Pre-op Consult

[Planktonmd]

Could it be what I mentioned in this post?

OK,
Since no one seems to want to participate I will keep going here:
The dizziness that the patient describes could be caused by vertebro-basilar insufficiency in the presence of carotid stenosis which limits the ability of the carotid circulation to compensate for the vertebro-basilar circulation.
The hypotensive episodes might very well be secondary to the vagal response caused by the vertigo.
At this point I don't think there is anything to optimize about this patient and I think the carotid surgery might actually improve his quality of life.
I would proceed without any further workup.
I don't think a TEE would help change any thing I do.
What do you guys think?

Ok we discussed one of the things I wanted to address in CEA's in general. But there is another issue here. Everyone just assumed that the dizziness due to ototoxicity was real and the fact that he has a DDD pacer in place didn't alert anyone to the other possibility. TO recap, he has episodes of hypotension with dizziness whenever he stands leaving him wheelchair bound. Family does report syncope or near syncope with standing. Anyone have any ideas? Remember, he has had a CEA back in 2005 and these symptoms occurred after that surgery.

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[Noyac]

Could it be what I mentioned in this post?

Yes Plank, it could be. But I'm thinking of something else here.
What if I said he had episodes of short pauses or asystole b/4 his pacer?

 

[Noyac]

You could have some neurological symptoms (syncope), what the patient calls "dizziness," from pacemaker malfunction (e.g., battery life, electrolyte imbalances). Has the pacemaker recently been evaluated? Any lab abnormalities?

Yes, the pacer was evaluated and found to have a faulty ventricular lead about a year ago. The lead was replaced and he feels the dizziness is better. But he is still in a wheelchair because his family says he can't walk due to this.

 

[Robert Loblaw]

Ok we discussed one of the things I wanted to address in CEA's in general. But there is another issue here. Everyone just assumed that the dizziness due to ototoxicity was real and the fact that he has a DDD pacer in place didn't alert anyone to the other possibility. TO recap, he has episodes of hypotension with dizziness whenever he stands leaving him wheelchair bound. Family does report syncope or near syncope with standing. Anyone have any ideas? Remember, he has had a CEA back in 2005 and these symptoms occurred after that surgery.

i'd be concerned about the functioning of his carotid sinuses--sounds like orthostatic hypotension, with one carotid surgically manipulated and the other atherosclerosed...

 

[Planktonmd]

i'd be concerned about the functioning of his carotid sinuses--sounds like orthostatic hypotension, with one carotid surgically manipulated and the other atherosclerosed...

But how do you distinguish that from vertebro-basilar insufficiency?

 

[Robert Loblaw]

But how do you distinguish that from vertebro-basilar insufficiency?

you first suggest VBI as the etiology to the presenter. then, when he acknowledges the possibility and re-asks the question, you think of another possible etiology.

i'm not sure how the best way to distinguish this would be, not the least as part of preoperative assessment. i don't recall the diagnosis of vbi, but i suppose an mra or TCDs might suggest this. i suspect there is some way to assess carotid sinus function--maybe heavy prolonged carotid massage? my endpoint would be stroke--watershed suggests appropriate sinus function, embolic confirms the indication for endarterectomy...

 

[Robert Loblaw]

OK,
Since no one seems to want to participate I will keep going here:
The dizziness that the patient describes could be caused by vertebro-basilar insufficiency in the presence of carotid stenosis which limits the ability of the carotid circulation to compensate for the vertebro-basilar circulation.
The hypotensive episodes might very well be secondary to the vagal response caused by the vertigo.

