Thoracic epidural complication

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lonelobo

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Wondering if any one had any ideas on this.

Toady I performed thoracic interlaminar epidural T7-8 on 80 yo man with complaints of mid-upper back pain for last year that has not responded to P.T., accupuncture,massage, TPI's, medications- sent to me on oxycodone 10 mg Q6hwith minimal relief. MRI showed typical spondylitic findings. Exam show diffusetenderness along paraspinals bu not focal findings. Decided to try ESI as pt was desperate for relief, though I let pt know this probably was a reach.
PMH: CAD with CABG x2 in 1955, on aggrenox for TIA's, though pt looks generally healthy.

Procedure:
Performed at ASC with local, after obtaining epiduragram with no apparent vascular spread performed test dose with 2cc 1% lidocaine, then injected solution of 80 mg of kenalog ad 2cc .25% marcaine.
Pt tolerated well. After he was cleaned up we sat him up and he reported feeling "dizzy". Monitors showed pt was brady, so IV was started and fluids
began. Pt remained with dizzy feeling and EMS was called, Brady protocol was started and pt responded to 1cc of EPI and his vitals responded nicely.
He still complained of not feeling well, so 12 lead EKG was performed ( showed sinus brady) continued with fluids and EMS arrived.
on transfer pt was stable and conversing with wife.
enroute to hospital pt arrested and had to be (30 min)resuscitated.
He is currently in CCU on vent, unresponsive, fixed dilated pupils.

Talked to wife and son and they are handling it well, as you can imagine I feel like crap- especially for elective pain procedure.

I am fellowship trained and have performed about 1500 procedures since I have been in private practice over last two years- this is 1st serious complication I have had.

I am obviously not sure what happened but it appeared pt had vasovagal response and his heart just didn't respond.
Wondering if got high spinal that effecting cardiac fibers, but timing seems a little quick for that.

any thoughts would be appreciated

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OMG...what a horrible thing to happen to you, and of course the patient....
My bet would be the high spinal from the 6 cc of injectate that could easily reach the T4 level (lower cardiac accelerator sympathetic fibers) and probably higher. The sympathetics seem to be far more sensitive and have a more rapid onset than the somatic fibers. Another possibility would be a subdural or subarachnoid injection. Subdural placement is particularly difficult to recognize and subarachnoid placement may not result in any CSF efflux from the needle. My sincere condolences to you and the family. Sometimes bad things just happen during procedures.
 
Wondering if any one had any ideas on this.

Toady I performed thoracic interlaminar epidural T7-8 on 80 yo man with complaints of mid-upper back pain for last year that has not responded to P.T., accupuncture,massage, TPI's, medications- sent to me on oxycodone 10 mg Q6hwith minimal relief. MRI showed typical spondylitic findings. Exam show diffusetenderness along paraspinals bu not focal findings. Decided to try ESI as pt was desperate for relief, though I let pt know this probably was a reach.
PMH: CAD with CABG x2 in 1955, on aggrenox for TIA's, though pt looks generally healthy.

Procedure:
Performed at ASC with local, after obtaining epiduragram with no apparent vascular spread performed test dose with 2cc 1% lidocaine, then injected solution of 80 mg of kenalog ad 2cc .25% marcaine.
Pt tolerated well. After he was cleaned up we sat him up and he reported feeling "dizzy". Monitors showed pt was brady, so IV was started and fluids
began. Pt remained with dizzy feeling and EMS was called, Brady protocol was started and pt responded to 1cc of EPI and his vitals responded nicely.
He still complained of not feeling well, so 12 lead EKG was performed ( showed sinus brady) continued with fluids and EMS arrived.
on transfer pt was stable and conversing with wife.
enroute to hospital pt arrested and had to be (30 min)resuscitated.
He is currently in CCU on vent, unresponsive, fixed dilated pupils.

Talked to wife and son and they are handling it well, as you can imagine I feel like crap- especially for elective pain procedure.

