Have you guys heard of this?

[ucsfgaspain]

Hello All,

I went to one of those drug dinners this week cuz I wanted to try out a restaurant I'd never been to. Paul White (Chair at UT southwestern) was giving a presentation.

He had an interesting premise and I wanted to see if any of you guys have been doing what he preaches.

He states that a typical anesthestic regimen consists of 1) multimodal analgesia sparing opioids i.e. nsaids, lots of local by the surgeon, iv acetaminophen (if we had it here in the US) 2) 1/2 mac of vapor 3) esmolol infusion. Now he states that these patients reallly don't need much post op opioid with this regimen. He states that he hardly ever gives any intraoperative narcotic and gives like 1 mg of morphine post op and that's all the patient needs. Advantage of this regimen, is quick discharge and quicker return to ADL's.

Being a skeptical guy by nature and pretty much having never met a chair of an academic program who actually passes gas, I'm a little wary of his advice.

Now I'm open to doing new stuff. I could only come up with 2 mechanisms why his proposal would work

1) beta blockers have analgesic properties that outlast their pharmakokinetics i.e. esmolol should have been long gone in the post op perioid

2) the dosages that we use for typical cases i.e. 250-500 ug of fentanyl for a lap chole lead to hyperalgesia

Anyone got insight into this? He states that he learned his regimen from Wender down at Cedars? So Cal Peeps got any clue?

This would have huge ramifications for the pain world. We do know that beta blockers do cause in some cognitive changes i.e. anxiolysis and depression in some. What do you guys think? Anything here? Or B.S.?

P.S. Hope everyone is doing well. Damn market is messing with my F U account! Peace.

---

Members don't see this ad.

 

[dhb]

I would think beta blockers don't have any analgesic properties. I agree that once you start hitting someone with suf/fent they will be more resistent to the effect of morphine compared with someone who is naive to opiods.

If you use local generously at every location that could be painfull there is no reason you should experience post-op pain. For a lap chole you infiltrate each inscision and spray the peritoneum with local your good to go.

Actually if you think of it a lot of operations can be performed under local or peripheral nerve block alone: appendix, hernias, ortho, eyes, carotides etc...

 

[huktonfonix]

yeah its more likely the rest of the stuff acetaminophen, NSAIDS, local will provide decent analgesia for most surgeries as long as you need less local than will exceed your max dose. The beta blockers are probably more for managing hemodynamics. I personally think opioids are overused in minor surgeries also, and that better use of local is often warranted. Does he use neurontin as well?

 

[Gern Blansten]

The "Chairman" at UTSW is NOT Paul White. He was chair there for a brief time years ago and held an endowed "chair" position, which he has held on to since that time. It can be misleading the way that it is put forward in his title, but I assure you, he is not the chairman.

It would be interesting to know exactly how much time he spends in direct patient care since he has a research lab which churns out ~50 papers a year, is a hired gun speaker for several companies and travels extensively.

 

[bigdan]

IV Tylenol is on its way...Phase 3 trials right now, I think...

dc

 

[SleepIsGood]

If I recall correctly there is a guy at Bay State that endorses this type of multimodal analgesia.

In addition, I do believe pregablin/neurontin is used.

I think the dose of tylenol is in lines of 1 gram !

Apparently this stuffworks. It just takes a lot of 'coordinating' since pts have to be on these meds (celebrex, neurontin ) for a few days preceding and I believe 7-14 days post op.

 

[UTSouthwestern]

The "Chairman" at UTSW is NOT Paul White. He was chair there for a brief time years ago and held an endowed "chair" position, which he has held on to since that time. It can be misleading the way that it is put forward in his title, but I assure you, he is not the chairman.

It would be interesting to know exactly how much time he spends in direct patient care since he has a research lab which churns out ~50 papers a year, is a hired gun speaker for several companies and travels extensively.

Paul worked pretty extensively with residents up to four years ago when I was there. Quite a few of those protocols he lectures on were tested by the residents on the Zale rotation and some were quite good. The key was extensive local infiltration pre incision and at closure.

