In view of Jet's recent post: Interesting case

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floridaboy18

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Had an interesting patient in regional the other day. PMH of SLE, ESRD 2/2 lupus nephritis, CAD s/p RCA and LAD stenting, HTN, HLD, hx LLE DVT, seizure disorder and bipolar. I'll place the setting, you tell me what you think went wrong. Go slow for those who want to learn (as I did as a current CA-1) from this case.

Case: AV fistula ligation
Block: Supraclavicular Block with 30 cc of 1.5% mepi with clonidine and epi
What happened? An hour and a half after the patient's block (which was sucessful) with the patient's O2 sats started dropping and the patient started having respiratory failure, tachycardic to 140s, hypertensive to SBP of 200 on non-invasive BP cuff.

What do you do next? What's on the differential?
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floridaboy18 said:
Had an interesting patient in regional the other day. PMH of SLE, ESRD 2/2 lupus nephritis, CAD s/p RCA and LAD stenting, HTN, HLD, hx LLE DVT, seizure disorder and bipolar. I'll place the setting, you tell me what you think went wrong. Go slow for those who want to learn (as I did as a current CA-1) from this case.

Case: AV fistula ligation
Block: Supraclavicular Block with 30 cc of 1.5% mepi with clonidine and epi
What happened? An hour and a half after the patient's block (which was sucessful) with the patient's O2 sats started dropping and the patient started having respiratory failure, tachycardic to 140s, hypertensive to SBP of 200 on non-invasive BP cuff.
What do you do next? What's on the differential?
Click to expand...

Im a 3rd yr med student, so take whatever I say with a pound of salt.

Maybe pneumothorax.. with some epi/clonidine getting into the subclavian?

Im just thinking on my own, without looking anything up, so go easy on me. :)
 
A pneumothorax is definitely a possibility, particularly presenting this acutely. Shot a CXR and only real immediate comment was some bilateral infiltrates they thought were consistent with possible pneumonia. No pneumo.

(The Epi was injected with no aspiration of blood and would not cause tachycardia, hypertension an hour and a half after. Would be immediately after injection. Good thought though).
 
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Also a 3rd year student. Please add my pound of salt to the dish:

H/O Lupus with DVTs - possible antiphospholipid antibody syndrome.

Got a DVT and threw a PE.
 
Also not an anesthesiologist so I will bring some salt to the table too...

- when was the last dialysis? Do we have recent electrolytes?
- for Ddx, many causes, but I'd be concerned about serotonin syndrome, given the psych and seizure history and injection of clonidine.

I never met a psychotropic drug that I could trust, they are all squirrelly.

Have some other ideas about reversal of a high preload, high afterload state but I'll contribute one thought at a time.

Thanks for the interesting case.
 
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I'm a nurse. You should defer to the CRNA
 
floridaboy18 said:
A pneumothorax is definitely a possibility, particularly presenting this acutely. Shot a CXR and only real immediate comment was some bilateral infiltrates they thought were consistent with possible pneumonia. No pneumo.

(The Epi was injected with no aspiration of blood and would not cause tachycardia, hypertension an hour and a half after. Would be immediately after injection. Good thought though).
Click to expand...

ahh.. Didnt see the time frame... hmm... possible pneumonia.... any preop PFTs?
 
hypertension and tachycardia as well as hypoxia is sort of an unusual combination.....if it was PE, etc, I'd more likely expect hypotension.

Perhaps he got a delayed onset of phrenic paralysis (less likely with supraclavicular, but possible...), already had some underlying nerve pathology on the other side as well, and now with respiratory distress/hypoxia is getting agitated causing the hypertension and tachycardia.
 
Libertas - you are right. I forgot that hypotension would be more likely. Wasn't thinking straight.

I retract my previous guess er... diagnosis...

New differential:

Clonidine withdrawal (alpha 2 agonist rebound hypertension)
Late absorption of the sympathomimetics systemically
Early acute intraoperative MI
Early malignant hyperthermia
 
Also - question for the experienced folks here -

Autonomic dysreflexia. For example, if someone forgot to place a Foley, is autonomic dysreflexia possible on a healthy individual? In my understanding, it is mostly in spinal cord injury patients - but I'm still learning about anesthetic drugs.
 
It cannot be autonomic hyperreflexia (you need a chronic high spinal lesion for that, with lower spinal stimulation, or some really bad autonomic neuropathy in diabetes or degenerative neurologic disease etc.).

It cannot be malignant hyperthermia, if it was a MAC and the patient only had contact with a nasal cannula on the accessory oxygen port.

Serotonin syndrome would probably need high doses of clonidine.