I am fellowship trained and have performed about 1500 procedures since I have been in private practice over last two years- this is 1st serious complication I have had.

I am obviously not sure what happened but it appeared pt had vasovagal response and his heart just didn't respond.
Wondering if got high spinal that effecting cardiac fibers, but timing seems a little quick for that.

any thoughts would be appreciated


1. Would have done facets instead of ESI, though both lack sufficient literature to support, the radiographic and clinical findings are more suggestive of a posterior column source of pain.

2. Did he stop the Aggrenox? And if so, does this matter- you will get people splittingthe fence on this though there are clearly some professional guidelines suggesting that it is fine and dandy to perform ESI's while on ASA.

3. What did you do wrong? Unless you gave him a spinal with a large amount of Marcaine (which you say you did not, and you even mention test dosing the patient), maybe itwas the stress of the procedure in an ASA3 patient.

4. Postulate what could have gone wrong? Sympathetic blockade from the ESI allowing cardiac decelerator brady and hypotension creating cardiac ischemia, cord stick, hematoma, medication reaction, etc.

5. The questions to be answered in this M&M will have to be the time frame you got done what you did, and what else could have been done? Cannot comment without knowing BP, O2 sat, etc.

Sht happens. Doing nothing wrong does not mean everything will be alright, but it means you better have some excellent documentation and a good relationship with the family. Go bedside, it happened on your watch and likely had nothing to do with you, but you have to be there for your patient even if you are no longer involved in his care.
 
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Dear lonelobo,

I'm so sorry to hear of this. Algos' comments were along my line of thinking as well. The amount of LA used is up to practitioner preference at this time and there is not a gold standard regarding LA use or no LA use, or even the volume of LA use.

That said, though I have personally not had any major complications yet, I expect to have a few over my career doing these procedures. The when and where is the anxiety provoking issue. Nobody that does these on a routine basis can expect to be complication free, NOBODY.

I'd also suggest that since this is a public forum, moving this topic to the private Pain Rounds Physicians forum, which is limited to verified physicians. I'm always leery of the lawyers probing this website looking for victims.

I wish you the very best and will keep you and your patient in my prayers.
 
I think Algos is on the right track with this one...I recently had a "sub-dural" pattern of contrast on a thoracic ESI at about the same level you did your injection. I injected a very small amount of contrast and saw a "bulbous" epidurogram that produced 2-3 level spread with like 0.75 ml of injectate. I repositioned and did the injection a level lower. The thoracics can be tricky as you know...thinner ligament; smaller epidural space, etc.
 
1. Would have done facets instead of ESI, though both lack sufficient literature to support, the radiographic and clinical findings are more suggestive of a posterior column source of pain.

2. Did he stop the Aggrenox? And if so, does this matter- you will get people splittingthe fence on this though there are clearly some professional guidelines suggesting that it is fine and dandy to perform ESI's while on ASA.

3. What did you do wrong? Unless you gave him a spinal with a large amount of Marcaine (which you say you did not, and you even mention test dosing the patient), maybe itwas the stress of the procedure in an ASA3 patient.

4. Postulate what could have gone wrong? Sympathetic blockade from the ESI allowing cardiac decelerator brady and hypotension creating cardiac ischemia, cord stick, hematoma, medication reaction, etc.

5. The questions to be answered in this M&M will have to be the time frame you got done what you did, and what else could have been done? Cannot comment without knowing BP, O2 sat, etc.

Sht happens. Doing nothing wrong does not mean everything will be alright, but it means you better have some excellent documentation and a good relationship with the family. Go bedside, it happened on your watch and likely had nothing to do with you, but you have to be there for your patient even if you are no longer involved in his care.



1.Facets were a thought, my thinking was 1st try ESI kinda of shotgun one time and access results, know not a lot of support in literature but Anectdotally have had a few that have responded.

2. Yes aggrenox was stopped for 5 days( after getting OK by Cardio), though as you say many do not stop it and that is true in my area- I prefer to stop all anticoags.

