Intraoperative stroke

[Laurel123]

This weekend I had an 85 year old woman with a bowel obstruction due to an incarcerated inguinal hernia. She has severe Mitral Regurg which is chronic. Both atria are enlarged, especially the left. She is in A fib which is chronic and rate controlled. Her EF is 65 percent on echo, though I assume that is total EF, not forward flow EF. She has had a few episodes of pulmonary edema the last few years but no MI. On exam pressure is 111/61, rate of 71, awake, alert. MR murmer, lungs are clear. Peripheral perfusion is poor, fingers are cool and a little dusky and the pulse ox tracing is so-so. She was on coumadin, but it was stopped when she was admitted to the hospital. Echo on admission showed no clots in heart. So it is now five days after admission and she is finally coming to the OR. Coags are normal.

I do a general anesthetic and she does OK. A little hypotension before incision to 79/45 which lasted only one bp reading as it corrected itself after incision. I kept bp probably a little below her baseline to baseline, which is pretty low to begin with. But given her regurg and CHF, I believe this is a good strategy.

Surgery about 3 hours. Ended up doing a brief ex lap. Post op she is awake and her eyes track and she nods and shakes her head appropriately, she never speaks. I am not concerned at this point because she is old and frail and had a pretty long GA. VSS.

Next day, shes still not speaking, and now the family believes she is not tracking or responding appropriately. Hospitalist believes she had an intraoperative stroke due to hypotension. But she is moving all extremities - and to me it is not consistant with watershed insult. I believe it could be emboli.

Two days later, same mental status - and CT shows a very large area of ischemia on the right side. They look through the anesthesia record and wonder it the hypotensive episode at the beginning caused the stroke or the lowish BP throughout the case worsened the stroke. It's possible - but I dont think it explains the stroke..

Thoughts? any else had a patient with an intraop stroke before?

By the way, as of today, there has been resolution to the case after days of discussion - so I just wanted you guys thoughts on the event and the possible causes.

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[Planktonmd]

This weekend I had an 85 year old woman with a bowel obstruction due to an incarcerated inguinal hernia. She has severe Mitral Regurg which is chronic. Both atria are enlarged, especially the left. She is in A fib which is chronic and rate controlled. Her EF is 65 percent on echo, though I assume that is total EF, not forward flow EF. She has had a few episodes of pulmonary edema the last few years but no MI. On exam pressure is 111/61, rate of 71, awake, alert. MR murmer, lungs are clear. Peripheral perfusion is poor, fingers are cool and a little dusky and the pulse ox tracing is so-so. She was on coumadin, but it was stopped when she was admitted to the hospital. Echo on admission showed no clots in heart. So it is now five days after admission and she is finally coming to the OR. Coags are normal.

I do a general anesthetic and she does OK. A little hypotension before incision to 79/45 which lasted only one bp reading as it corrected itself after incision. I kept bp probably a little below her baseline to baseline, which is pretty low to begin with. But given her regurg and CHF, I believe this is a good strategy.

Surgery about 3 hours. Ended up doing a brief ex lap. Post op she is awake and her eyes track and she nods and shakes her head appropriately, she never speaks. I am not concerned at this point because she is old and frail and had a pretty long GA. VSS.

Next day, shes still not speaking, and now the family believes she is not tracking or responding appropriately. Hospitalist believes she had an intraoperative stroke due to hypotension. But she is moving all extremities - and to me it is not consistant with watershed insult. I believe it could be emboli.

Two days later, same mental status - and CT shows a very large area of ischemia on the right side. They look through the anesthesia record and wonder it the hypotensive episode at the beginning caused the stroke or the lowish BP throughout the case worsened the stroke. It's possible - but I dont think it explains the stroke..

Thoughts? any else had a patient with an intraop stroke before?

By the way, as of today, there has been resolution to the case after days of discussion - so I just wanted you guys thoughts on the event and the possible causes.

Here is the list of problems this patient has:
1- She has AFIB
2- She is not anticoagulated
3- She has dilated atria
4- She has severe MR
5- She has Bowel obstruction with possible inflammatory response.
6- She is 85 Y/O
Each one of the above mentioned problems is an independent risk for intracardiac thrombus formation and embolic event.
The fact that the transthoracic echo was negative 5 days ago is meaningless because:
A- It was 5 days ago,
B- they did not do a TEE which means they might have missed the thrombus.
So, this is an embolic event from cardiac origin caused by all these risk factors and nothing you did caused it.
You, Doctor, did your best and gave this woman the appropriate anesthetic because she needed this emergent surgery.
My advice:
1-DO NOT discuss this case any further with anyone including Hospital risk management (they are not your friends)
2-Do not write any personal opinions or explanations to what happened in the chart.
3-Follow her progress and talk to the family and answer any questions they have, but remember: you did not do anything wrong.
4- Your management was appropriate.

 

[Laurel123]

Thanks for the response. I totally agree. In fact, when I discovered that she had had a stroke at some point intraop or immediately postop, I immediately pointed to emboli. I mean her atria were huge, especially the left. It seemed most logical.
But they were fixated on hypotension, especially because of one documented low number. A systolic below eighty FREAKS out these hospitalists and surgeons. I dont love it either, but I manage it. They kept explaining their concern that the bp could have been low for the 4 minutes before and after the measurement accounting for 8 minutes of hypotension.

 

[Planktonmd]

Thanks for the response. I totally agree. In fact, when I discovered that she had had a stroke at some point intraop or immediately postop, I immediately pointed to emboli. I mean her atria were huge, especially the left. It seemed most logical.
But they were fixated on hypotension, especially because of one documented low number. A systolic below eighty FREAKS out these hospitalists and surgeons. I dont love it either, but I manage it. They kept explaining their concern that the bp could have been low for the 4 minutes before and after the measurement accounting for 8 minutes of hypotension.

