tourniquet pain

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likeaboss

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Does anybody have a good understanding of what causes tourniquet pain? How big of a problem is it for those of you doing lots of ortho cases? How do you manage it?

Thank you everybody.

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Ischemia causes it. For cases under GA, I will give esmolol or sometimes labetalol if HR or BP get away from where I'm comfortable. Don't chase it ... avoid the urge to give opiates. Tourniquet pain is very resistant to opiates and it's easy to screw yourself with an over-narc'd patient once the tourniquet is down.

For cases where the patient is awake or just sedated, it can be a nuisance. I usually go with extra propofol or midazolam, or a little fentanyl. The real solution is for the surgeon to hurry up and let the tourniquet down. 🙂
 
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There is also the early tourniquet pain the instant it goes on, which is all somatic. Anxious awake patients can totally lose it and freak out if they don't have enough narcs on board, or enough nerve block coverage. At the 1-2 hr mark you start to get the ischemic stuff that is harder to treat.
 
If I anticipate long tourniquet time, I will give pre-emptive bolus dosing of ketamine 0.25-0.5 mg/kg (one time dose)-really effective as ketamine has some peripheral effects. Also, can use bolus dosing of 20 mg at a time during the case if you are hesitant to give a pre-emptive larger bolus as above.
 
If I feel like the pt has enough narcs/anesthesia on board and BP's are still getting outta control I like to bolus Nicardipine 100-200mcg at a time. Works great and is short acting enough that you don't have to worry about the pt's BP crashing once the tourniquet somes down.
 
If I feel like the pt has enough narcs/anesthesia on board and BP's are still getting outta control I like to bolus Nicardipine 100-200mcg at a time. Works great and is short acting enough that you don't have to worry about the pt's BP crashing once the tourniquet somes down.

While that may work nice, isn't that a pretty expensive fix to a pretty simple problem?
 
So if you were to bring the tourniquet down for about 3 min and then reinflate, would that "reset" the tourniquet time back to zero, pain wise? What if you repositioned the tourniquet proximally or distally once the patient showed signs of tourniquet pain?
 
Tourniquet pain is not thought to be soley a result of neural pathways but also the release of vaso-active mediators in the setting of limb ischemia. Thus regional anesthesia is not always effective just like pgg mentioned.

I agree nicardipine is pricey but we have a few surgeons that push 2-2.5hrs of tourniquet time regularly and you gotta do something. Using cheaper longer acting agents (labetalol, hydralazine) often results in marked hypotension after tourniquet release, and I'm too much of a whimp to use nipride sans a-line
 
Tourniquet pain is not thought to be soley a result of neural pathways but also the release of vaso-active mediators in the setting of limb ischemia. Thus regional anesthesia is not always effective just like pgg mentioned.

I agree nicardipine is pricey but we have a few surgeons that push 2-2.5hrs of tourniquet time regularly and you gotta do something. Using cheaper longer acting agents (labetalol, hydralazine) often results in marked hypotension after tourniquet release, and I'm too much of a whimp to use nipride sans a-line

there are a million ways to lower blood pressure. Nitroglycerin is pretty cheap. Labetalol doesn't last terribly long. Cranking up the gas doesn't cost much. A smidge of fentanyl rarely messes up your wake up.

Just pointing out that routinely using nicardipine for tourniquet pain probably adds up to a ton of money over the course of a year. And it's not like there is a lot of cash to go around in healthcare these days.
 
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😕

Not everybody is a candidate for regional. By the time the tourniquet pain manifests, it's a bit too late to change plans.

Also, you've never seen tourniquet pain bleed through a spinal?

Sure, not every patient is a candidate for regional...
I did not say that you should wait for the pain to start then consider regional anesthesia!
I meant if a procedure involves a tourniquet maybe you should do it under regional.
And if tourniquet pain "bleeds" through your spinal then your spinal is simply not at the right level.
Sorry if I confused you 🙂
 
Tourniquet pain is not thought to be soley a result of neural pathways but also the release of vaso-active mediators in the setting of limb ischemia. Thus regional anesthesia is not always effective just like pgg mentioned.

I agree nicardipine is pricey but we have a few surgeons that push 2-2.5hrs of tourniquet time regularly and you gotta do something. Using cheaper longer acting agents (labetalol, hydralazine) often results in marked hypotension after tourniquet release, and I'm too much of a whimp to use nipride sans a-line

I disagree!
Tourniquet pain is caused by actual local ischemia + nerve compression and it can be relieved completely by a regional anesthetic.
When you have a good spinal and after a while you start seeing the BP and HR going up this is simply because the level of your spinal had gone down not because the pain is "bleeding" through the regional or circulating mediators.
With the tourniquet inflated all circulating mediators are mechanically trapped within the ischemic area after the tourniquet and they don't circulate until the tourniquet is deflated.
 