 

[periopdoc]

I routinely use a mixture of gabapentin 900 mg, celebrex 400 mg and tylenol 975 mg orally pre-op for most outpatient and total joint cases. No need to give it for days before the operation, just a single dose in preop. If there is a lot of postop pain expected, you can continue post-operatively. I don't notice a huge difference in my operative opiate use, it is pretty minimal anyway, but my patients get less opiates in PACU and leave a few minutes earlier.

Of course we could discuss whether this is due to an inherent decrease in their NEED for opiates and PACU care or just a mental decrease in my PACU nurses PERCEPTION of the patient's requirements when hear about all of these new "fancy pain medications" in my report.

-pod

 

[dhb]

I think the dose of tylenol is in lines of 1 gram !

Routine dosage: iv tylenol comes in 1g bottle for adults and 500mg for children; 0.15mg/kg / 6h

 

[urge]

Paul worked pretty extensively with residents up to four years ago when I was there. Quite a few of those protocols he lectures on were tested by the residents on the Zale rotation and some were quite good. The key was extensive local infiltration pre incision and at closure.

How do you infiltrate for a Whipple?
As for a lap Lap Chole, why are we even talking about this?

The whole thing doesn't make sense to me.

 

[dhb]

How do you infiltrate for a Whipple?
As for a lap Lap Chole, why are we even talking about this?

The whole thing doesn't make sense to me.

We're not talking about no narcs for Whipple's but less narcs for moderately painfull procedures

 

[rsgillmd]

Routine dosage: iv tylenol comes in 1g bottle for adults and 500mg for children; 0.15mg/kg / 6h

dhb, the dosage in terms of mg/kg doesn't sound right. Take a 70 kg person, they would 105 mg. At most 420 mg in 24 hrs according to your dosing. Why provide a 1 gm bottle?

Also, for T&As, and many others peds procedures, we give 30 mg/kg as a one time dose PR. You're saying there is a 200 fold reduction by giving it IV. That just seems hard to believe.

I'm not saying you're wrong. I have no clue how to dose IV tylenol. I'm just saying it sounds hard to believe. Would you mind giving your source?

 

[fakin' the funk]

How do you infiltrate for a Whipple?
As for a lap Lap Chole, why are we even talking about this?

Newbie here...you mean, because it doesn't hurt a lot if local is used appropriately?

 

[MTGas2B]

I've heard of the beta blocker stuff before. Never tried it. There a little out there to support it.

Intraoperative esmolol infusion in the absence of opioids spares postoperative fentanyl in patients undergoing ambulatory laparoscopic cholecystectomy.
Collard V, Mistraletti G, Taqi A, Asenjo JF, Feldman LS, Fried GM, Carli F.

Department of Anesthesia, Steinberg-Bernstein Centre for Minimally Invasive Surgery, McGill University Health Centre, Montreal, Quebec, Canada.

BACKGROUND: The use of opioids during ambulatory surgery can delay hospital discharge or cause unexpected hospital admission. Preliminary studies using an intraoperative continuous infusion of esmolol in place of an opioid have inconsistently reported a postoperative opioid-sparing effect. In this study, we compared esmolol versus either intermittent fentanyl or continuous remifentanil on postoperative opioid-sparing, side effects, and time of discharge. METHODS: Ninety patients (consisting of three groups) were enrolled in this prospective, randomized, and observer-blinded study. The control group (n = 30) received intermittent doses of fentanyl, the esmolol group (n = 30) received a continuous infusion of esmolol (5-15 microg x kg(-1) x min(-1)) and no supplemental opioids during surgery, and the remifentanil group (n = 30) received a continuous infusion of remifentanil (0.1-0.5 mixrog x kg(-1) x min(-1)). General anesthesia was standardized, and adjuvant medications included acetaminophen, ketorolac, local anesthetics in the skin incisions, dexamethasone, and droperidol. Postoperative analgesia included fentanyl. RESULTS: The amount of fentanyl in the postanesthesia care unit was significantly less in the esmolol group, 91.5 +/- 42.7 microg, compared with the other two groups, remifentanil, 237.8 +/- 54.7 microg, control, 168.1 +/- 96.8 microg (P < 0.0001). The incidence of nausea was more frequent in the control (66.7%) and remifentanil (67.9%) groups compared with the esmolol group (30%) (P < 0.01). The esmolol group reached the White-Song score of 12 of 14 faster than the remifentanil group (P < 0.01), and left the hospital 45-60 min earlier (P < 0.004). CONCLUSIONS: Intraoperative IV infusion of esmolol contributes to a significant decrease in postoperative administration of fentanyl and ondansetron and facilitates earlier discharge.