It is easy for a hospitalist to point fingers because this is their chance to point out how bad we anesthesiologists are, they love to do that whenever they get a chance.
For the surgeon, blaming you is the natural thing to do because then he can try to say that his surgery did not hurt the patient but it was your anesthesia.
They simply have no idea what caused the stroke but blaming you is the easy way out
As I said above, if I were you I wouldn't talk to any of these people about the case anymore.
And you might need to report the event to your liability carrier.

 

[militarymd]

1) shi t happens.

2) who was taking care of the patient when the sh it happened?



I'm not saying you did anything wrong.....but YOU WERE taking care of the patient when something bad happened....right?

Or were you not the patient's doctor when she was hypotensive.....the cause of the majority of complications in the OR??????

Shifting the blame and not accepting responsibility like someone is advising you is the WORST thing to do.

Having been through a couple of these...I KNOW.

 

[Planktonmd]

1) shi t happens.

2) who was taking care of the patient when the sh it happened?



I'm not saying you did anything wrong.....but YOU WERE taking care of the patient when something bad happened....right?

Or were you not the patient's doctor when she was hypotensive.....the cause of the majority of complications in the OR??????

Shifting the blame and not accepting responsibility like someone is advising you is the WORST thing to do.

Having been through a couple of these...I KNOW.

Are you implying that she needs to accept the hospitalist's assumption that she caused the stroke because of a systolic of 80?
If every elderly having surgery who has a systolic pressure of 80 has a stroke then we wouldn't be doing this business.
I did not say shift the blame but I said there are multiple risk factors in this patient that can cause the stroke that are completely unrelated to anesthesia.
The most stupid thing any practicing physician could do is accept blame or responsibility for an event without being certain what caused it, man you are advising her to do what every plaintiff attorney dreams of: A physician that takes responsibility for an adverse event although they did not do anything to cause it.
My advice is simple and I emphasize it:
When you are in a situation where an adverse event has happened and people are pointing fingers at you, you need to protect yourself and you need to think that everything you say or do can come back to bite you down the road.
Everyone involved will be protecting themselves and if you don't you will lose.

 

[militarymd]

I like that.

I'm the great doctor taking care of your old and sick and infirmed.....better than any nurse can....

Oh...but if something bad happens....it's not my fault.....don't point fingers at me...

yes ...good strategy..

oh wait....now a days....it's all about Gabba and his crap.

It's the "system" ' s fault...we need to analyze the system that allows old, and sick and infirmed people have surgery.....

 

[9french]

Not every complication is preventable. The only thing we can be expected to do is to prevent the preventable complications.

In this case, the patient had an embolic stroke. She has every last risk factor. If the stroke was secondary to GLOBAL hypotension or hypoxia, you would generally expect more diffuse injury, as opposed to a focal finding (as described on the CT).

Lets say instead of these findings being found post-op, instead, the patient walked into the E.R. with these sx. Do you think any competent E.R. physician or Neurologist, would suggest this was from a global hypotensive event as opposed to an embolic stroke? I've said this before, but it is absolutely ridiculous that the internists write in the chart (A LEGAL DOCUMENT) their theories about us causing a serious complication without any evidence, without any understanding of the actions of general anesthetic medications, and without speaking to the Anesthesiologist.

As a resident, I would have your attending speak to the internist who wrote that in the chart and let them know it is not appreciated.

 

[ozzie20]

Not every complication is preventable. The only thing we can be expected to do is to prevent the preventable complications.

In this case, the patient had an embolic stroke. She has every last risk factor. If the stroke was secondary to GLOBAL hypotension or hypoxia, you would generally expect more diffuse injury, as opposed to a focal finding (as described on the CT).

Lets say instead of these findings being found post-op, instead, the patient walked into the E.R. with these sx. Do you think any competent E.R. physician or Neurologist, would suggest this was from a global hypotensive event as opposed to an embolic stroke? I've said this before, but it is absolutely ridiculous that the internists write in the chart (A LEGAL DOCUMENT) their theories about us causing a serious complication without any evidence, without any understanding of the actions of general anesthetic medications, and without speaking to the Anesthesiologist.

As a resident, I would have your attending speak to the internist who wrote that in the chart and let them know it is not appreciated.

I agree, With a global issue like hypotension, you would expect global results. Focal issue like a clot = focal results like those seen on the CT. If there were multiple focal points, then I could buy the hypotension being more of an issue, but it wasnt. If anything, the hypotension would reduce the incidence of the clot occurring, and it happened anyway.

You can put the blame on the anesthesiologist for the issue of having hypotension, but to state that a single episode of LOW blood pressure that lasted MAX of 8 mins somehow sent the patient into a thrombotic episode is ******ed. Stranger things have happened, but in medicine you become a kind of betting man, betting that the odds are such and such happened over so and so. And the odds are for her that given she has A-fib, not anticoagulated, underwent an emergent surgery, had enlarged atria gave her a stroke is MUCH more likely than 8 mins of isolated hypotension doing any damage.

 

[militarymd]

1) shi t happens.

2) who was taking care of the patient when the sh it happened?



I'm not saying you did anything wrong.....but YOU WERE taking care of the patient when something bad happened....right?

Or were you not the patient's doctor when she was hypotensive.....the cause of the majority of complications in the OR??????

Shifting the blame and not accepting responsibility like someone is advising you is the WORST thing to do.

Having been through a couple of these...I KNOW.

You guys aren't listening....or in this case reading....

Hypotension IS a known cause of perioperative stroke (9%) based on some data....along with other known causes.

Fighting/arguing with consultants about how they're "wrong" is not a good approach.

As for the actual cause....you're never going to know...regardless of what the images show.

 

[militarymd]

I was thinking about this a little bit....let me ask you guys this.

Although much more rare than perioperative Myocardial infarctions, I think of strokes as just a "brain attack"....people have heart attacks sometimes and sometimes they have brain attacks when they have surgery.