i guess being serious and with a little more thought: if we are to implicate the carotid stenosis as an etiology of what is, essentially, orthostatic VBI, then, as i understand the pathophysiology, unilateral carotid stenosis plus vertebral insufficiency alone should not cause orthostatic dizziness/hypotension, etc. and we must postulatate the existence of a second lesion. for example, vertebral artery stenosis, unilateral carotid stenosis:
- AND incomplete circle of willis thus preventing the apparently patent other carotid from retrograde perfusing of the vertebral system
- AND failed previous CEA or restenosis of the other carotid or significant (possibly multiple) high grade stenosis in other downstream vasculature, thus preventing the apparently patent other carotid from retrograde perfusing of the vertebral system
- AND bilateral carotid sinus dysfunction resulting in orthostatic hypotension, thus preventing the carotids from retrograde perfusing of the vertebral system

as i'm writing this i'm recalling that carotid dopplers are not part of a syncope workup, so i'd bet that if it is true orthostatic VBI, one of the above three concomittant lesions (and probably more than one) are likely present in this vasculopath. alternatively, i could be wrong about the pathophysiology. either way, i doubt that we will have a satisfying answer...or will we?

 

[Noyac]

But how do you distinguish that from vertebro-basilar insufficiency?

Plank, you are absolutely right that it could be VBI.

Unfortunately, I didn't present this case as well I as could have because I didn't come up with what I think is the true cause of all his problems until later. I thought the stent in the RV was interesting enough but as I thought more about this guy and then subsequently performed his CEA I came to the conclusion that he was suffering from something else.

This guy had a CEA in 2005. His dizziness and syncope began shortly after this. He had a very involved workup and the geniuses at Mayo came up with ototoxicity, In the meantime he had a pacemaker placed (DDD mode nontheless) and his symptoms markedly improved. However, he gained so much weight that he still needed the wheelchair and the family believes its due to dizziness but i reality its due to exercise intolerance. So I surmised that he was suffering from "Carotid Sinus Syndrome". Excellent call Robert Loblaw.
HOw I came up with this is that he had a CEA, then the sx's started and after he received a pacer they improved. Long shot, I know. But you ask how does one distinguish b/w VBI and CSS. Well CSS has episodes of asystole lasting >3 sec. The cardinal symptom is syncope or near syncope. It is caused by carotid sinus hypersensitivity and is a know complication of CEA. It isn't absolutely necessary to have asystole to have CSS. A decrease in SBP >50 mmHg ocurs with carotid massage. So the way to determine this is carotid massage.
Type 1 is cardioinhibitory: asystole >3 sec with CBM (carotid body massage)
Type 2 is vasodepressor: decrease SBP >50 mmHg independent of HR.
Type 3 is mixed: characteristics of both.

So this is a exaggerated response of the carotid baroreceptor to mechanical stimulation. The symptoms of dizziness and syncope result from baroreceptor-mediated cerebral hypoperfusion due to bradycardia/asystole (cardioinhibitory), hypotension (vasodepressor), or both (mixed). So Plank, you are right that the cause of the symptoms is hypoperfusion but the cause of the hypoperfusion in my opinion is CSS not VBI.

The treatment is VVI or DDD pacer in the cardioinhibitory type 1, carotid sinus surgical ablation in the vasodepressor type if the pacer doesn't do the trick. And if neither one of these things work a glossopharyngeal nerve block may do the trick.

I found this to be a very interesting case in more ways than one. Yes, in PP we still do interesting cases. They don't all go to the Ivory Towers for a million dollar w/u and then receive the same procedure that they were originally scheduled for. This guy came to our facility was scheduled for a CEA and in the process was seen and his condition which has stumped the "Mayo Clinic" was also pinpointed by an anesthesiologist. Not a neurologist or a cardiologist.

I did the case last week and he went home POD #2 still wheezing.

Nice job guys.

 

[Planktonmd]

Excellent thread Noy.

 

[Southpaw]

This was so far above my level my head was spinning, but it was a great read. Thanks Noy!

 

[Noyac]

This was so far above my level my head was spinning, but it was a great read. Thanks Noy!

Don't worry, it was above the vascular surgeon and the cardiologists heads as well. The cardiologist that put the stent in the RV was too concerned with how she looked in the eyes of the medical staff to even grasp what was going on.

 

[Robert Loblaw]

Excellent call Robert Loblaw.

Call me Bob...Bob Loblaw (not my exceedingly brilliant pun, unfortunately. Credit Mitch Hurwitz).

