Transforaminal ESI's

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pain chimp

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I'm curious...when you guys do transforaminal LESI's do you purposefully get a concordant paresthesia when placing the needle? Does it make you feel better or worse when you do? Or indifferent? If you do get a paresthesia, obviously you pull back the needle a little bit and inject. But what if the patient can't tolerate the injection no matter how far you pull the needle back?

I used to never give transforaminal ESI's much thought until a few recent patients came back and complained of worsened pain for a few days after the injection. I'm probably just a little gunshy because I know this happends with interlaminars as well.

Thanks.

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I'm curious...when you guys do transforaminal LESI's do you purposefully get a concordant paresthesia when placing the needle? Does it make you feel better or worse when you do? Or indifferent? If you do get a paresthesia, obviously you pull back the needle a little bit and inject. But what if the patient can't tolerate the injection no matter how far you pull the needle back?

I used to never give transforaminal ESI's much thought until a few recent patients came back and complained of worsened pain for a few days after the injection. I'm probably just a little gunshy because I know this happends with interlaminars as well.

Thanks.

One should NEVER try to obtain parasthesias during a TFESI. If the patient can't tolerate the injection, the needle is 95% of the time in the wrong location. or you are injecting your bolus too quickly.
 
One should NEVER try to obtain parasthesias during a TFESI. If the patient can't tolerate the injection, the needle is 95% of the time in the wrong location. or you are injecting your bolus too quickly.



i agree
 
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One should NEVER try to obtain parasthesias during a TFESI. If the patient can't tolerate the injection, the needle is 95% of the time in the wrong location. or you are injecting your bolus too quickly.




I agree with this as well which is why i use minimal sedation (ie oral valium). I have had more than one patient who seemed to have an unusual response during needle placement/contrast injection. I quickly withdrew the needle. I do not feel that I would have had this information with deep sedation. I cant bill 99144 but I dont care.
 
that's why i don't sedate >99% of my cases...
 
I understand that one should never spear the nerve during needle placement but it seems reasonable to me (and perhaps I am wrong) that when advancing the needle mm by mm into it's final location a slight concordant paresthesia is appropriate followed by needle withdraw and injection. It also seems reasonable to me that when injecting some discomfort is expected but it should not be intolerable and you should never inject forcefully. I have plenty of patients that complain of uncomfortable pain during interlaminar esi's (with no herniated disc or other major pathology).
 
I understand that one should never spear the nerve during needle placement but it seems reasonable to me (and perhaps I am wrong) that when advancing the needle mm by mm into it's final location a slight concordant paresthesia is appropriate followed by needle withdraw and injection. It also seems reasonable to me that when injecting some discomfort is expected but it should not be intolerable and you should never inject forcefully. I have plenty of patients that complain of uncomfortable pain during interlaminar esi's (with no herniated disc or other major pathology).


yeah, dude, you're fine and you're not wrong, IMHO. there are some other practitioners on this forum who claim that 95% of the time, their injections are pain-free (paresthesia-free - whatever). i think that is complete BS. i dont think you should necessarily TRY to get paresthesias, but you are injecting fluid right around a nerve that is sometimes in a very tight space (stenosis), they are going to feel it. if you keep withdrawing your needle, a transforaminal very quickly becomes a multifidis injection. as long as you are not intraneural or intravascular, you are ok. sometimes they feel interlaminars as well. thats ok.

abort the procedure if there are paresthesias? what? really? im assuming you still bill for it, though. i really dont think this is a technique issue, but rather our perception.misperception of what the patient is actually feeling.
 
i abort the procedure if the parasthesia persists despite needle repositioning...

similar cases have gone to court and the pain doc got fried for INJECTING despite the persistent complaint of pain --- in that case he did not document in his note that he withdrew the needle before injecting (he just used the template as his note).

this happens VERY rarely (maybe once or twice a year), as most parasthesias abate.
 
yeah, dude, you're fine and you're not wrong, IMHO. there are some other practitioners on this forum who claim that 95% of the time, their injections are pain-free (paresthesia-free - whatever). i think that is complete BS. i dont think you should necessarily TRY to get paresthesias, but you are injecting fluid right around a nerve that is sometimes in a very tight space (stenosis), they are going to feel it. if you keep withdrawing your needle, a transforaminal very quickly becomes a multifidis injection. as long as you are not intraneural or intravascular, you are ok. sometimes they feel interlaminars as well. thats ok.

abort the procedure if there are paresthesias? what? really? im assuming you still bill for it, though. i really dont think this is a technique issue, but rather our perception.misperception of what the patient is actually feeling.
Hey Chimp, I thing you might have hit a nerve there (sorry, SOMEONE had to say it ;))
 
Just a quick tangential question...what are people using for test doses during TFESI? Also is there a good reference...
 