So if someone is a victim of a perioperative myocardial infarction secondary to hypotension intraoperatively.....what do their post op echocardiograms look like?

do they have GLOBAL biventricular dysfunction with their rise in enzymes...or do they have new REGIONAL wall motion abnormalities ?

I'm assuming that most people agree that hypotension causes periop MI's.....or has everyone given that up and have gone with the unstable coronary thrombus theory....and just tolerate the hypotension now and ignore the cardiologists?

 

[Noyac]

All of you are right IMO. I think of it this way. This pt is a setup for clot formation and stoke, a fib, dilated chamber, no anticoagulants, etc. I believe that this is a embolic event that may or may not have occurred due to hypotension. The hypotension will exacerbate the situation by allowing clot formation, right. I'm not totally sure how much hypotension it takes but this seems right here. 8 minutes doesn't seem like much in the grand scheme of things though.
In my opinion, everyone is responsible. The internist should have covered the pt with lovenox or heparin pre-op. The surgeon should have made sure she was covered then held it for the appropriate amount of time then restarted it and the anesthesiologist should have caught it albeit, you probably didn't see this pt til the day of surgery long after these issues were missed by others. But you went along with the surgery and therefore you are partly responsible. Its unfortunate, but its part of the game. You need to know your medicine and risk being the bad guy when you see something not right.

I had a very similar case last year. Lady with a surgical condition had 2 cardiac stents less than 6 months ago. Internist stops plavix and gets cardiac and surgical consults. Pt sits on the floor 5 days without anticoagulation waiting for surgery. We (anesthesiologist) are not involved until day 5, not really remembering all the details. Surgeon wants to go to OR now. I see the pt and say WAIT. She isn't protected. Everyone has a cow. Before we can argue the point, pt starts to have crushing CP and CHF. I TOLD YOU SO. Surgeon cancels case. Internist blames everyone including me. Pt did fine though. I brought internist b/4 PROC and well needless to say much respect was garnered on my part from the others and she is still bitter. Well then do your f*cking job, idiot.

 

[urge]

Agree with Mil. Hypotension COULD have caused it. An emboli, TOO. There was definite hypotension. There hasn't been any evidence of clot (atrial). It's hard to support the embolic ethiology this way. I'm not much of a radiologist or neurologist, but I remember there are hints as to the cause of the stroke by the ct images. What did the radiologist say? Has a repeat echo been done. Are there any clots?

All people saying that since hypotension is global, hence she must have global stroke, did you go to med school? That's like the most ******ed thing ever posted in this forum.

OP, you had a bad outcome. It was going to happen sooner or later. I would talk to the family and say I was sorry for the incident since it happened under my care.

 

[Noyac]

I was thinking about this a little bit....let me ask you guys this.

Although much more rare than perioperative Myocardial infarctions, I think of strokes as just a "brain attack"....people have heart attacks sometimes and sometimes they have brain attacks when they have surgery.

So if someone is a victim of a perioperative myocardial infarction secondary to hypotension intraoperatively.....what do their post op echocardiograms look like?

do they have GLOBAL biventricular dysfunction with their rise in enzymes...or do they have new REGIONAL wall motion abnormalities ?

I'm assuming that most people agree that hypotension causes periop MI's.....or has everyone given that up and have gone with the unstable coronary thrombus theory....and just tolerate the hypotension now and ignore the cardiologists?

I see your point Mil but I look at it differently. The heart has plaque buildup in the coronaries that is not universal throughout the coronaries. Seen as 90% stenosis in the LAD, minimal elsewhere in some cases. These areas become vulnerable. The brain on the other hand has multiple "watershed" areas with the circle of willis and the flow is rerouted better therefore better protected. You need a global decrease in perfusion to affect the brain in this case. Focal areas become injured by focal insults, emboli.
Sure anything is possible but to me it seems as though if this were from hypotension alone there would be more areas of insult. Think about the strokes we see after CEA's.

 

[militarymd]

I see your point Mil but I look at it differently. The heart has plaque buildup in the coronaries that is not universal throughout the coronaries. Seen as 90% stenosis in the LAD, minimal elsewhere in some cases. These areas become vulnerable. The brain on the other hand has multiple "watershed" areas with the circle of willis and the flow is rerouted better therefore better protected. You need a global decrease in perfusion to affect the brain in this case. Focal areas become injured by focal insults, emboli.
Sure anything is possible but to me it seems as though if this were from hypotension alone there would be more areas of insult. Think about the strokes we see after CEA's.

The reason you are differentiating between the brain and the heart is because we (anesthesiologists) have been taught that way.

From a Internists POV. They're the same. The risk factors for CAD and CVD are the same. The plaques that exist in the coronaries also exist in the cerebral circulation (arteries are arteries...they all build plaques)....accounting for the fact that 90% (number may be off) of strokes are "bland" strokes....ie the same mechanism as "unstable coronary thrombus"....

The mechanical/locational nature of cerebral location puts it at risk of embolism that the coronary circulation is protected from...and hemorrhage is another mechanism that does not exist in the coronary circulation, but the majority of "brain attacks" occur the same way as "heart attacks"....in the outpatient setting....

And I would submit that the majority of non-carotid/non CABG type surgically related "brain attacks" occur in the same mechanistic fashion as "heart attacks"

 

[Planktonmd]

You guys aren't listening....or in this case reading....

Hypotension IS a known cause of perioperative stroke (9%) based on some data....along with other known causes.

Fighting/arguing with consultants about how they're "wrong" is not a good approach.

As for the actual cause....you're never going to know...regardless of what the images show.

You are the one who is not listening and I truly think that you see our specialty as inferior to all the other specialties and this is why you always rush to criticizing the anesthesiologists because for some mysterious reason you convinced yourself that you are above this specialty.
If you don't think we are "consultants" and that our opinions are as valuable as all the other "consultants" then stop calling yourself an anesthesiologist and go hang out with the internists maybe they will accept you.