In truth, I must be honest and admit that I would not have guessed CSS firstly. In truth, neither did I guess it secondly, given the obvious prerequisite of having to have been aware of its existence in order to do so. I was simply postulating that the carotid sinuses could be involved--hypofunctioning, I thought, actually. My tongue-in-cheek answer of carotid massage as a means of differentiation is particularly ironic in retrospect. Watershed infarct would confirm the diagnosis, I suppose. If at least I wasn't aware of the syndrome, I will take the credit for understanding physiology, however.

Either way, in addition to being a very interesting case, it's the rare case in which a zebra is suspected and actually found. Very gratifying, I'm sure.

Curious, did you confirm the diagnosis at some point with intraoperative asystole or did you take the improvement with pacing as indirect confirmation? I will remind you that House, M.D. would barge, fully clothed and hepped up on "vikes," into your OR and massage this mans sterile neck with his bare greasy palms, dramatically stop his heart, and confirm the diagnosis--or would he be scrubbed, performing the combined CABG/removal of foreign body from ventrical/carotid endarterectomy/renal transplant, the later procedure now necessary after boxing this gentleman's kidneys from IV dye administered during an angiogram (again, performed personally by the gruffy internist) of his entire vasculature tree in search of a fungal vasculitis that was suggested by the finding of a woman's hair in the foyer of the patient's home, itself obtained by his fellows during a routine history/physical/home invasion.

 

[Noyac]

Call me Bob...Bob Loblaw (not my exceedingly brilliant pun, unfortunately. Credit Mitch Hurwitz).

In truth, I must be honest and admit that I would not have guessed CSS firstly. In truth, neither did I guess it secondly, given the obvious prerequisite of having to have been aware of its existence in order to do so. I was simply postulating that the carotid sinuses could be involved--hypofunctioning, I thought, actually. My tongue-in-cheek answer of carotid massage as a means of differentiation is particularly ironic in retrospect. Watershed infarct would confirm the diagnosis, I suppose. If at least I wasn't aware of the syndrome, I will take the credit for understanding physiology, however.

Either way, in addition to being a very interesting case, it's the rare case in which a zebra is suspected and actually found. Very gratifying, I'm sure.

Curious, did you confirm the diagnosis at some point with intraoperative asystole or did you take the improvement with pacing as indirect confirmation? I will remind you that House, M.D. would barge, fully clothed and hepped up on "vikes," into your OR and massage this mans sterile neck with his bare greasy palms, dramatically stop his heart, and confirm the diagnosis--or would he be scrubbed, performing the combined CABG/removal of foreign body from ventrical/carotid endarterectomy/renal transplant, the later procedure now necessary after boxing this gentleman's kidneys from IV dye administered during an angiogram (again, performed personally by the gruffy internist) of his entire vasculature tree in search of a fungal vasculitis that was suggested by the finding of a woman's hair in the foyer of the patient's home, itself obtained by his fellows during a routine history/physical/home invasion.

Holy **** Bob your killing me here.
Nice job with the physiology. You should be teaching at one of the "Ivory Towers".
As far as your question goes, I never turned off his DDD pacer so I made this diagnosis by the sequence of events.

And the carotid sinus is hypersensitive in CSS. We are all aware of the hypersensitivity of the carotid sinus after a CEA leading to persistent hypotension post-op. But this usually wanes over the next 24 hrs. Not in this guy.

So since this case has so much going on with it. How would you guys proceed with the CEA? Do the case, more workup, cancel and treat the current problem, send to one of the "Ivory Towers"?

 

[Robert Loblaw]

Plank, you are absolutely right that it could be VBI.

This guy had a CEA in 2005. His dizziness and syncope began shortly after this. He had a very involved workup and the geniuses at Mayo came up with ototoxicity, In the meantime he had a pacemaker placed (DDD mode nontheless) and his symptoms markedly improved. However, he gained so much weight that he still needed the wheelchair and the family believes its due to dizziness but i reality its due to exercise intolerance. So I surmised that he was suffering from "Carotid Sinus Syndrome".

this, by the way, is one of the things i love most about our specialty. it is easy to stuck a tube in and whip out the iphone--or you can get academic about just about anything scientific that suits your fancy or passes your time...for no other reason than because you can. this time/thought luxury is somewhat unique to our one-patient-at-a-time specialty.