Pneumonia doesn't happen in 90 minutes and it's typically not associated with hypertension.

Would not consider rebound from slowly absorbed tissue clonidine. Plus it has a longer action than 90 minutes.

How fast did the desat and sympathetic response set in?

P.S. I don't want to guess; this thread should be for trainees.
 
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I'm out of ideas, then.

I think libertas' idea of the phrenic nerve block is most likely. A block involves injecting into tissues, and then the medication can spread and redistribute from there.

I also don't know if pneumonia is completely ruled out. The xray is suggestive of it - it does not develop in 90 minutes, true... but perhaps it was already smoldering and the patient just lost the ability to compensate.

I'm going to stew on this some more...

Edit:
Just thought of some patient factors:

Alcohol or other substance withdrawal
Failure to take home BP meds prior to surgery

And a surgeon based one:

Ligating the AV bypass increased total peripheral resistance when the venous shunt was closed off. This lead to the hypertension. Throughput failure on a patient with known cardiac disease and likely pre-existing hypertension related to renal failure meant flash pulmonary edema, explaining the rapid onset respiratory failure.

Med student speculation all done. I'm going to sit back and see how this pans out now...

Edit 2: clarifying
 
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I agree with Libertas as to most likely cause. Other thoughts:

-If you left the fluid wide open you could send the patient into circulatory overload, which would account for the resp failure and hypertension, and by extension I guess the tachycardia.
-You said the block was successful, but if not, and the patient got hypertensive/tachycardic from pain, that could also cause a flash pulmonary edema and then resp failure.
-Turns out, you know what else presents with hypertension, tachycardia, and respiratory failure: accidental administration of paralytic to a mostly awake patient. But I'm guessing that's not what happened here.

Also, unless I missed a chapter somewhere, what does clonidine have to do with serotonin syndrome? A cursory Google search results in something called high-dose clonidine motor syndrome, otherwise I haven't heard/read/pharmacologically understand an association between the two.
 
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BobtheDoc said:
Ligating the AV bypass increased total peripheral resistance when the venous shunt was closed off. This lead to the hypertension. Throughput failure on a patient with known cardiac disease and likely hypertension related to renal failure meant flash pulmonary edema, explaining the rapid onset respiratory failure.
Click to expand...

I'm not sure what "throughput failure" is, but if you mean the patient was in high output cardiac failure from a grossly enlarged fistula, then yes, that's a good line of reasoning. I would think it would have to be a pretty significant fistula to create that kind of hemodynamic change, but closing it off could lead to a large increase in SVR and acute decompensated CHF.
 
BobtheDoc said:
Ligating the AV bypass increased total peripheral resistance when the venous shunt was closed off. This lead to the hypertension. Throughput failure on a patient with known cardiac disease and likely hypertension related to renal failure meant flash pulmonary edema, explaining the rapid onset respiratory failure.
Click to expand...

I would go with this one. Probably developed a lot of MR from the high afterload.
 
By "throughput failure" I was trying to get across the idea that the high afterload prevented blood moving through - everything backed up causing the pulmonary edema... probably not the right words. Basically, this patient has known cardiac risk factors, so it is difficult to know how how tenuous their cardiac tolerance was...

If this is what was going on, then I think proper management would be to intubate and start positive pressure ventilation with a high PEEP, and then give an antihypertensive that works via systemic vasodilation to reduce afterload. An agent with inotropic action would be beneficial, potentially. Phosphodiesterase III inhibitors or hydralazine.

Not saying this is the correct diagnosis, but for those here who know, IF it was - would nitroglycerin or clonidine be appropriate to reduce afterload here?
 
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A lot of great thoughts guys. A few other details to add (I might not have been clear with the original post):
- The patient never left the regional bay, the case in the OR before got delayed a bit hence the patient sitting in regional for an hour and a half. Thankfully, they were not induced for general anesthesia (even though this is a small consideration because 1.5% mepi is anesthetic dosing and GA wasn't on the table).
-This all occurred over about 20 minutes, starting about an hour to an hour and a half after the block.