 

[Noyac]

The reason you are differentiating between the brain and the heart is because we (anesthesiologists) have been taught that way.

From a Internists POV. They're the same. The risk factors for CAD and CVD are the same. The plaques that exist in the coronaries also exist in the cerebral circulation (arteries are arteries...they all build plaques)....accounting for the fact that 90% (number may be off) of strokes are "bland" strokes....ie the same mechanism as "unstable coronary thrombus"....

The mechanical/locational nature of cerebral location puts it at risk of embolism that the coronary circulation is protected from...and hemorrhage is another mechanism that does not exist in the coronary circulation, but the majority of "brain attacks" occur the same way as "heart attacks"....in the outpatient setting....

And I would submit that the majority of non-carotid/non CABG type surgically related "brain attacks" occur in the same mechanistic fashion as "heart attacks"

Over 80% of strokes are ischemic caused by blockage of the artery leading to decreased flow. Plaque can cause blockage of the artery and ischemic strokes are either thombotic, embolic, lacunar or cryptogenic. I am not arguing the likelihood of the stroke here with you and I didn't read the CT results that Laurel posted when I responded. I just went with the clinical picture of a fib, no anticoagulation and large chamber. The CT showed large area of ischemia on R side. I think thrombotic ischemia fits the bill. Just like an MI. But it could have been a large clot as well.

 

[9french]

T

And I would submit that the majority of non-carotid/non CABG type surgically related "brain attacks" occur in the same mechanistic fashion as "heart attacks"

I would disagree with this. As you know, there are both STEMIs and NSTEMIs. The mechanism of the perioperative STEMI is that increased sympathetic tone, leads to increase in shear forces, which cause plaque disruption, which exposes tissue factor to the blood, which leads to an acute thrombus, which completely blocks the artery, which leads to severe ischemia. This is aided by the perioperative period inducing a hypercoaguable state plus the withholding of anti-platelet medications due to fear of bleeding. Of note, the degree of vessel stenosis does not acurately predict the risk of STEMI, i.e, a vessel with 30% stenosis is at risk just like a vessel with 90% stenosis. The NSTEMI is caused by a supply/demand mismatch. Normally the amount of myocardial injury is significantly less than that of a STEMI. A tight, fixed coronary lesion is strong risk factor. Hypotension can cause NSTEMI.

Strokes really have really two mechanisms. The first is hemmorhage, which has nothing to do with this discussion. The second is that of a thromboembolic event. A thrombus will form either in the carotids or in the Left atrium. This thrombus will come dislodged and wind up in a cerebral vessel completely occluding it. Hypertension is a risk factor.

Hypotension is not a risk factor for embolic stroke. If there is a cerebral vessel with a stenotic lesion, obviously you want to maintain a good blood pressure to avoid supply/demand mismatch, such as with management of vasospasm following SAH, or even carotid clamping. However, without a fixed, tight lesion in a cerebral artery, hypotension should not cause a single, focal area of ischemia. What I would expect would be multiple, small punctate lesions seen on CT if there was significant, prolonged hypotension. Now, there can be a million "what ifs." However, in this particular patient, as part of the stroke w/u, she should have gotten an MRA and carotid dopplers to look for a fixed lesion. If a fixed lesion is not present, hypotension causing a focal ischemic area is far less likely than a thromboembolic event. So again, the hospitalist should not blame the Anesthesiologist for the stroke without an adequate w/u, without a basic knowledge of anesthetic drugs, and without speaking to the Anesthesiologist.

Lastly, keep in mind that most of our anesthetic agents are likely protective against ischemia.

 

[Planktonmd]

Over 80% of strokes are ischemic caused by blockage of the artery leading to decreased flow. Plaque can cause blockage of the artery and ischemic strokes are either thombotic, embolic, lacunar or cryptogenic. I am not arguing the likelihood of the stroke here with you and I didn't read the CT results that Laurel posted when I responded. I just went with the clinical picture of a fib, no anticoagulation and large chamber. The CT showed large area of ischemia on R side. I think thrombotic ischemia fits the bill. Just like an MI. But it could have been a large clot as well.

The most common reason for perioperative stroke is overwhelmingly embolism.

 

[mille125]

Here is the list of problems this patient has:
1- She has AFIB
2- She is not anticoagulated
3- She has dilated atria
4- She has severe MR
5- She has Bowel obstruction with possible inflammatory response.
6- She is 85 Y/O
Each one of the above mentioned problems is an independent risk for intracardiac thrombus formation and embolic event.
The fact that the transthoracic echo was negative 5 days ago is meaningless because:
A- It was 5 days ago,
B- they did not do a TEE which means they might have missed the thrombus.
So, this is an embolic event from cardiac origin caused by all these risk factors and nothing you did caused it.
You, Doctor, did your best and gave this woman the appropriate anesthetic because she needed this emergent surgery.
My advice:
1-DO NOT discuss this case any further with anyone including Hospital risk management (they are not your friends)
2-Do not write any personal opinions or explanations to what happened in the chart.
3-Follow her progress and talk to the family and answer any questions they have, but remember: you did not do anything wrong.
4- Your management was appropriate.

laurel listen to plankton on this one he is giving you very good advice...

 

[mille125]

You guys aren't listening....or in this case reading....

Hypotension IS a known cause of perioperative stroke (9%) based on some data....along with other known causes.

Fighting/arguing with consultants about how they're "wrong" is not a good approach.

As for the actual cause....you're never going to know...regardless of what the images show.

give me a freaking break...


Your logic is absurd. You should not accept fault just because a patient has a bad event on your watch. Complications are a part of the risk of surgery. This patient had many risk factors for intraoperative stroke. To accept blame because of one isolated incident of hypotension is foolhardy. Mil, you seem like a smart guy but your advice here is laughable and actually somewhat amateurish.

With that said, there are some events where you may need to accept responsibility:

1) Patient requests epidural anesthesia for post op pain. You see an obvious wet tap. Patient develops PDPH.