Think what you mention in #4 maybe to blame, I just thought onset was a little quick, unfortunately situation is extremely bleak for this man thay are completing workup this evening (CT scan,etc) tonight. Not sure I will ever know for sure.

appreciate the thoughts
 
Dear lonelobo,

I'm so sorry to hear of this. Algos' comments were along my line of thinking as well. The amount of LA used is up to practitioner preference at this time and there is not a gold standard regarding LA use or no LA use, or even the volume of LA use.

That said, though I have personally not had any major complications yet, I expect to have a few over my career doing these procedures. The when and where is the anxiety provoking issue. Nobody that does these on a routine basis can expect to be complication free, NOBODY.

I'd also suggest that since this is a public forum, moving this topic to the private Pain Rounds Physicians forum, which is limited to verified physicians. I'm always leery of the lawyers probing this website looking for victims.

I wish you the very best and will keep you and your patient in my prayers.

Lig,

As long as no identifying information is used, and lonelobo is comfortable with it, I think it is okay to keep it out in the general area...it takes a lot of courage to share complications and others (potential fellowship applicants, residents, med students, etc) should appreciate that there is inherent risk in what we do.
 
I do not think this was a subdural injection because that would have presented with a rapid respiratory and cardiovascular decompensation. It was likely a block of the cardiac accelerator fibers, which lie between T4-T6 by the local anesthetic, which responded well to epi, but the epi simply wore off and the patient subsequently had an MI.
I think this is a complication of a procedure which was handled well initially, but in the transfer of this patient there was a breakdown. I think whoever said the patient was stable for transfer failed at their job.
 
I think this is all of our's nightmare. This is also why I no longer use any local with the spinal needle - only for the skin. The last time I used local the patient got numb up through the chest, followed by a spinal headache - obviously an inadvertant spinal. She did fine. Scared the crap outta me.

If you haven't already, contact your malpractice ASAP. If they never sue you for it, then thank God. If they do, your lawyers have a running start on them. If he dies, the blame game is going to start very fast.

Make sure you have documented the living hell outta this case. You might even talk with one of your malpractice's lawyers before you sign off on dictations, etc.

I would also keep very open lines of communication with the patient's family, and him when he recovers - patients and families are reportedly less likely to sue if they feel their concerns are being addressed.

If not done already, consider getting the admit team to get a cervical and thoracic MRI to see if there was epidural hematoma or similar. Not too long ago, I did 2 LESI's on a patient which went well and helped short term, no complications, no blood at the time. She had surgery a few weeks later and the neurosurgeon documented an epidural hematoma when he opened her up. I bet it happens more than we think.

Good luck, and let us know anyway we can help support you.

:(
 
Consider a Bezold-Jarisch reflex..several reports of young patients arresting after intrathecal "controlled" spinal anesthetics. Typically due to a hyperdynamic left ventricle, low preload, and syncope. There is a nice review article in Anesthesiology a couple years ago. I had a patient post-spinal for a TURP brady down and arrest on me in the PACU. He survived with CPR and pressors. This would assume intrathecal or subdural spread. maybe a possibility

Hope this helps...
 
Consider a Bezold-Jarisch reflex..several reports of young patients arresting after intrathecal "controlled" spinal anesthetics. Typically due to a hyperdynamic left ventricle, low preload, and syncope. There is a nice review article in Anesthesiology a couple years ago. I had a patient post-spinal for a TURP brady down and arrest on me in the PACU. He survived with CPR and pressors. This would assume intrathecal or subdural spread. maybe a possibility

Hope this helps...

Stim,

Can you post the reference? This is a great case for people to learn from.
 
Also consider the effects on splanchnic blood flow for vasomotor responses (see the last reference). As a result the patient may not have been able to compensate with an adequate cardiac output. Rembember CO=SV x HR.


: Acta Anaesthesiol Scand. 1980;24(1):11-6. Links
Effects of thoracic epidural block and prenalterol on coronary vascular resistance and myocardial metabolism in patients with coronary artery disease.