DDx so far from what I have read:
-Potential PE: Likely would expect more hypotension than hypertension but the acuity of the situation certainly pointed towards this possibility. Remote history of DVT on coumadin.
-Delayed Phrenic nerve paralysis: For my fellow residents/students, phrenic nerve paralysis following a supraclavicular block is not uncommon. This is why it is essential to consider your patient's pulmonary history before doing this block. Our patient was a terrible historian, but we felt gave enough information to proceed. This also would have been seen on a CXR with an elevated diaphragm. The diaphragm was normal appearing on both sides.
-Delayed intravascular consumption of Epi: I presume this is possible and could explain her vitals, but don't really know how that would relate to her new onset respiratory failure
-Serotonin syndrome: Interesting thought. No flushing was noted on/by the patient. Interesting thought though!
-Pulmonary edema 2/2 volume overload. The fluids were not left wide open, but she had been sitting there with them dripping over the mentioned time period. She had recent dialysis (1-2 days prior). Her most recent (2011) echo showed mild MR. This as probably 2nd on our list to a potential PE given the acuity of the respiratory failure. The CXR we were reading also came off of a machine, and wasn't the best picture of sorts while we were figuring this out.
-Pneumothorax: Vitals don't really point towards this either, we thought this was a possibility initially given the procedure location and acuity...but CXR did not show anything.

More answers to come. This is what happened next. We gave her some antihypertensives (labetalol I believe) given her tachycardia and hypertension prior to what happened next.

So, the patient's mental status starts to wain. Sats in low 90's now on 15 L non re breather. We elect to intubate her in regional. I'd ask for your thoughts on induction agents, but I'll just tell you we did propofol/sux/tube given the acuity of the situation, available meds, and her recent dialysis session. Her potassium was 4.1 on that morning's BMP. Intubation goes fine.... then....

This previosuly tachycardic, hypertensive patient's blood pressure plummets after induction. We have to place a femoral a-line and central line for quick access. She is hypotensive to the point of requiring infusions of pressers (phenylephrine and epinephrine) to increase her MAP to goal of 65.

What do you do next? Change your differential? (I am learning as we go, too).
 
Holy cow! My bet was on the PE or volume overload. Now I would add a coronary event, and that pneumonia doesn't sound half bad.
 
I think this is one of those ideal cases to grab the ultrasound probe and stick it on the patient's heart and lungs for a quick look to figure out what the F is going on ..... conveniently you're in the regional bay! Check the lungs for ptx, check the IVC, and rv/lv function.

So if this all happened while the patient is in the regional suite still, the block probably has SOMETHING to do with it, but the presentation still seems unusual to me. Delayed LAST? Seems a little unlikely, given the time course, initial hypertension, though that was a reasonably hefty dose of mepiv, I guess...what the hell, maybe give intralipid. It seems like last can really present in unpredictable ways. I suppose some sort of RV pathology (RV infarct, pe...) but again the initial hypertension makes less sense to me.

Last crazy guess---you punctured some bad vessel doing the block, they have some sort of expanding badness in their neck, leading to respiratory distress first, and eventually circulatory instability.
 
Good case guys!

I realize I'm talking with a bit more info than the inital post, but:

- Obstruction and hypercarbia could have given you the entire holding area picture; I agree with intubation.
- Any chance this is LAST? You have a pt with seizure d/o who now has a seizure-causing med in her body. Timing is a little off, but maybe some weird seizure presentation? You gave propofol, a known AED and hypotension causing agent...maybe you broke seizure and with it went the hyperstimulation that was causing the high HR and HTN.
- I too thought PE, but that's a lot of BP for a symptomatic PE
- PTX was on my list; I think you have to say it given the procedure, but again, lots of BP for a pt with a tension PTX. But the PPV and subsequent CV collapse sorta fits.
- Primary cardiac (MI, CHF) definitely on list, even with HTN
 
Persistent/refractory hypotension after induction/intubation makes me think of a few things; the most common unifying factor being a pre-load dependent patient. Positive pressure ventilation and then game over. You see it a lot with septic bowel patients who are under-resuscitated, but that doesn't sound like this case. Her RCA stent could have gone down causing RV failure which would also fall in the preload-dependent category.

Also like the LAST theory and would consider running some intralipid and see if it improves.
 
I have never used mepivacaine, but emedicine says that the toxic dose is 7 mg/kg, not to exceed 400 mg (patient had 450).
 
LAST? Not sure what this is an acronym for. Could someone enlighten me? Dr. Google didn't know...
 
Couple of thoughts:

1). LAST stands for local anesthetic systemic toxicity. Typically, what it is referring to is systemic toxicity to the heart or brain. Remember, local anesthetic block sodium channels. In the brain, this leads to seizure. In the heart, this leads to heart block or other dysrhythmias. Inter lipid (1.5 cc/kg) is usually the dose used to help bind the lipophillic anesthetic and attempt to reverse the damage. I don't have a ton of experience with this being a Ca-1 but I would think an hour and a half later is a little long.