Just a quick tangential question...what are people using for test doses during TFESI? Also is there a good reference...

Test dose?

Omni 180 injected under digital subtraction looking for a neurogram and no vascular uptake. That's it. We reserve 'test dose' 1.5% lido with epi for celiacs, LSBs, and hypogastric plexus blocks.
 
Pain Med. 2004 Jun;5(2):202-5.
Temporary neurologic deficit after cervical transforaminal injection of local anesthetic.

Karasek M, Bogduk N.
Northwest Spine Group, Eugene, Oregon, USA.

OBJECTIVE: To describe the effects of spinal cord block after injection of local anesthetic into a cervical radicular artery. DESIGN: Case report.

SETTING: Neurology practice specializing in spinal pain. Interventions. A patient underwent a C6-7 transforaminal injection. Contrast medium indicated correct and safe placement of the needle.

RESULTS: After the injection of local anesthetic, the patient developed quadriplegia. The injection was terminated. The neurologic impairment resolved after 20 minutes observation.

CONCLUSION: Despite correct placement of the needle for a cervical transforaminal injection, injectate may nevertheless enter a cervical radicular artery. Whereas local anesthetic, so injected, appears to have only a temporary effect on spinal cord function, particulate steroids may act as an embolus and cause permanent impairment.


Spine J. 2002 Jan-Feb;2(1):70-5.
Paraplegia after lumbosacral nerve root block: report of three cases.

Houten JK, Errico TJ.
Department of Neurosurgery, New York University School of Medicine, New York, NY 10016, USA.

BACKGROUND CONTEXT: Lumbar nerve root blocks and epidural steroid injections are frequently employed in the management of degenerative conditions of the lumbar spine, but relatively few papers have been published that address the complications associated with these interventions. Serious complications include epidural abscess, arachnoiditis, epidural hematoma, cerebrospinal fluid fistula and hypersensitivity reaction to injectate. Although transient paraparesis has been described after inadvertent intrathecal injection, an immediate and lasting deficit has not been previously described as sequelae of a nerve root block.

PURPOSE: We present three cases in which either persisting paraplegia or paraparesis occurred immediately after administration of a lumbar nerve root block and propose a mechanism for this devastating but previously unreported complication.

STUDY DESIGN/SETTING: Case reports of three patients.

PATIENT SAMPLE: Three patients, two women and one man ranging in age from 42 to 64 years, underwent three procedures performed at three different facilities, in the hands of two different injectionists. In each instance, penetration of the dura was not thought to have occurred. In two procedures the needles were placed transforamenally, one at L3-4 on the left and one at L3-4 on the right, and in the third the needle tip was placed immediately lateral to the S1 nerve root.

OUTCOME MEASURES: Patient follow-up data from medical office records.

METHODS: In each case, needle placement was verified with injection of a contrast media in conjunction with either computerized tomography or biplanar fluoroscopy. No backbleeding or cerebrospinal fluid was encountered upon aspiration in any of the procedures. Magnetic resonance imaging (MRI) was performed within 48 hours of injury in all patients.

RESULTS: In each patient, paraplegia suddenly ensued after instillation of the steroid solution and, in each instance, postprocedure MRI revealed increased signal in the low thoracic spinal cord on T2-weighted imaging consistent with edema. The sudden onset of neurological deficit and the imaging changes noted in the spinal cord point to a vascular explanation for these injuries. We postulate that in these patients the spinal needle either penetrated or caused injury to an abnormally low dominant radiculomedullary artery, a recognized anatomical variant. This vessel, also known as the artery of Adamkiewicz, in 85% of individuals arises between T9 and L2, usually from the left, but in a minority of people may arise from the lower lumbar spine and rarely even from as low as S1. The artery of Adamkiewicz travels with the nerve root through the neural foramen and irrigates the anterior spinal artery. Injury of it or injection of particulate matter into it, as what may happen with the commonly used epidural steroid injectates, may result in infarction of the lower thoracic spinal cord, producing the clinical and imaging findings seen in these three patients.