2) Tooth is chipped during the course of airway management in a patient with a difficult airway.

Both of these adverse outcomes were clearly "anesthetic complications". You should be honest with the patient and their family. Yet these complications are risks of surgery/anesthesia and should have been addressed before the operation.


To say, "the patient had a stroke because of one episode of hypotension" in Laurel's complex patient is rushing to a quick and easy (and probably erroneous) conclusion. The anesthesia attending and the hospitalist should have a discussion about the inappropriate entry that was placed in the chart. It would have also been appropriate for the hospitalist to talk with the actual care team before making a conclusion with limited facts.

 

[mille125]

You are the one who is not listening and I truly think that you see our specialty as inferior to all the other specialties and this is why you always rush to criticizing the anesthesiologists because for some mysterious reason you convinced yourself that you are above this specialty.
If you don't think we are "consultants" and that our opinions are as valuable as all the other "consultants" then stop calling yourself an anesthesiologist and go hang out with the internists maybe they will accept you.

or better call yourself a trial attorney with your "i accept blame" philosophy

 

[militarymd]

How many STEMI have you seen in the perioperative period?

In my 10 years of watching closely....none.

I would disagree with this. As you know, there are both STEMIs and NSTEMIs. The mechanism of the perioperative STEMI is that increased sympathetic tone, leads to increase in shear forces, which cause plaque disruption, which exposes tissue factor to the blood, which leads to an acute thrombus, which completely blocks the artery, which leads to severe ischemia. This is aided by the perioperative period inducing a hypercoaguable state plus the withholding of anti-platelet medications due to fear of bleeding. Of note, the degree of vessel stenosis does not acurately predict the risk of STEMI, i.e, a vessel with 30% stenosis is at risk just like a vessel with 90% stenosis. The NSTEMI is caused by a supply/demand mismatch. Normally the amount of myocardial injury is significantly less than that of a STEMI. A tight, fixed coronary lesion is strong risk factor. Hypotension can cause NSTEMI.

Strokes really have really two mechanisms. The first is hemmorhage, which has nothing to do with this discussion. The second is that of a thromboembolic event. A thrombus will form either in the carotids or in the Left atrium. This thrombus will come dislodged and wind up in a cerebral vessel completely occluding it. Hypertension is a risk factor.

Hypotension is not a risk factor for embolic stroke. If there is a cerebral vessel with a stenotic lesion, obviously you want to maintain a good blood pressure to avoid supply/demand mismatch, such as with management of vasospasm following SAH, or even carotid clamping. However, without a fixed, tight lesion in a cerebral artery, hypotension should not cause a single, focal area of ischemia. What I would expect would be multiple, small punctate lesions seen on CT if there was significant, prolonged hypotension. Now, there can be a million "what ifs." However, in this particular patient, as part of the stroke w/u, she should have gotten an MRA and carotid dopplers to look for a fixed lesion. If a fixed lesion is not present, hypotension causing a focal ischemic area is far less likely than a thromboembolic event. So again, the hospitalist should not blame the Anesthesiologist for the stroke without an adequate w/u, without a basic knowledge of anesthetic drugs, and without speaking to the Anesthesiologist.

Lastly, keep in mind that most of our anesthetic agents are likely protective against ischemia.

 

[militarymd]

The most common reason for perioperative stroke is overwhelmingly embolism.

Show me your reference.

The latest I'm aware of is a study looking at CABG patients...in which case what you say is true.

In non-CABG/non-CAROTID surgery.....I don't think so.

 

[militarymd]

so thrombus never form in the MCA...like it does in the LAD?

I would disagree with this. As you know, there are both STEMIs and NSTEMIs. The mechanism of the perioperative STEMI is that increased sympathetic tone, leads to increase in shear forces, which cause plaque disruption, which exposes tissue factor to the blood, which leads to an acute thrombus, which completely blocks the artery, which leads to severe ischemia. This is aided by the perioperative period inducing a hypercoaguable state plus the withholding of anti-platelet medications due to fear of bleeding. Of note, the degree of vessel stenosis does not acurately predict the risk of STEMI, i.e, a vessel with 30% stenosis is at risk just like a vessel with 90% stenosis. The NSTEMI is caused by a supply/demand mismatch. Normally the amount of myocardial injury is significantly less than that of a STEMI. A tight, fixed coronary lesion is strong risk factor. Hypotension can cause NSTEMI.

Strokes really have really two mechanisms. The first is hemmorhage, which has nothing to do with this discussion. The second is that of a thromboembolic event. A thrombus will form either in the carotids or in the Left atrium. This thrombus will come dislodged and wind up in a cerebral vessel completely occluding it. Hypertension is a risk factor.

Hypotension is not a risk factor for embolic stroke. If there is a cerebral vessel with a stenotic lesion, obviously you want to maintain a good blood pressure to avoid supply/demand mismatch, such as with management of vasospasm following SAH, or even carotid clamping. However, without a fixed, tight lesion in a cerebral artery, hypotension should not cause a single, focal area of ischemia. What I would expect would be multiple, small punctate lesions seen on CT if there was significant, prolonged hypotension. Now, there can be a million "what ifs." However, in this particular patient, as part of the stroke w/u, she should have gotten an MRA and carotid dopplers to look for a fixed lesion. If a fixed lesion is not present, hypotension causing a focal ischemic area is far less likely than a thromboembolic event. So again, the hospitalist should not blame the Anesthesiologist for the stroke without an adequate w/u, without a basic knowledge of anesthetic drugs, and without speaking to the Anesthesiologist.

Lastly, keep in mind that most of our anesthetic agents are likely protective against ischemia.

 

[militarymd]

You are the one who is not listening and I truly think that you see our specialty as inferior to all the other specialties and this is why you always rush to criticizing the anesthesiologists because for some mysterious reason you convinced yourself that you are above this specialty.
If you don't think we are "consultants" and that our opinions are as valuable as all the other "consultants" then stop calling yourself an anesthesiologist and go hang out with the internists maybe they will accept you.