2). The patient did receive 450 mg of mepivacaine, and I am used to quoting the 7 mg per kilogram toxic dose. However, my understanding is that those numbers are not exactly cut and dry. The patient wait over 130 kg. Her BMI was between 40 and 45. Given that there's no intravascular aspiration I don't think this played a part. Maybe though. Another good thought.

What happened next. After we gain central access and an arterial line, patient was started on pressers. We then got a TTE which demonstrated moderate to severe MR. The MR was significantly worse than what had been seen on the previous echo. Once we are able to do the chest x-ray on actual computer screen, it didn't look that that's the consistent with a volume overload sort of picture.

I thought this was an interesting case given the differential and the location and setting of where this happened. We definitely considered hee hee, pneumothorax, phrenic nerve process, new onset pneumonia potentially new onset sepsis, and the corresponding overload in place in stage renal disease patient.

Patient ended up requiring dialysis anyway, but I did find it interesting that the patient potassium jump from 4.1 to 6 after our dosage succinylcholine. I noticed when the t waves started looking peaked on the monitor. Stat abs showed us that.

For the med students: treating hyperkalemia. Remember C-BIG-KD.

In order. Calcium gluconate. Most important. Stabilizes cardiac membrane so that threshold to cause deadly arrhythmia is raised. B for beta agonists, which push k intravascular. Insulin for I which does the same. We give "D" (dextrose) with that. Only two ways to remove k from body (kayexolate and dialysis) for KD.
 
Looks like the patient is not the only bad historian around. Next thing we will hear is that the patient was on a MAO inhibitor for the bipolar disorder and they used epi for the block.

LAST is local anesthetic systemic toxicity. Silly new acronym.

That dose of mepivacaine does not look very Impressive. You guys should have seen regional performed before ultrasound. Blocks only worked back then when you have one ml per kilo. Toxicity wasn't that common.
 
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Thanks for the updates Florida,

Just a couple of thoughts:

- Initially I considered that by ligating the fistula you are reversing a high afterload, high preload state and that if the pt had a preload dependent lesion it would be exacerbated, as others eluded to above. Do you think the exacerbation of the MR was due to intrinsic disease of the valve due to SLE, rupture of a papillary muscle due to recurrent MI, or other cause because I don't see why the drop in afterload wouldn't actually help the MR? Can't wrap my head around it.

- Also, did you consider adrenal insufficiency as a cause of the hypotension? Was the patient on long term corticosteroids due to the SLE? Its something I might have tried if the pt remained hypotensive.

- I come from the pediatrics world, and I would have considered milrinone if this pt had poor contractility as well, especially since it does not change myocardial oxygen demand and this patient has 2 stents, and it also helps calcium uptake of the myocardium which would assist you if the potassium was increasing. Did you guys discuss this? I dont see it used much in adult medicine but would be interested what your thoughts are.

Thanks again for the interesting discussion.
 
But what caused the pt to end up in sudden chf from severe MR. The patient was able to live outside of the hospital prior to coming to your regional bay for an elective procedure…so you always have to ask yourself what the hell did we just do that changed this patients course.

Did you have an ABG prior to intubation? If not did the vent you have available have an ETCO2 reading on it after intubation?
How much sedation and pain medication did the patient get in the regional suite before and during the block?
One of my first thoughts was a progressing pneumothorax that wasn't seen on the initial CXR and was going to be chalked up to an occult pneumo that progressed
My second thought was the pt become hypercarbic secondary to sedation or phrenic block leading to tachycardia and increased SVR resulting in the initial vitals and CXR reading….what vasopressors were the pt started on prior to the echo?
You mentioned the K was 6 how long after sux was this lab obtained? Was the patient acidotic at this time?
 
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Thank you for a very interesting case. I must admit the worsening of the MR without fluid overload or coronary event (or some other cause of acute LV dysfunction) was not high on my list. But what caused the exacerbation? What are the chances that it was spontaneous? ;)
 
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In short, I would have to look back At the record. I'll take another look when I get home. I think that the patient did receive probably 1 L in regional over that hour and a half. She ended up receiving more when she was put on pressers. I think potentially it could have been volume overload from fluids.

A question I had actually about this myself is will phrenic nerve paralysis always show up on a CXR? I mean if it's blocked you'd think it would be elevated, but I haven't seen it yet.

She ended up getting dilaysis and the tube came out a day or tube later so it's also a possibility she missed a dialysis session (though she said she went two days ago on that friday).
 
Also I will say that the MR was severe enough that it ended up warranting a CT surgery consult who will not be replacing the valve emergently, but did want to follow back up once she was more stable in terms of her ESRD/dialysis to consider replacing it.