PMID: 17959952 [PubMed - indexed for MEDLINE]

 

[dhb]

dhb, the dosage in terms of mg/kg doesn't sound right. Take a 70 kg person, they would 105 mg. At most 420 mg in 24 hrs according to your dosing. Why provide a 1 gm bottle?

Also, for T&As, and many others peds procedures, we give 30 mg/kg as a one time dose PR. You're saying there is a 200 fold reduction by giving it IV. That just seems hard to believe.

I'm not saying you're wrong. I have no clue how to dose IV tylenol. I'm just saying it sounds hard to believe. Would you mind giving your source?

oops my bad 15mg/kg which gives you 1g for 70kg
some people give a 30mg/kg one time dose since you're still below the level at which you start to see toxicity (60mg/kg)

 

[huktonfonix]

If you think about it, it makes sense. Its the same reason why people use esmolol instead of more induction agent or narcotic to control hemodynamics during intubation. some moments may cause sympathetic stimulation but not necessarily pain and esmolol is a great quick on, quick off medication to control sympathetic stimulation. I personally used to do this during residency since there was often a long wait after induction until incision and the blood pressures tended to drift down with the narcotics at intubation.

 

[RT2MD]

Esmolol is pretty Beta-1 specific isn't it? Just thinking that using something that isn't as specific could be a bad idea for some of these reactive airway dx patients that require beta-2 agonists... or is that something that is seen much intra-operatively (bronchospasm due to beta blockers)?

Thanks,

 

[militarymd]

If you think about it, it makes sense. Its the same reason why people use esmolol instead of more induction agent or narcotic to control hemodynamics during intubation. some moments may cause sympathetic stimulation but not necessarily pain and esmolol is a great quick on, quick off medication to control sympathetic stimulation. I personally used to do this during residency since there was often a long wait after induction until incision and the blood pressures tended to drift down with the narcotics at intubation.

we treat pain.

we treat hypovolemia

we treat anemia

we treat hypoxia



so why don't we treat the hyper adrenergic state that exists in the perioperative period?

drum roll please.....


we don't have a serum catecholamine monitor.

 

[Jeff05]

patients with severe reactive airway dz could have bronchospasm even with selective beta-blockers.

Esmolol is pretty Beta-1 specific isn't it? Just thinking that using something that isn't as specific could be a bad idea for some of these reactive airway dx patients that require beta-2 agonists... or is that something that is seen much intra-operatively (bronchospasm due to beta blockers)?

Thanks,

 

[dfk]

patients with severe reactive airway dz could have bronchospasm even with selective beta-blockers.

that's where dilt comes in. M&M (p. 251) states labetalol may actually have B2 agonist properties. imagine that.

 

[fakin' the funk]

M&M (p. 251) states labetalol may actually have B2 agonist properties. imagine that.

It does. From G&G:

Labetalol (NORMODYNE, TRANDATE, others) is representative of a class of drugs that act as competitive antagonists at both a1 and b receptors. Labetalol has two optical centers, and the formulation used clinically contains equal amounts of the four diastereomers. The pharmacological properties of the drug are complex, because each isomer displays different relative activities. The properties of the mixture include selective blockade of a1 receptors (as compared with the a2 subtype), blockade of b1 and b2 receptors, partial agonist activity at b2 receptors, and inhibition of neuronal uptake of norepinephrine (cocaine-like effect) (see Chapter 6). The potency of the mixture for b receptor blockade is fivefold to tenfold that for a1 receptor blockade.