I did a LOT of 4-5 hour total knees in residency with CSEs - tetracaine + epi spinals. We'd have dense blocks for hours, and 90 minutes into the tourniquet HR & BP predictably go up, and patients would get squirmy.

Mind you, this is while the orthopods are getting medieval on the knee with their carpentry tools. Tourniquet down for a while at the 2 hr mark, patient stops squirming, tourniquet back up, more knee chopping.

I don't think this can be explained by just a receding spinal. I admit I don't fully understand the mechanism, but I've seen it in patients I know had good levels still.

I don't run into this problem now because our surgeons are fast.
 
It seems there is a specific issue with Tetracaine where the C fibers do return to activity before other thicker fibers and that seems to explain why a Tetracaine spinal could continue to appear OK while the patient is experiencing Tourniquet pain.
I am pretty sure there was an article about that a few years back comparing Tetracaine to Bupivacaine and showed less Tourniquet pain with Bupivacaine.
I'll try to find it for you.
 
It seems there is a specific issue with Tetracaine where the C fibers do return to activity before other thicker fibers and that seems to explain why a Tetracaine spinal could continue to appear OK while the patient is experiencing Tourniquet pain.
I am pretty sure there was an article about that a few years back comparing Tetracaine to Bupivacaine and showed less Tourniquet pain with Bupivacaine.
I'll try to find it for you.

There:

http://www.ncbi.nlm.nih.gov/pubmed/3414992
 
I wonder if you could get any relief of the hypertension with a bit of nitro paste? Put it on at around an hour when the pressure starts to climb and wipe it off when they are closing? We don't have ready access to it, so I can't give it a try. I wouldn't think it lasts very long after you wipe it off and it's got to be dirt cheap.
 
I wonder if you could get any relief of the hypertension with a bit of nitro paste? Put it on at around an hour when the pressure starts to climb and wipe it off when they are closing? We don't have ready access to it, so I can't give it a try. I wouldn't think it lasts very long after you wipe it off and it's got to be dirt cheap.

Propofol is a simple way to do the same thing.
 
Just thinking out loud here.

If tourniquet pain is due to ischemia... would lowering the BP actually decrease perfusion to the affected extremity making ischemia worse? Is hypertension a way in which the body tries to maintain perfusion to that extremity or is it solely a pain response?

Do awake patients feel any better once you drop their BPs with antihypertensives? I can't imagine it does as you are just treating BPs and not the pain intself.

I don't do awake totals and rarely do I encounter tourniquet pain... but our knees take about 45 minutes @275-300mmhg. I would generally let the tourniquet pain ride unless they have cardiac issues. If you treat it and then the tourniquet goes down, you are likely to encounter some hypotension from CO2 buildup in the extremity + whatever antihypertensive is given to treat the HTN while the tourniquet is up.

I agree that treating tourniquet pain with opiods is not a good idea.
 

Interesting, thanks.

I'm not wholly convinced though. I've done painfully long TKAs with bupivacaine too, sometimes with CSEs where the level is kept at an adequate level with epidural boluses ... and a receding level just doesn't explain why these patients will get tourniquet pain but have solid coverage of the knee itself.

These knee patients are having tourniquet pain at 90-120 min but they're not having knee pain. (As evidenced by the fact that the pain goes away when the tourniquet goes down, even though Bob The Builder is still hammering away at the knee.)

Dermatomes aren't horizontal in the leg the way they are in the trunk; it's the same spinal nerves that get anterior thigh and anterior knee. Except for the most superior portion of the anterior thigh which is L1. I would expect that a spinal that doesn't cover the anterior thigh also wouldn't cover the anterior knee.
 
would lowering the BP actually decrease perfusion to the affected extremity making ischemia worse?

I wouldn't think so.

If the tourniquet's at 300, the tissue isn't getting perfused by a BP of 140/90 any better than it is at 110/60. There's zero flow in both cases.
 
OR time is pretty expensive.

that's why you do a residency so you can learn how to wake the patient up on a dime in a variety of scenarios. An extra 50 mcg of fentanyl isn't going to slow down your extubation unless you don't know what you are doing. Same thing with having the peak concentration of gas a little higher. And I'm pretty sure nitroglycerin or esmolol also don't slow down wake up.
 