CONCLUSIONS: We present the cases of three patients who had lasting paraplegia or paraparesis after the performance of a nerve root block. We propose that the mechanism for this rare but devastating complication is the concurrence of two uncommon circumstances, the presence of an unusually low origin of the artery of Adamkiewicz and an undetected intraarterial penetration of the procedure needle.
 
Last edited:
Pain Med. 2004 Jun;5(2):202-5.


Spine J. 2002 Jan-Feb;2(1):70-5.
Paraplegia after lumbosacral nerve root block: report of three cases.

Houten JK, Errico TJ.
Department of Neurosurgery, New York University School of Medicine, New York, NY 10016, USA.

BACKGROUND CONTEXT: Lumbar nerve root blocks and epidural steroid injections are frequently employed in the management of degenerative conditions of the lumbar spine, but relatively few papers have been published that address the complications associated with these interventions. Serious complications include epidural abscess, arachnoiditis, epidural hematoma, cerebrospinal fluid fistula and hypersensitivity reaction to injectate. Although transient paraparesis has been described after inadvertent intrathecal injection, an immediate and lasting deficit has not been previously described as sequelae of a nerve root block.

PURPOSE: We present three cases in which either persisting paraplegia or paraparesis occurred immediately after administration of a lumbar nerve root block and propose a mechanism for this devastating but previously unreported complication. STUDY

DESIGN/SETTING: Case reports of three patients.

PATIENT SAMPLE: Three patients, two women and one man ranging in age from 42 to 64 years, underwent three procedures performed at three different facilities, in the hands of two different injectionists. In each instance, penetration of the dura was not thought to have occurred. In two procedures the needles were placed transforamenally, one at L3-4 on the left and one at L3-4 on the right, and in the third the needle tip was placed immediately lateral to the S1 nerve root.

OUTCOME MEASURES: Patient follow-up data from medical office records. METHODS: In each case, needle placement was verified with injection of a contrast media in conjunction with either computerized tomography or biplanar fluoroscopy. No backbleeding or cerebrospinal fluid was encountered upon aspiration in any of the procedures. Magnetic resonance imaging (MRI) was performed within 48 hours of injury in all patients.

RESULTS: In each patient, paraplegia suddenly ensued after instillation of the steroid solution and, in each instance, postprocedure MRI revealed increased signal in the low thoracic spinal cord on T2-weighted imaging consistent with edema. The sudden onset of neurological deficit and the imaging changes noted in the spinal cord point to a vascular explanation for these injuries. We postulate that in these patients the spinal needle either penetrated or caused injury to an abnormally low dominant radiculomedullary artery, a recognized anatomical variant. This vessel, also known as the artery of Adamkiewicz, in 85% of individuals arises between T9 and L2, usually from the left, but in a minority of people may arise from the lower lumbar spine and rarely even from as low as S1. The artery of Adamkiewicz travels with the nerve root through the neural foramen and irrigates the anterior spinal artery. Injury of it or injection of particulate matter into it, as what may happen with the commonly used epidural steroid injectates, may result in infarction of the lower thoracic spinal cord, producing the clinical and imaging findings seen in these three patients.

CONCLUSIONS: We present the cases of three patients who had lasting paraplegia or paraparesis after the performance of a nerve root block. We propose that the mechanism for this rare but devastating complication is the concurrence of two uncommon circumstances, the presence of an unusually low origin of the artery of Adamkiewicz and an undetected intraarterial penetration of the procedure needle.

i didnt read the full text of the above article, but it sounds like they didnt use live flouro. also, it didnt say which steroid they used. adamkiewicz on the right at S1 is hard for me to swallow as a rationale.

i know that everyone out there is not doing test doses. im not, but i guess im thinking about it. id love a quick "yay or nay" on whether or not people are doing test doses.
 