Reiz S, Nath S, Rais O.
A thoracic epidural block from T1 to T12 was performed with plain prilocaine in four patients with coronary artery disease who were scheduled for abdominal aortic aneurysm surgery. The hemodynamic effects of the block consisted of marked reduction in arterial blood pressure due to impairment of cardiac performance and reduction in systemic vascular resistance. The heart rate decreased moderatetly. The epidural block induced a marked reduction in coronary vascular resistance with only a moderate decrease in coronary sinus blood flow. The myocardial oxygen and lactate utilization decreased in parallel to the decrease in cardiac work. In spite of the absence of arrhythmias and ST-T-segment changes following the epidural block, regional myocardial dysoxia could not be ruled out with the present methods. Administration of the cardioselective beta 1-adrenoreceptor agonist prenalterol increased cardiac performance and thereby arterial blood pressure, but did not affect the systemic or coronary vascular resistance.
PMID: 7376799 [PubMed - indexed for MEDLINE]


1: Acta Anaesthesiol Scand. 1979 Feb;23(1):93-6. Links
Hemodynamic effects of prenalterol, a beta1-adrenoreceptor agonist, in hypotension induced by high thoracic epidural block in man.

Reiz S, Nath S, Pontén E.
The hemodynamic effects of prenalterol, a new beta1-adrenoreceptor agonist, on hypotension induced by a thoracic epidural block extending between T1 and T12 and thereby blocking the cardiac sympathetic supply have been studied in eight patients scheduled for abdominal aortic aneurysm resection. The thoracic epidural block induced a drop in blood pressure, due to a reduction in cardiac output and systemic vascular resistance. Intravenous infusion of 10 mg of prenalterol rapidly and effectively reversed the hypotension by an increase in cardiac output without any effects on systemic vascular resistance or heart rate. The results indicate that prenalterol is a pure beta1 agonist with a marked inotropic but no chronotropic property.
PMID: 34312 [PubMed - indexed for MEDLINE]

1: Br J Anaesth. 2002 Sep;89(3):446-51. Links
Effect of thoracic epidural anaesthesia on colonic blood flow.

Gould TH, Grace K, Thorne G, Thomas M.
Sir Humphrey Davy Department of Anaesthesia, Bristol Royal Infirmary, Marlborough Street, Bristol BS8 2HW, UK.
BACKGROUND: The effect of thoracic epidural block on splanchnic blood flow is unclear. It remains to be resolved if sympathetic block, increases or decreases regional splanchnic blood flow and whether regional splanchnic flow becomes dependent on cardiac output or perfusion pressure. A clear understanding of the regional haemodynamic consequences of an epidural block may modify practice with respect to epidural anaesthesia. METHODS: Fifteen patients, who underwent anterior resection for rectal cancer, had invasive intraoperative monitoring of arterial pressure, central venous pressure, cardiac output, inferior mesenteric artery flow (Doppler flow probe), and colonic serosal red cell flux (laser Doppler probe), while an epidural block was established with local anaesthetic. In three consecutive time periods, arterial pressure was first allowed to fall (to a mean arterial pressure of 60 mm Hg), then treated with colloid fluid resuscitation and finally by vasopressors until the pre-epidural arterial pressure had been restored. RESULTS: On induction of epidural block, there was a reduction in mean colonic serosal red cell flux to 65% and inferior mesenteric artery flow to 80% (mean) of pre-epidural levels. There was a strong association between mean arterial pressure and both measured inferior mesenteric artery blood flow (P < 0.004) and colonic serosal red cell flux (P < 0.0001). Changes in cardiac output were poorly associated with either inferior mesenteric artery blood flow (P = 0.638) or colonic serosal red cell flux (P = 0.265). Inferior mesenteric artery blood flow and colonic serosal red cell flux were restored to pre-epidural levels after arterial pressure had been improved with a vasopressor. CONCLUSION: Once intraoperative epidural block has been established, colonic serosal red cell flux and inferior mesenteric artery flow are more closely associated with changes in mean arterial pressure than changes in cardiac output. The measured reduction in colonic flow does not respond to an increase in cardiac output with fluid resuscitation, but requires the use of a vasopressor to increase arterial pressure, before colonic blood flow is improved.
PMID: 12402724 [PubMed - indexed for MEDLINE]
 