The problem with our specialty, as so well represented by your attitudes, is that we are tooo narrow minded.

Our care of the patient encompasses a tiny fraction of a percent of their lives...albeit sometimes a critical fraction of a percent.

Our impact in the overall well being of a patient represents a tiny fraction of a percent of their lives...and once again...sometimes a critical fraction.

And so when it DOES matter....like in this case where something REALLY bad has happened....what do guys like you say?

"it's not my fault".......

this is why people like you will never have any respect.

 

[Planktonmd]

Show me your reference.

The latest I'm aware of is a study looking at CABG patients...in which case what you say is true.

In non-CABG/non-CAROTID surgery.....I don't think so.

Yes, the data is from post CABG patients and it was published in the NEJM last year.
This article stated specifically that deliberate hypotension did not seem to be a factor in the incidence of perioperative stroke and that most of these strokes were embolic.
I would paste the article but it would be a copy right violation.
Since this is the only data we have I think it must be more credible than your personal opinion based on your personal analysis, wouldn't you agree with that?

 

[Planktonmd]

The problem with our specialty, as so well represented by your attitudes, is that we are tooo narrow minded.

Our care of the patient encompasses a tiny fraction of a percent of their lives...albeit sometimes a critical fraction of a percent.

Our impact in the overall well being of a patient represents a tiny fraction of a percent of their lives...and once again...sometimes a critical fraction.

And so when it DOES matter....like in this case where something REALLY bad has happened....what do guys like you say?

"it's not my fault".......

this is why people like you will never have any respect.

Arguing with you has proven to be futile every single time, so I will stop here, but I still have to repeat my suggestion to you: If you feel that our specialty is not good enough for you go ahead and call yourself something else other than an anesthesiologist.

 

[Pooh & Annie]

The problem with our specialty, as so well represented by your attitudes, is that we are tooo narrow minded.

Our care of the patient encompasses a tiny fraction of a percent of their lives...albeit sometimes a critical fraction of a percent.

Our impact in the overall well being of a patient represents a tiny fraction of a percent of their lives...and once again...sometimes a critical fraction.

And so when it DOES matter....like in this case where something REALLY bad has happened....what do guys like you say?

"it's not my fault".......

this is why people like you will never have any respect.

I bet they really respect you at your place where all the other physicians know you'll take the blame for ANY incident that has the slightest chance of being anesthetic related. Dangerous attitude for you AND your colleagues.

 

[DET0897]

Things to consider:

1) What do her carotids look like/sound like? If there is a critical stenosis in the right carotid then a hypotensive episode could certainly cause focal ischemia if the right hemisphere was dependent on good collateral circulation from the left carotid territory. The definition of hyptonsion in this case, <80 SBP, is relative if pre-op her SBP is 150 or so. Then, SBP in the low 100's could also disrupt the collateral circulation to the right hemisphere. What was her pre-op BP?

2) With the CT scan on POD3, whose to say that her stroke wasn't on POD#0, 1 ,or 2. Today's CT's can detect ischemia <24hours, especially if large. To a trained eye, large infarcts can be seen much sooner than that. Given that her exam changed between PACU and being on the floor, its hard to say the event was intra-op vs periop. An MRI with diffusion weighted images could help give a temporal picture, but again it would be hard to determine the timing down to a specific hour, or even day, with DWI.

3) Is the patient left handed? You describe a motor/expressive aphasia which is typically a left hemipshere cortical sign, rather than right hemisphere. Perhaps she was more abulic, which could be right hemipshere but usually with sens/motor signs.

4) its not uncommon to to see an obvious clot in the MCA (dense MCA sign), and still see nothing on TEE bubble. A post-op TEE would be neither sensitive (rule out) or specific (rule in) for embolic event in this (legal) case, but could direct therapy

 

[9french]

How many STEMI have you seen in the perioperative period?

In my 10 years of watching closely....none.

I am aware of several. Fortunately, none occurred in either the O.R. or PACU. Approximately 50% of fatal perioperative MIs are thrombotic in nature. I should add that a thrombus which does not completely occlude a coronary may present as a NSTEMI.

Dawood, M, Gutpa, DK, Southern, J, et al Pathology of fatal perioperative myocardial infarction: implications regarding pathophysiology and prevention. Int J Cardiol 1996;57,37-44

 

[9french]

so thrombus never form in the MCA...like it does in the LAD?

Of course it can and it does. Strokes can be be both embolic and thrombotic. I do not know offhand the percentages of each. MIs, on the other hand, are very rarely embolic. This is the big mechanistic difference between ischemic stroke and MI in my view.

 

[militarymd]

Of course it can and it does. Strokes can be be both embolic and thrombotic. I do not know offhand the percentages of each. MIs, on the other hand, are very rarely embolic. This is the big mechanistic difference between ischemic stroke and MI in my view.

the problem with plank's statement is that he is quoting wrong patient population...he says NEJM 2007...that's also not correct...the original data was published in 2003 in Stroke...and it specifically addresses CABG surgery which has an inherrently high risk of embolism.

I have done several lit searches (for grand rounds) on stroke in NonCABG/non carotid surgery....I have not been able to find data.

Based on personal experience over 10 years. I have seen 2 strokes (not CABG/not Carotid) in the periop period. One a colon resection...one a ACDF...both patients had no risk factors other than HTN and Diabetes.....and , heaven forbid....short periods of hypotension in the OR.

Post op work up ....unable to find a source of embolism....but imaging studies showed localized ischemic areas.

 

[militarymd]

I am aware of several. Fortunately, none occurred in either the O.R. or PACU. Approximately 50% of fatal perioperative MIs are thrombotic in nature. I should add that a thrombus which does not completely occlude a coronary may present as a NSTEMI.