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i didnt read the full text of the above article, but it sounds like they didnt use live flouro. also, it didnt say which steroid they used. adamkiewicz on the right at S1 is hard for me to swallow as a rationale.

i know that everyone out there is not doing test doses. im not, but i guess im thinking about it. id love a quick "yay or nay" on whether or not people are doing test doses.

Nay; I feel it will serve to obfuscate a developing epdural hematoma or nerve injury. Also the minute movement and time seperation between contrast to local to steroid may be enough time to have the needle move into another micro-vessel from step one to step three.

I use a three way stop-cock with a catheter attached to the needle so it does not move at all. step one: inject contrast under live or DSA fluoro; step two; move selector arm on three way stopcock to steroid syringe and inject steroid. Nothing has been moved and no time has been wasted "changing" syringes between contrast injection and steroid injection.

I'm not saying my way is the best but its an option.
 
Just outta curosity ampa, what steroid did they use in the article you quoted! Iuse Kenacort rather than depomedrol, as acc. to P. raj kenacort doesn't make big particles as does depo. also I wish to know what steroid most of the guys are using for TFESI!!
 
Just outta curosity ampa, what steroid did they use in the article you quoted! Iuse Kenacort rather than depomedrol, as acc. to P. raj kenacort doesn't make big particles as does depo. also I wish to know what steroid most of the guys are using for TFESI!!

bailey -

I'll speak for ampa cause I'm in his head :D The only steroid that is truly nonparticulate is dexamethasone, that is also the only steroid that has never been implicated in a catastrophic epidural complication in the literature. Some argue that betamethasone is nonparticulate as well but it is. Triamcinolone is not that much diff than depo. I only use test doses for cervical TFESIs and I use 0.8cc 2% lido based on the above article. And I don't try and get a paresthesia. Sometimes it happens and I apologize. And most patients "feel pressure"/discomfort during my TFESIs. I had one recently cry out in pain during the injection, even after repositioning several times. I gave up and re-examined the MRI. Turns out his neuroforamen were tighter than I had thought. I'm guessing that's why it hurt so much. And powermd, your test dose with epi. Is it 1:100000 epi or 1:200000 epi?
 
Does that mean you are using Dexa for TFESI (C,T,L)! I'll happily switch once I have some ref for that matter....;)
 
bailey -

I'll speak for ampa cause I'm in his head :D The only steroid that is truly nonparticulate is dexamethasone, that is also the only steroid that has never been implicated in a catastrophic epidural complication in the literature. Some argue that betamethasone is nonparticulate as well but it is. Triamcinolone is not that much diff than depo. I only use test doses for cervical TFESIs and I use 0.8cc 2% lido based on the above article. And I don't try and get a paresthesia. Sometimes it happens and I apologize. And most patients "feel pressure"/discomfort during my TFESIs. I had one recently cry out in pain during the injection, even after repositioning several times. I gave up and re-examined the MRI. Turns out his neuroforamen were tighter than I had thought. I'm guessing that's why it hurt so much. And powermd, your test dose with epi. Is it 1:100000 epi or 1:200000 epi?

That post was during my fellowship where we did NOT do a test dose. Dye is injected under DSA. In PP I don't have DSA, so I just look for a persisting neurogram/epidurogram (and neg asp) to r/o intravascular placement. I'm also tending toward less use of local with the injectate because if the patient has a catastrophic complication I want to be sure of what it is ASAP. As I said in my last post, in fellowship we only did test doses (with 1:200K epi) for high volume sympathetic blocks.
 
Powermd, that is what I was referring to... test doses for hypogastics, celiacs etc. Just wasn't sure if it was 1:100k or 200k, thanks

And baily, I only use dexa for cervical and thoracic TFESIs not lumbar. Some would argue and use dexa for everything. There was one article looking at efficacy of dexa vs triamcinolone I believe, and it did show that triamcinolone was more effective however failed to reach statistical significance. Take that for what it's worth
 
Another option for TFESIs is using a peripheral nerve stimulator. I used to use it but don't really think it works that well. Seems like, by the time the pt feels the stim, you are on top of the nerve root anyway. I use Epimed blunt tip needles. I have to belive they are less traumatic to the nerve root. I don't routinely use dexa, agree with Club, it is the safest, but maybe not as effective.
 