Interesting, thanks.

I'm not wholly convinced though. I've done painfully long TKAs with bupivacaine too, sometimes with CSEs where the level is kept at an adequate level with epidural boluses ... and a receding level just doesn't explain why these patients will get tourniquet pain but have solid coverage of the knee itself.

These knee patients are having tourniquet pain at 90-120 min but they're not having knee pain. (As evidenced by the fact that the pain goes away when the tourniquet goes down, even though Bob The Builder is still hammering away at the knee.)

Dermatomes aren't horizontal in the leg the way they are in the trunk; it's the same spinal nerves that get anterior thigh and anterior knee. Except for the most superior portion of the anterior thigh which is L1. I would expect that a spinal that doesn't cover the anterior thigh also wouldn't cover the anterior knee.
Actually I think with a CSE a receding level is the explanation: While your spinal recedes you are replacing it with a less dense epidural block that could conceivably allow the severe pain of the tourniquet (more severe than bone pain) to pass through.
 
I wouldn't think so.

If the tourniquet's at 300, the tissue isn't getting perfused by a BP of 140/90 any better than it is at 110/60. There's zero flow in both cases.

Yeah....you are probably right.

We've all seen blood loss in the surgical field despite the application of a tourniquet @ 300mmhg. The likely cause is medullary bleeding from the bone or arterial calcification that does not compress despite the use of a tourniquet (not the norm).

I'd love to see a study that looked at microvascular blood flow to the sciatic nerve with the use of a tourniquet. I was thinking that blood flow might not be completely occluded due to the sciatic nerve location (under the femur and surrounded by muscle) and in those patients with adipose rich thighs.

Femoral nerve is obviously vulnerable not only to ischemic factors but to direct mechanical stress as well.
 
I did a LOT of 4-5 hour total knees in residency with CSEs - tetracaine + epi spinals. We'd have dense blocks for hours, and 90 minutes into the tourniquet HR & BP predictably go up, and patients would get squirmy.

Same here and i've never touched a vial of tetracaine
 
Actually I think with a CSE a receding level is the explanation: While your spinal recedes you are replacing it with a less dense epidural block that could conceivably allow the severe pain of the tourniquet (more severe than bone pain) to pass through.

Is it really more painful than bone pain?
 
We can find out:
Why don't you to try to inflate a blood pressure cuff around you arm to 300 mm Hg and see how long you can tolerate it?


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:claps:


Nice plank... I've been waiting for someone to make me chuckle on here...
 
Actually I think with a CSE a receding level is the explanation: While your spinal recedes you are replacing it with a less dense epidural block that could conceivably allow the severe pain of the tourniquet (more severe than bone pain) to pass through.

It still doesn't explain why there's a perceived difference in surgical knee pain vs tourniquet pain. It's the same dermatome for anterior knee and anterior thigh (and we know the posterior thigh is more densely covered since it's several dermatomes lower than the knee).

Maybe there's something to that fast/slow fiber resistance to -caine you mentioned earlier, and it's simply harder to block the slow burning ischemic pain fibers than the fast stabbing surgical pain fibers. It's the most plausible explanation I can think of.
 
Interesting discussion.

I personally don't believe the statement "With the tourniquet inflated all circulating mediators are mechanically trapped within the ischemic area after the tourniquet and they don't circulate until the tourniquet is deflated" Just can't accept that without proof.
 
Interesting discussion.

I personally don't believe the statement "With the tourniquet inflated all circulating mediators are mechanically trapped within the ischemic area after the tourniquet and they don't circulate until the tourniquet is deflated" Just can't accept that without proof.

Do you know of any study showing "mediators" passing through an inflated cuff to 250-300 mmHg and causing hypertension and tachycardia?
What mediators are you referring to by the way?
 
Do you know of any study showing "mediators" passing through an inflated cuff to 250-300 mmHg and causing hypertension and tachycardia?
What mediators are you referring to by the way?

I'm guessing he's referring to evil humors released from the proximal side of the cuff. Maybe you can bleed them off with leeches?
My money is on pain receptors and nerve transmission.
How high do you think you need to raise the cuff to stop nerve transmission?




🙂
 
I'm guessing he's referring to evil humors released from the proximal side of the cuff. Maybe you can bleed them off with leeches?
My money is on pain receptors and nerve transmission.
How high do you think you need to raise the cuff to stop nerve transmission?
🙂

Since my foot falls asleep when I cross my leg at the movie, I'm guessing--at least for some nerves--the necessary amount of cuff pressure is small.