Dawood, M, Gutpa, DK, Southern, J, et al Pathology of fatal perioperative myocardial infarction: implications regarding pathophysiology and prevention. Int J Cardiol 1996;57,37-44

so what kind of MIs do you get with hypotension? NSTEMI with global hypokinesis?

 

[militarymd]

Yes, the data is from post CABG patients and it was published in the NEJM last year.
This article stated specifically that deliberate hypotension did not seem to be a factor in the incidence of perioperative stroke and that most of these strokes were embolic.
I would paste the article but it would be a copy right violation.
Since this is the only data we have I think it must be more credible than your personal opinion based on your personal analysis, wouldn't you agree with that?

Having run a journal club for 5 years for residents, you just made one of the most common rookie mistakes in interpreting literature.....you extrapolated data from one patient population (CABG) to another patient population.

In CABG/Carotid surgery, the risks of embolism are high and known and OBVIOUS...you're sticking a hugh cannula into the aorta...duhhhh.

I would have thought you would be better trained in your journal clubs.

 

[mille125]

Arguing with you has proven to be futile every single time, so I will stop here, but I still have to repeat my suggestion to you: If you feel that our specialty is not good enough for you go ahead and call yourself something else other than an anesthesiologist.

as i said before, it is likely telling a schizophrenic that their hallucinations aren't real..

 

[mille125]

The problem with our specialty, as so well represented by your attitudes, is that we are tooo narrow minded.

Our care of the patient encompasses a tiny fraction of a percent of their lives...albeit sometimes a critical fraction of a percent.

Our impact in the overall well being of a patient represents a tiny fraction of a percent of their lives...and once again...sometimes a critical fraction.

And so when it DOES matter....like in this case where something REALLY bad has happened....what do guys like you say?

"it's not my fault".......

this is why people like you will never have any respect.

Mil....i just dont understand you sometimes

How many times does the surgeon take complete blame for a bad outcome? Close to never. I remember being involved in a liver resection as a resident. By the end of the case the surgeon lost near 3 liters of blood which was obviously excessive (it should not have been a difficult case). The patient had a relatively high lactate level despite the massive resuscitation effort. The patient ultimately did well. Do you know what he told the ICU attending. He said that all of the morbidity was related to hypotension during anesthesia. If you look at the anesthesia record you would see about a total of 10 minutes of a six hour case with a MAP below 65.


We see this kind of thing from surgeons all the time. You could also argue that "the surgeons impact in the overall well being of a patient represents a tiny fraction of a percent of their lives". What does this have to do with anything?

I do agree that physicians should be accountable for their actions. However, what you are suggesting is downright foolish (their is no other way to put it). Your earlier CRNA statement is also puzzling. You have a habit of frequently comparing those of dissenting opinions to "physicians who are no better than CRNAs". Again I must say that your thoughts on this subject are much closer to the thinking of a nurse.

 

[Laurel123]

Thanks for the discussion guys.

I just wanted to clarify that the surgeon and the hospitalist did not put anything in the chart about the cause of the stroke when they initially discussed it with me. We simply reviewed the chart together initially after a stroke was suspected. I was just disagreeing with them because my initial feeling was emboli and they were thinking watershed and we had a discussion about the events during surgery and her risk factors. But they were going to get all the appropriate studies to look for a cause before any 'hypothesis' was documented. I just wanted to bring the discussion to other seasoned anesthesiologists to get an idea of whether anyone has ever seen a intraoperative stroke due to transient hypotension. Theoretically, it is definitely possible - but again, in this patient, my first thought was emboli.

Just to update - I was at a different hospital for the rest of the week and fairly swamped, so when I returned to this hospital days later - the surgeon caught me in the lounge and said that it was determined to be embolic. Unfortunately I don't know any details of the studies done to determine this but I have ordered the chart for Monday to review.

BTW, the surgeon had actually been very frank in his original consent for surgery with the family and said it was very possible that the patient could suffer a cardiac or brain insult. The family was very accepting of this, as they believed the patient had been depressed since the loss of her husband and they had all considered not even bringing her to the hospital because she had been in and out of the hospital frequently and was miserable being poked and proded. However, the bowel obstruction made her so miserable they decided it would be a terrible way to go - so they brought her in and agreed to surgery hoping to bring her comfort. After the stroke, they all felt she seemed comfortable and made her comfort care - she died 5 days post op.

But I will update Monday after I have gone through the chart. But the discussion on when to accept blame and when to deny is very thought provoking now that I am in private practice.

 

[Planktonmd]

Having run a journal club for 5 years for residents, you just made one of the most common rookie mistakes in interpreting literature.....you extrapolated data from one patient population (CABG) to another patient population.

In CABG/Carotid surgery, the risks of embolism are high and known and OBVIOUS...you're sticking a hugh cannula into the aorta...duhhhh.

I would have thought you would be better trained in your journal clubs.

Is it possible for you to concentrate on the subject we are discussing without repeatedly telling us the glorious history of your wonderful achievements?
We already know everything about your distinguished academic career.

 

[militarymd]

Is it possible for you to concentrate on the subject we are discussing without repeatedly telling us the glorious history of your wonderful achievements?
We already know everything about your distinguished academic career.

So then...are you saying that extrapolating data generated from CABG surgery and applying it to a general surgery patient population is intellectually correct?

 

[Planktonmd]

So then...are you saying that extrapolating data generated from CABG surgery and applying it to a general surgery patient population is intellectually correct?

Yes, I am.
There is no other data, only your personal opinion.
But wait, I already told you that I am not continuing this discussion with you.

 

[militarymd]

Yes, I am.
There is no other data, only your personal opinion.
But wait, I already told you that I am not continuing this discussion with you.

I just wanted to be clear....that you realize your mistake in interpreting the literature....ie wrong patient population.

I merely stated that there is no data.

You stated your opinion as if it were fact based on an error in reading an article.

 

[deleted126335]

.