Than I'll continue with my Triamcinolene as it usually works well for me!
 
Powermd, that is what I was referring to... test doses for hypogastics, celiacs etc. Just wasn't sure if it was 1:100k or 200k, thanks

And baily, I only use dexa for cervical and thoracic TFESIs not lumbar. Some would argue and use dexa for everything. There was one article looking at efficacy of dexa vs triamcinolone I believe, and it did show that triamcinolone was more effective however failed to reach statistical significance. Take that for what it's worth
Betamethasone is the smallest particulate. There is no justifiable reason to put your patient at greater risk with larger particles. (Tiso RL, Cutler T, Catania JA, Whalen K. Adverse central nervous system sequelae after selective transforaminal block: The role of corticosteroids. Spine J. 2004;4:468–474.)

O’Donnell C, Cano W, Eramo G. Comparison of triamcinolone to dexamethasone in the treatment of low back pain and leg pain via lumbar transforaminal epidural steroid injection. Spine J. 2008;8:65S demonstrated that, when you compare therapeutic doses of particulate to a known sub-therapeutic does of dexamethasone, the non-particulate (not surprisingly) doesn't work as well.

A trend that does not reach statistical significance is, be definition, insignificant. The Dreyfuss study (Dreyfuss P, Baker R, Bogduk N. Comparative effectiveness of cervical transforaminal injections with particulate and nonparticulate corticosteroid preparations for cervical radicular pain. Pain Med. 2006 May-Jun;7(3):237-42.) concludes "A theoretically safer nonparticulant agent appears to be a valid alternative to particulate agents that have been used to date, and which have been associated with hazard."

I don't use non-particulates in the lumbar spine is illogical.. I don't use them below where Adamkiewicz is likely to lie (i.e. below L4) at least has some construct validity.
 
"I don't use non-particulates in the lumbar spine is illogical.. I don't use them below where Adamkiewicz is likely to lie (i.e. below L4) at least has some construct validity."

Yeah, that's basically what I meant. I'm actually always thinking about Adamki whenever I do TFESIs and often go nonparticulate on my higher lumbar TFESIs, with a lower threshold when I inject on the left side . . . .
 
Betamethasone is the smallest particulate. There is no justifiable reason to put your patient at greater risk with larger particles.

So would you argue that pain docs should use betamethasone in lieu of triamcinolone for the usual lumbar transforaminals at L5,S1? Is there any literature to back this up?

I use dexamethasone for cervical, thoracic, and upper lumbar transforaminals (L1-L3), and I use triamcinolone for lower lumbar transforaminals and for interlaminar epidurals at all levels.

Is there any evidence in the literature that we should be using betamethasone over triamcinolone for lower lumbar transforaminals/interlaminars?

I guess there is also the argument that it's possible to acquire preservative free betamethasone, but not preservative free triamcinolone.
 
So would you argue that pain docs should use betamethasone in lieu of triamcinolone for the usual lumbar transforaminals at L5,S1? Is there any literature to back this up?

I use dexamethasone for cervical, thoracic, and upper lumbar transforaminals (L1-L3), and I use triamcinolone for lower lumbar transforaminals and for interlaminar epidurals at all levels.

Is there any evidence in the literature that we should be using betamethasone over triamcinolone for lower lumbar transforaminals/interlaminars?

I guess there is also the argument that it's possible to acquire preservative free betamethasone, but not preservative free triamcinolone.

amp will chime in but in reviewing the literature last year I remember betamethasone being implicated in a couple catastrophic complications from TFESIs. Dexa, on the other hand, has not. And I can't remember if triamcinolone or beta was cited more often. I think triamcinolone was which is what one would expect based on particle size....
 
I remember Aprill quoting a study done in St. Louis showing that piggy vertebral arteries injected with ANY particulate steroid (depomedrol, celestone, kenalog) caused thrombosis whereas dex was the only med that did not. I'll let ampa or someone else chime in on the actual study details. I never could find it.
 
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