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I agree with Kwijibo. The local picked off the cardiac accelerators and the block outlasted the epi that was given, which was to be expected since IV epi doesn't last very long but the LA block does. Based on the LA used, the block could last for over an hour (lidocaine) and possibly several hours (bupivacaine), indicating a need for prolonged monitoring and administration of chronotropic (or other) agents.

Was the patient on a beta blocker? Beta blocker + epi = more alpha than beta effect from epi.

I would have used atropine and volume expansion initially in this case. If bringing up the HR and preload didn't raise BP, that would indicate either ischemic pump failure or profound splanchnic vasodilation. Then I'd start something that's mixed alpha and beta since without a PA catheter it would be hard to tell what is going on. I don't think I'd use pure alpha like phenylephrine in an 80 year old diseased heart. If you're lucky the increased diastolic pressure will perfuse the coronaries and kick the heart into high gear, but if it's pump failure the increased afterload would worsen the situation. I'd go for a mixed inotrope-pressor. Dopamine would probably be my drug of choice if atropine and volume failed. Until then, boluses of ephedrine would probably be best.

I stopped using local for my neuraxial injections a long time ago. Nothing but trouble and I have seen no difference in outcomes using saline.

Lonelobo, if you're anything like others (myself included) who have had this type of experience be prepared for some personal misery. Don't be surprised if you wake up every morning thinking about it, or if it's sitting on your shoulder during every damn case for the next 2 years. That just means you're normal.

One thing I have noticed over the years is that doctors who have had a bad outcome or have been sued suffer in silence and in solitude. I think that is very destructive, but we are trained to never show weakness or uncertainty. Also, your malpractice carrier will tell you to keep your mouth shut. Legally that's good advice, but in terms of mental health it's dangerous. I have seen colleagues who were totally devastated by things like this. One excellent FP quit medicine when he was sued for malpractice. One of the best neurologists I have ever known was a total wreck for several years.

Don't let this happen. Talk to a therapist because if you are a decent person you are going to beat yourself up. Only sociopaths hurt people without caring. A couple of sessions with a psychologist can get your mindset into the proper perspective, which is that you just proved quite convincingly that you're not God. You're still a good doctor but you will need some reminding. More than once, and over an extended period.

Consider an anti-depressant if you find yourself obsessing over it and losing sleep. There's no shame in it - half your colleagues are taking them already. Waking up at 3 a.m. stressing over it and going to work sleep-deprived will just make everything worse.

Bad things happen to good doctors all the time. In the long run you'll be ok, and you'll be ok sooner if you take my advice and talk it out (and use an SSRI if you are obsessing or losing sleep), and it will make you a little more charitable when someone else has a complication. Even if you get sued you'll be ok, and even if you lose the lawsuit you'll be ok. You will still survive and thrive.

Stercus accidit.
 
i agree - talking about it is good - especially face to face with colleagues you REALLY trust - because all of them can sympathize...
 
Just came back from seeing Pt and family
Had EEG which was read as consistent with severe anoxic injury.
As EMS reported PEA for about 10-15 min.
Family is deciding when to withdraw life support.

Toughest thing has been talking to his wife about how this happened.
I have been going up to see her daily and asking her to call or let me
know if I can serve as intermediary for her with other Docs.
She has been very understanding.

It has obviously been a difficult couple days to keep focused at work.
I have always heard horror stories and many will say that if you practice
long enough it will happen-but not easy to swallow only couple years
out of training. Things like these definitely put things into perspective.

Thanks everyone for advice and helpful info
 
:(

If any good comes out of this at all, it's that you've reminded us all how fallible we are. We get very comfortable with the 100's or more of cases that go well every time, only to be blindsided by one like this.