 

[9french]

..

 

[militarymd]

Question for military:

Do you treat every single reading of hypotension akin to that presented by the original poster immediately with pressors? Or do you wait to see if it persists, or wait for the surgical stimulation that you know is coming if it is preincisional?

I practice the way the OP does.... but I probably give vasoactive drugs sooner than she would........

And each time that I wait..to see if the BP will come up....It's feels like gambling to me.

There's a reason why all those consultants (cardiologists, nephrologists, neurologists, internists, gastroenterologists, etc) notes say "avoid hypotension"

 

[9french]

so what kind of MIs do you get with hypotension? NSTEMI with global hypokinesis?

With severe, prolonged hypoxia and hypotension such as s/p arrest, you can definitely get global hypokinesis. More commonly, in an older individual with, say, a 95% RCA lesion and several hours of hypotension, you would more likely get a regional wall motion abnormality. Although in this latter case, the patient may have an increase in troponin necessitating the dx of MI as opposed to angina, rarely will it lead to a massive MI.

However this does not have a direct correlation to the brain. Both the brain and cerebral vasculature are more sensitive to ischemia and there is not a true anginal equivalent in the brain (TIA is NOT an anginal equivalent). Furthermore although there is a term called "vasospasm" in the brain, it is actually a remodeling of the affected vasculature. This is very different than coronary vasospasm. "Brain attack" and "heart attack" are both lay terms. Although they both are ischemic injuries, when you get down to epidemiology, etiology, diagnosis, treatment, and prevention they are very different.

I still stand by my original point that this is an embolic injury, and is not at all c/w a global hypotensive event.

 

[militarymd]

..

this where we disagree

Unstable Angina/NSTEMI >>>>> ACS ........TIA>>>>stroke

They seem mechanistically the same to me....risk factors, primary/secondary prevention strategies, treatment modalities...the differences lie in the organs affected.

Whether hypotension TRULY causes these entities in the periop timeframe....I honestly don't know....but it is in the "medical lore"

I will submit this....if you have a narrowed vessel with compromised blood flow distal to it (whether it be in the brain or the heart), then if you decrease the pressure, it would appear to me that the tissue distal to it can suffer from ischemia and cell death, in a non-global fashion.....especially if a plaque also forms during the period of low flow.

I know you're going to say the brain has collaterals.....but I will submit that despite these collaterals, people who suffer from bland strokes (and most are NOT embolic) occluding that MCA will lead to infarction.

 

[Planktonmd]

I just wanted to be clear....that you realize your mistake in interpreting the literature....ie wrong patient population.

I merely stated that there is no data.

You stated your opinion as if it were fact based on an error in reading an article.

What can I say!

 

[9french]

this where we disagree

Unstable Angina/NSTEMI >>>>> ACS ........TIA>>>>stroke

They seem mechanistically the same to me....risk factors, primary/secondary prevention strategies, treatment modalities...the differences lie in the organs affected.

Whether hypotension TRULY causes these entities in the periop timeframe....I honestly don't know....but it is in the "medical lore"

I will submit this....if you have a narrowed vessel with compromised blood flow distal to it (whether it be in the brain or the heart), then if you decrease the pressure, it would appear to me that the tissue distal to it can suffer from ischemia and cell death, in a non-global fashion.....especially if a plaque also forms during the period of low flow.

I know you're going to say the brain has collaterals.....but I will submit that despite these collaterals, people who suffer from bland strokes (and most are NOT embolic) occluding that MCA will lead to infarction.

Unstable angina is simply a change in anginal sx over a period less than 2 weeks. Most angina is from supply/demand mismatch. You put a patient with severe CAD on a treadmill, the supply will not be able to keep up with demand, and they will get chest pain. In Printzleman's (sp) angina, vasospasm may lead to chest pain, often at rest. TIAs are caused by small thrombi or emboli which lyse before damage is done. Hence TIA does not equal angina.

In a diseased heart, the heart, too, may develop collaterals. As far as I'm aware, the distal cerebral circulation does not have great collateralization, so I would only suggest the proximal circulation, i.e., circle of Willis is well collateralized. Lastly, of course, the cerebral vasculature is highly sensitive to hypoxia and hypercarbia, which is protective against ischemia.

 

[mille125]

Thanks for the discussion guys.

I just wanted to clarify that the surgeon and the hospitalist did not put anything in the chart about the cause of the stroke when they initially discussed it with me. We simply reviewed the chart together initially after a stroke was suspected. I was just disagreeing with them because my initial feeling was emboli and they were thinking watershed and we had a discussion about the events during surgery and her risk factors. But they were going to get all the appropriate studies to look for a cause before any 'hypothesis' was documented. I just wanted to bring the discussion to other seasoned anesthesiologists to get an idea of whether anyone has ever seen a intraoperative stroke due to transient hypotension. Theoretically, it is definitely possible - but again, in this patient, my first thought was emboli.

Just to update - I was at a different hospital for the rest of the week and fairly swamped, so when I returned to this hospital days later - the surgeon caught me in the lounge and said that it was determined to be embolic. Unfortunately I don't know any details of the studies done to determine this but I have ordered the chart for Monday to review.

BTW, the surgeon had actually been very frank in his original consent for surgery with the family and said it was very possible that the patient could suffer a cardiac or brain insult. The family was very accepting of this, as they believed the patient had been depressed since the loss of her husband and they had all considered not even bringing her to the hospital because she had been in and out of the hospital frequently and was miserable being poked and proded. However, the bowel obstruction made her so miserable they decided it would be a terrible way to go - so they brought her in and agreed to surgery hoping to bring her comfort. After the stroke, they all felt she seemed comfortable and made her comfort care - she died 5 days post op.

But I will update Monday after I have gone through the chart. But the discussion on when to accept blame and when to deny is very thought provoking now that I am in private practice.

it sounds like you worked with a good team. obviously you should not have "accepted blame" in this case...