And if I had all the answers I wouldn't be putting this on here :) it was a strange/interesting case.

And I agree with the sentiment of "what the hell did we do to her" considering her stability before the block. I'll look up the first ABG we can find, though we manually bag valve masked her for a good bit before transferring her to the PACU.
 
My best guess is that you had a patient with mod MR, probably worsening over time (not sure how recent the previous echo was). She might be barely compensating, but is also 2 days out from dialysis, and you paralyze her phrenic. Over the next hour and a half she tires out, starts getting air hungry and maybe anxious, leading to hypertension and more pulm edema. You then give someone who's in distress labetalol and block their sympathetic tone. Inducing them and completely removing their air-hunger-driven sympathetic drive shortly after the labetalol might have caused that severe hypotension, especially since I'm guessing you didn't go super light on the prop due to the urgent RSI, recent HTN setting. Not to mention her LV might not be the greatest with chronic MR.

I think for the MR alone to cause all that in that time frame is unlikely, and would have to be torrential, maybe set off by a pap rupture, but that doesn't sound like this case...

Thanks for the case
 
Itwasalladream, I think you are spot on with almost all of that. Still a question for my learning... How often do you get phrenic nerve paralysis without an elevated hemidiaphragm on plain film?
 
i think it becomes a chicken or egg argument ultimately. i think its unlikely that she had acute nonischemic worsening of her MR, and there is no reaosn to suspect an acute coronary event in holding.

i wager she is less than compliant with her antihypertensives, perhaps got a little sedative for the block, got a little phrenic nerve paralysis, maybe got hypercapneic? that plus a little fluid sent her into volume overload, manifested by high catecholamine state (tachycardia and hypertension). her MR worsened acutely due to the afterload and preload perturbations and she developed pulmonary edema. you then intubated her, took away her catecholamine surge and work of breathing, and she crumped.

so, i think her MR worsened due to the other things going on, which were likely small, but added together to create drama, i wager with correction of volume and pH status her echo would look very similar to baseline.
 
floridaboy18 said:
Itwasalladream, I think you are spot on with almost all of that. Still a question for my learning... How often do you get phrenic nerve paralysis without an elevated hemidiaphragm on plain film?
Click to expand...

it can happen but i think its unlikely to be of clinical significance unless you can see volume loss. however, any PNP had likely resolved by this point but that doesnt mean it didnt happen and wasnt a contributing factor to her decompensation
 
It is always easy to pick apart a situation like this when looking in the rear view mirror….hindsight is a bitch to deal with but this is the exact kind of case were a lot of learning occurs. What was going to just be another simple supraclav turned into a a complicated situation and this has happened to me multiple times throughout my training. Great learning case and thanks for posting. Below is an example I had recently others can learn from.

Several months ago I had a patient that was progressing rapidly into hepatorenal syndrome after he was brought back to the SICU following an umbilical hernia repair secondary to it perfing from high output ascites. Pt was put on vasopressin and his non invasive read 50/30, pt desaturating on pulse ox, I place an art line and blood is dark but is pulsatile. I was second guessing the line secondary to the color of the blood so hook it up to a transducer which correlated with NIBP. Send a gas it it returns with a Sat of 70% which correlated with the pulse ox so I begin treating the pt based of these readings. Pt acidotic, non responsive to vasopressin, gave intermittent boluses of epi and bicarb with minimal response in his BP. The junior resident on the service then feels the femoral pulse and it is bounding. Redo the art line more proximal at the brachial level and the pt BP is 190/100. Essentially the pt was so clamped down the pulse ox was unreliable and my initial art line was in a vein and it was pulsatile secondary to the pt significant TR from plum HTN. Like I said….hindsight is often a bitch and I beat myself up over this for sometime bc I went through multiple checks to ensure it was arterial and a simple maneuver of checking a femoral pulse would have prevented the patient being harmed by be giving him unnecessary medications….but if the puzzle pieces are not fitting like they should most likely you are missing something and this is just another good example.
 
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Sorry to bump an old thread. I was searching something and came across this case. It reminded me so much of a case I had seen particularly the part were she is hypertensive and then crashes into shock.

The case I had seen was a pt with undiagnosed pheo, went into flash Pulm edema from hypertensive crisis on the day after some minor surgery, got intubtated and a couple of hours later went hypotensive with no response to pressors and died. Autopsy showed pheo. Turns out pheo crises do this where they are hypertensive and then crash after receptors kind of get saturated.

Very similarly to above scenario where pt was getting minor procedure -> hypertensive crisis and flash Pulm edema-> shock. Might be a stretch but just reminded me of that case.
 
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