I've already used this as an example to our ASC's nursing staff as to how bad a simple ESI can go bad so quick, and making sure we are prepared to handle it.

My prayers and thoughts are with you.
 
I agree with Kwijibo. The local picked off the cardiac accelerators and the block outlasted the epi that was given, which was to be expected since IV epi doesn't last very long but the LA block does. Based on the LA used, the block could last for over an hour (lidocaine) and possibly several hours (bupivacaine), indicating a need for prolonged monitoring and administration of chronotropic (or other) agents.

Was the patient on a beta blocker? Beta blocker + epi = more alpha than beta effect from epi.

I would have used atropine and volume expansion initially in this case. If bringing up the HR and preload didn't raise BP, that would indicate either ischemic pump failure or profound splanchnic vasodilation. Then I'd start something that's mixed alpha and beta since without a PA catheter it would be hard to tell what is going on. I don't think I'd use pure alpha like phenylephrine in an 80 year old diseased heart. If you're lucky the increased diastolic pressure will perfuse the coronaries and kick the heart into high gear, but if it's pump failure the increased afterload would worsen the situation. I'd go for a mixed inotrope-pressor. Dopamine would probably be my drug of choice if atropine and volume failed. Until then, boluses of ephedrine would probably be best.

I stopped using local for my neuraxial injections a long time ago. Nothing but trouble and I have seen no difference in outcomes using saline.

Lonelobo, if you're anything like others (myself included) who have had this type of experience be prepared for some personal misery. Don't be surprised if you wake up every morning thinking about it, or if it's sitting on your shoulder during every damn case for the next 2 years. That just means you're normal.

One thing I have noticed over the years is that doctors who have had a bad outcome or have been sued suffer in silence and in solitude. I think that is very destructive, but we are trained to never show weakness or uncertainty. Also, your malpractice carrier will tell you to keep your mouth shut. Legally that's good advice, but in terms of mental health it's dangerous. I have seen colleagues who were totally devastated by things like this. One excellent FP quit medicine when he was sued for malpractice. One of the best neurologists I have ever known was a total wreck for several years.

Don't let this happen. Talk to a therapist because if you are a decent person you are going to beat yourself up. Only sociopaths hurt people without caring. A couple of sessions with a psychologist can get your mindset into the proper perspective, which is that you just proved quite convincingly that you're not God. You're still a good doctor but you will need some reminding. More than once, and over an extended period.

Consider an anti-depressant if you find yourself obsessing over it and losing sleep. There's no shame in it - half your colleagues are taking them already. Waking up at 3 a.m. stressing over it and going to work sleep-deprived will just make everything worse.

Bad things happen to good doctors all the time. In the long run you'll be ok, and you'll be ok sooner if you take my advice and talk it out (and use an SSRI if you are obsessing or losing sleep), and it will make you a little more charitable when someone else has a complication. Even if you get sued you'll be ok, and even if you lose the lawsuit you'll be ok. You will still survive and thrive.

Stercus accidit.

you are a good man gorback...

i hope all goes well for you in the future lonelobo
 
I stopped using local for my neuraxial injections a long time ago. Nothing but trouble and I have seen no difference in outcomes using saline.

This thread has convinced me, at least for thoracics and cervicals.
 
This thread has convinced me, at least for thoracics and cervicals.

Lonelobo, to be clear for you, You should know that using LA vs. no LA for epidurals is still up for contention and there is no gold standard regarding this issue. I'd estimate 99% of epidurals are still done with some LA, whether the docs on this board agree or not.
 
Lonelobo, to be clear for you, You should know that using LA vs. no LA for epidurals is still up for contention and there is no gold standard regarding this issue. I'd estimate 99% of epidurals are still done with some LA, whether the docs on this board agree or not.
I wondered what others thought about the use of marcaine vs lidocaine in this set of circumstances, and whether anyone thought it would have made any difference?
 
bump.....good reread and good luck to lonelobo......no marcaine for me anywhere except lumbar.

T
 
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