Dopamine is more common in acute pain (some pain guru may correct me if I am wrong). This is not to say that these excitatory neurotransmitters are not causing the same problem when we give an anesthetic.

I do quite a bit of spine cases currently and i have seen the drop in BP you describe but it almost always responds to neo and fluids. I mostly, attribute it to hypovolemia.

As far as diuresis, well maybe but it ain't the only cause. I suspect it has a minimal effect if any. But it is exacerbated by the NPO status, position changes in the case, possible down regulation of receptors, etc.

 

[fakin' the funk]

I have found these guys often require a dopamine gtt, but certainly my p value for these situations is quite low.

Good ole patient variability.....makes life interesting.

???

 

[toughlife]

???

Come on, you know CRNA statistics.

 

[rn29306]

Come on, you know CRNA statistics.

Damned Crown and Coke.

 

[armygas]

Please explain to everyone how chronic pain causes an increase in sympathetic outflow. Then how it causes diuresis.

Then tell us how long someone with chronic pain may actually have an increased sympathetic discharge.

Actually chronic pain causes a “depressive” phenotype in patients as a constant stress load can create hippocampal atrophy which in turn causes a disinhibition of the amygdala. Excitatory relay neurons from the amygdala to the hypothalamus can then cause the release of CRF which releases ACTH from the anterior pituitary gland. In turn the ACTH acts on the adrenal medulla to release not only endogenous steroids but also can increase the production of catecholamines. So you can end up with a cyclic response that generates increased endogenous steroid and catecholamine levels..... those two combined could answer your question.

 

[SexPanther]

Actually chronic pain causes a “depressive” phenotype in patients as a constant stress load can create hippocampal atrophy which in turn causes a disinhibition of the amygdala. Excitatory relay neurons from the amygdala to the hypothalamus can then cause the release of CRF which releases ACTH from the anterior pituitary gland. In turn the ACTH acts on the adrenal medulla to release not only endogenous steroids but also can increase the production of catecholamines. So you can end up with a cyclic response that generates increased endogenous steroid and catecholamine levels..... those two combined could answer your question.

That's fine and good (and a well written neuroscientist answer) but I'm still wanting the physiologic basis for the statement for increased sympathetic outflow leads to diuresis. See my previous post for why it seems counter-intuitive to me. Moreover, based on the generation of increased endogenous steroid production, you could make the argument that there will be some mineralocorticoid activity that will augment/enhance the actions of aldosterone/aldosterone receptor. I could try and look it up myself, but I only have a few more days of doing nothing left.

 

[armygas]

That's fine and good (and a well written neuroscientist answer) but I'm still wanting the physiologic basis for the statement for increased sympathetic outflow leads to diuresis. See my previous post for why it seems counter-intuitive to me. Moreover, based on the generation of increased endogenous steroid production, you could make the argument that there will be some mineralocorticoid activity that will augment/enhance the actions of aldosterone/aldosterone receptor. I could try and look it up myself, but I only have a few more days of doing nothing left.

Alpha adrenergic stimulation with norepinephrine may be associated with an increase in the renal excretion of solute-free water. It seems the likely mechanism is the inhibition of vasopressin release by norepinephrine.
If your interested this article is freely available here http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=302280

 

[SexPanther]

Alpha adrenergic stimulation with norepinephrine may be associated with an increase in the renal excretion of solute-free water. It seems the likely mechanism is the inhibition of vasopressin release by norepinephrine.
If your interested this article is freely available here http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=302280

Thanks for the link, I'll try to read it later today.