The pharmacological effects of labetalol have become clearer since the four isomers were separated and tested individually. The R,R isomer is about four times more potent as a b receptor antagonist than is racemic labetalol, and it accounts for much of the b blockade produced by the mixture of isomers, although it no longer is in development as a separate drug (dilevalol). As an a1 antagonist, this isomer is less than 20% as potent as the racemic mixture. The R,S isomer is almost devoid of both a and b blocking effects. The S,R isomer has almost no b blocking activity, yet is about five times more potent as an a1 blocker than is racemic labetalol. The S,S isomer is devoid of b blocking activity and has a potency similar to that of racemic labetalol as an a1 receptor antagonist. The R,R isomer has some intrinsic sympathomimetic activity at b2 adrenergic receptors; this may contribute to vasodilation. Labetalol also may have some direct vasodilating capacity.

The actions of labetalol on both a1 and b receptors contribute to the fall in blood pressure observed in patients with hypertension. a1 Receptor blockade leads to relaxation of arterial smooth muscle and vasodilation, particularly in the upright position. The b1 blockade also contributes to a fall in blood pressure, in part by blocking reflex sympathetic stimulation of the heart. In addition, the intrinsic sympathomimetic activity of labetalol at b2 receptors may contribute to vasodilation.

 

[dfk]

It does. From G&G:

Labetalol (NORMODYNE, TRANDATE, others) is representative of a class of drugs that act as competitive antagonists at both a1 and b receptors. Labetalol has two optical centers, and the formulation used clinically contains equal amounts of the four diastereomers. The pharmacological properties of the drug are complex, because each isomer displays different relative activities. The properties of the mixture include selective blockade of a1 receptors (as compared with the a2 subtype), blockade of b1 and b2 receptors, partial agonist activity at b2 receptors, and inhibition of neuronal uptake of norepinephrine (cocaine-like effect) (see Chapter 6). The potency of the mixture for b receptor blockade is fivefold to tenfold that for a1 receptor blockade.

The pharmacological effects of labetalol have become clearer since the four isomers were separated and tested individually. The R,R isomer is about four times more potent as a b receptor antagonist than is racemic labetalol, and it accounts for much of the b blockade produced by the mixture of isomers, although it no longer is in development as a separate drug (dilevalol). As an a1 antagonist, this isomer is less than 20% as potent as the racemic mixture. The R,S isomer is almost devoid of both a and b blocking effects. The S,R isomer has almost no b blocking activity, yet is about five times more potent as an a1 blocker than is racemic labetalol. The S,S isomer is devoid of b blocking activity and has a potency similar to that of racemic labetalol as an a1 receptor antagonist. The R,R isomer has some intrinsic sympathomimetic activity at b2 adrenergic receptors; this may contribute to vasodilation. Labetalol also may have some direct vasodilating capacity.

The actions of labetalol on both a1 and b receptors contribute to the fall in blood pressure observed in patients with hypertension. a1 Receptor blockade leads to relaxation of arterial smooth muscle and vasodilation, particularly in the upright position. The b1 blockade also contributes to a fall in blood pressure, in part by blocking reflex sympathetic stimulation of the heart. In addition, the intrinsic sympathomimetic activity of labetalol at b2 receptors may contribute to vasodilation.

thanks for the reference.

 

[Planktonmd]

dhb, the dosage in terms of mg/kg doesn't sound right. Take a 70 kg person, they would 105 mg. At most 420 mg in 24 hrs according to your dosing. Why provide a 1 gm bottle?

Also, for T&As, and many others peds procedures, we give 30 mg/kg as a one time dose PR. You're saying there is a 200 fold reduction by giving it IV. That just seems hard to believe.

I'm not saying you're wrong. I have no clue how to dose IV tylenol. I'm just saying it sounds hard to believe. Would you mind giving your source?

The adult dose of Prodafalgan (old prodrug of paracetamol used in Europe) is 2000 mg for adults.
And the dose of IV Paracetamol for adults is actually 1000 mg.
Here is a study comparing both:
http://cat.inist.fr/?aModele=afficheN&cpsidt=17154575

 

[Planktonmd]

Hello All,

I went to one of those drug dinners this week cuz I wanted to try out a restaurant I'd never been to. Paul White (Chair at UT southwestern) was giving a presentation.