 

[Southpaw]

this, by the way, is one of the things i love most about our specialty. it is easy to stuck a tube in and whip out the iphone--or you can get academic about just about anything scientific that suits your fancy or passes your time...for no other reason than because you can. this time/thought luxury is somewhat unique to our one-patient-at-a-time specialty.

i completely agree! very well said sir!

 

[Robert Loblaw]

Holy **** Bob your killing me here.
Nice job with the physiology. You should be teaching at one of the "Ivory Towers".
As far as your question goes, I never turned off his DDD pacer so I made this diagnosis by the sequence of events.

And the carotid sinus is hypersensitive in CSS. We are all aware of the hypersensitivity of the carotid sinus after a CEA leading to persistent hypotension post-op. But this usually wanes over the next 24 hrs. Not in this guy.

So since this case has so much going on with it. How would you guys proceed with the CEA? Do the case, more workup, cancel and treat the current problem, send to one of the "Ivory Towers"?

i was not aware of post-op hypersensitity--i've only done one cea, believe it or not, and haven't read much about the procedure, in particular. plenty of vascular to come in the next few months, though.

clearly, the case can be done safely since you did it--how close you were to disaster is unknown and unknowable. if hypersensitivity is the problem and it is related to his previous contralateral CEA (the vessel of which is not being manipulated), i would pay special attention to the positioning of contralateral neck, possibly egg carton/bubble wrap it, have a chaplain bless it, include its position in the operative time out, document the reverence with which i were treating it, and then forget about it, provided i had epinephrine/atropine within arms reach at all times. i'd probably have an extremely low threshold for epi bolus given the pathophysiologic similarity to the bezold-jarisch reflex.

the ivory towers myth centers around the fact that we ivorians see patients referred for surgical reasons. very few cases (if any) are referred to us for anesthetic ones. my experience during residency (at least at my high volume, high acuity training program) has been that the turnover times for our rooms (45 minutes to an hour) provide time for us to wax medical over our patients. in general, without a preop clinic to organize work-ups, the goldilocks effect is in full--patients either come with way to much are frighteningly not enough work up. rarely just right. my practice with these cases, which in my opinion should be every residents practice, is to figure out a way to (safely) do the case--not a way not to. we are doctor for crying out loud!

now, if reimbursements drop substantially i might not be willing to expose myself to the same risks with such paltry rewards...

 

[Robert Loblaw]

i completely agree! very well said sir!

in the interest of full disclosure, i do bring my iphone charger to work.

 

[Licoricestick]

Wow - what an education!
Thanks for posting Noyac and thanks to everyone else for the discussion.

 

[DreamMachine]

HOw I came up with this is that he had a CEA, then the sx's started and after he received a pacer they improved. Long shot, I know. But you ask how does one distinguish b/w VBI and CSS. Well CSS has episodes of asystole lasting >3 sec. The cardinal symptom is syncope or near syncope. It is caused by carotid sinus hypersensitivity and is a know complication of CEA. It isn't absolutely necessary to have asystole to have CSS. A decrease in SBP >50 mmHg ocurs with carotid massage. So the way to determine this is carotid massage.
Type 1 is cardioinhibitory: asystole >3 sec with CBM (carotid body massage)
Type 2 is vasodepressor: decrease SBP >50 mmHg independent of HR.
Type 3 is mixed: characteristics of both.

Badass thread...the best one in a long while.

Do they worry about doing a carotid massage in these patients, as in breaking off some clot and having it go the brain?

 

[Noyac]

Badass thread...the best one in a long while.

Do they worry about doing a carotid massage in these patients, as in breaking off some clot and having it go the brain?

Sure you do but the affected carotid sinus is on the side that had the CEA in 2005. That side is open and clean. So I wouldn't worry too much about it.

 

[urge]

Nevermind