I do not know of any study showing "mediators" passing through an inflated cuff, etc.
But I do know, the absence of my knowing of such a study certainly does not constitute a proof for me that "all circulating mediators are mechanically trapped."

Plausible counter arguments abound; iL offers proximal-cuff-stuff as one freebie.
 
I'm guessing he's referring to evil humors released from the proximal side of the cuff. Maybe you can bleed them off with leeches?
My money is on pain receptors and nerve transmission.
How high do you think you need to raise the cuff to stop nerve transmission?




🙂

I like the leeches idea 😀
 
In the good old days when we did Bier blocks we used a double tourniquet and we inflated the distal one then inflated the proximal one then deflated the distal one and kept only the proximal inflated.
Then if the case took too long and tourniquet pain started to appear we inflated the distal tourniquet and deflated the proximal one and this effectively relieved the tourniquet pain.
This indicates that there is no chemical mediators involved and that it is simply pain cause by the compression of nerves or other things under the tourniquet itself.
 
In the good old days when we did Bier blocks we used a double tourniquet and we inflated the distal one then inflated the proximal one then deflated the distal one and kept only the proximal inflated.
Then if the case took too long and tourniquet pain started to appear we inflated the distal tourniquet and deflated the proximal one and this effectively relieved the tourniquet pain.
This indicates that there is no chemical mediators involved and that it is simply pain cause by the compression of nerves or other things under the tourniquet itself.

I still do it that way (when there is a double tourniquet).
 
In the good old days when we did Bier blocks we used a double tourniquet and we inflated the distal one then inflated the proximal one then deflated the distal one and kept only the proximal inflated.
Then if the case took too long and tourniquet pain started to appear we inflated the distal tourniquet and deflated the proximal one and this effectively relieved the tourniquet pain.
This indicates that there is no chemical mediators involved and that it is simply pain cause by the compression of nerves or other things under the tourniquet itself.


Personally I think the "experiment" sheds light, but doesn't imply your conclusion (which of course could be true nevertheless).
 
In the good old days when we did Bier blocks we used a double tourniquet and we inflated the distal one then inflated the proximal one then deflated the distal one and kept only the proximal inflated.
Then if the case took too long and tourniquet pain started to appear we inflated the distal tourniquet and deflated the proximal one and this effectively relieved the tourniquet pain.
This indicates that there is no chemical mediators involved and that it is simply pain cause by the compression of nerves or other things under the tourniquet itself.

The good old days was 3 weeks ago for me. And we use the double when arm habitus allows.
 
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Although I'm not a huge fan due to it's lack of post-op pain control... it's def. a skill that is worth learning. They are excellent for the patient that doesn't want to go to sleep... and especially important when your hand surgeon requests them.
 
It seems there is a specific issue with Tetracaine where the C fibers do return to activity before other thicker fibers and that seems to explain why a Tetracaine spinal could continue to appear OK while the patient is experiencing Tourniquet pain.
I am pretty sure there was an article about that a few years back comparing Tetracaine to Bupivacaine and showed less Tourniquet pain with Bupivacaine.
I'll try to find it for you.

Upper limb tourniquet pain can be blocked by doing an intercostobrachial nerve block, in addition to a brachial plexus block as the intercostobrachial nerve is not covered by brachial plexus. I would imagine lower extremity tourniquet pain could be blocked by a similar blockade of cutaneous nerves, but I haven't heard of anything specific.

The reason tourniquet pain sets in, even in the presence of a dense peripheral nerve block, is because the unmyelinated C-fibers are more resistant to blockade by LA's...so as your local anesthestics are metabolized, the A-deltas may still be covered and surgical stimulation at the site doesn't cause bumps in HR/BP...but the slow C-fibers aren't covered anymore and you'll see a slowly rising HR and BP. Also, C-fibers are sensitive to compression and ischemia...both of which go hand-in-hand with tourniquets.

Opioids are pretty good at first, but eventually they hit a ceiling effect and by that time you may have over-dosed...which you'll find out as soon as the tourniquet drops and the sympathetic outflow drops.

Esmolol (load plus drip) is a cheap and effective way to block the sympathetic outflow...I had an attending that did her entire regional fellowship without a single opioid or benzo...guess what she used....esmolol...some theorize it has some activity at the substantia nigra in addition to its peripheral anti-adrenergics.
 
I had an attending that did her entire regional fellowship without a single opioid or benzo...guess what she used....esmolol...some theorize it has some activity at the substantia nigra in addition to its peripheral anti-adrenergics.

If you're going to loose a year of your life you might as well use some opioids. 😉
 
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