He had an interesting premise and I wanted to see if any of you guys have been doing what he preaches.

He states that a typical anesthestic regimen consists of 1) multimodal analgesia sparing opioids i.e. nsaids, lots of local by the surgeon, iv acetaminophen (if we had it here in the US) 2) 1/2 mac of vapor 3) esmolol infusion. Now he states that these patients reallly don't need much post op opioid with this regimen. He states that he hardly ever gives any intraoperative narcotic and gives like 1 mg of morphine post op and that's all the patient needs. Advantage of this regimen, is quick discharge and quicker return to ADL's.

Being a skeptical guy by nature and pretty much having never met a chair of an academic program who actually passes gas, I'm a little wary of his advice.

Now I'm open to doing new stuff. I could only come up with 2 mechanisms why his proposal would work

1) beta blockers have analgesic properties that outlast their pharmakokinetics i.e. esmolol should have been long gone in the post op perioid

2) the dosages that we use for typical cases i.e. 250-500 ug of fentanyl for a lap chole lead to hyperalgesia

Anyone got insight into this? He states that he learned his regimen from Wender down at Cedars? So Cal Peeps got any clue?

This would have huge ramifications for the pain world. We do know that beta blockers do cause in some cognitive changes i.e. anxiolysis and depression in some. What do you guys think? Anything here? Or B.S.?

P.S. Hope everyone is doing well. Damn market is messing with my F U account! Peace.

This anesthetic technique that you described makes perfect sense.
Multi-modal analgesia and intraop sympathetic blockade is what we all try to do when we administer anesthesia, the only difference is that we try to achieve the sympathetic blockade indirectly by giving more narcotics, this guy is doing sympathetic blockade directly.
This sympathetic blockade will eliminate the need to give extra intra-operative Narcotics and as a result decrease the incidence of postop hyperalgesia which as we know is very common.
It wouldn't be surprising if the Beta blocker also offers direct synergism with other analgesics by attenuating the stimulant effects of the sympathetic activity on the CNS.

 

[huktonfonix]

we treat pain.

we treat hypovolemia

we treat anemia

we treat hypoxia



so why don't we treat the hyper adrenergic state that exists in the perioperative period?

drum roll please.....


we don't have a serum catecholamine monitor.

No we dont. But we also dont have a pain monitor for patients under general anesthesia.

 

[Planktonmd]

No we dont. But we also dont have a pain monitor for patients under general anesthesia.

Correct,
But what is pain under anesthesia?
Does anyone know the definition of pain under General anesthesia?

 

[militarymd]

No we dont. But we also dont have a pain monitor for patients under general anesthesia.

when they wake up, they tell us they have PAIN...

they DO NOT wake up and tell us that their serum norepinephrine levels are high....or that their ADH level is 15 pg/ml....etc.etc.

 

[huktonfonix]

when they wake up, they tell us they have PAIN...

they DO NOT wake up and tell us that their serum norepinephrine levels are high....or that their ADH level is 15 pg/ml....etc.etc.

yes, but there are also plenty of surgeries during which they have an increase in HR, BP, etc in response to stimulus and wake up with no pain. And these surgeries are probably the ones more appropriate to use with the above mentioned technique.

 

[militarymd]

yes, but there are also plenty of surgeries during which they have an increase in HR, BP, etc in response to stimulus and wake up with no pain. And these surgeries are probably the ones more appropriate to use with the above mentioned technique.

you are confused about the differences between "hemodynamic response" and the "stress response"....

although they are intimatedly related, they are different.

 

[huktonfonix]

you are confused about the differences between "hemodynamic response" and the "stress response"....

although they are intimatedly related, they are different.

True, but I strongly doubt that the amount of opioid we use during most operations is effective in eliminating the stress response. Regional would be much more effective in this case, but it is usually not eliminated or even effectively blunted under general to my knowledge.