Vasopressors in ischemic stroke

[Nephro critical care]

I had a recent case where a woman who is chronically uncontrolled hypertensive presented to ED with ‘hypertensive urgency’. Her BP was about 220 systolic. Pt got started on IV antihypertensives gtt and then SBP plummeted to 90s. She then became unresponsive.
Moved to ICU. MRI shows bilateral mutiple infarct anterior and posterior circulation. Thought embolic or watershed. SBP now 100s. Getting fluids and has AKI.
I am thinking watershed infarcts from hypotension. How aggressive would you be with this pts BP ?? I think she chronically runs 200s.

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[Aldertonghen]

I may be completely wrong (PGY1 intern here) but at my program we typically allow permissive hypertension for 24-47 hours after the stroke- so basically only treat it if it’s more than 220/120. And then lower it by not more than 15% every 24 hours, usually with labetalol. That patient was treated too aggressively

If it’s an aneurysm then <160mm hg.
If it’s a bleed then 130-150mm Hg.

Those are the numbers I remember from my stroke rotation

 

[Nephro critical care]

I may be completely wrong (PGY1 intern here) but at my program we typically allow permissive hypertension for 24-47 hours after the stroke- so basically only treat it if it’s more than 220/120. And then lower it by not more than 15% every 24 hours, usually with labetalol. That patient was treated too aggressively

If it’s an aneurysm then <160mm hg.
If it’s a bleed then 130-150mm Hg.

Those are the numbers I remember from my stroke rotation

I meant how aggressively would you raise the blood pressure at this point if SBP 110. She is getting saline. Would you start vasopressors to keep SBP 160-180 mm Hg and place central and arterial lines to aggressively get BP to goal ?

 

[Telamir]

As far as I am aware there is no evidence for any of this. That being said, I’ve run into this scenario before where blood pressure drops and causes ischemic symptoms either worsening a stroke or causing it in the first place.

I’ve started pressors on these folks with mixed results.

From a purely (as far as I know) scant evidence standpoint I’d go 140-160. You’re unlikely to cause a bleed (depending on stroke size) or significant harm at those ranges.

 

[Radetzky]

I meant how aggressively would you raise the blood pressure at this point if SBP 110. She is getting saline. Would you start vasopressors to keep SBP 160-180 mm Hg and place central and arterial lines to aggressively get BP to goal ?

Yes I would, I would aim for a MAP of 80-100. I mean the ship has probably sailed but you can at least prevent further ischemic injury.

This is why we need to get rid of “hypertensive urgency” as an entity. Results in well meaning people assassinating patients.

 

[Nephro critical care]

In this case the pt was getting NS at but SBP still 120-130. Pt was unresponsive. I decided to throw the kitchen sink. I put CVL and started norepinephrine to keep SBP 160 - 180 mm Hg with instructions not to treat hypertension unless SBP > 220 mm Hg. Since I was using norepinephrine I knew I was playing with fire re risk of causing ICH and family was already mad. So I placed arterial line so nurses would react quickly to BP changes because otherwise I find they become extremely content with q30 cuff pressures.
Amazingly once SBP reached 180-200 mm Hg pt woke up and started talking. Now she is started on diet. I am curious should I repeat MRI to see if DWI changes are resolving ?

 

[Radetzky]

In this case the pt was getting NS at but SBP still 120-130. Pt was unresponsive. I decided to throw the kitchen sink. I put CVL and started norepinephrine to keep SBP 160 - 180 mm Hg with instructions not to treat hypertension unless SBP > 220 mm Hg. Since I was using norepinephrine I knew I was playing with fire re risk of causing ICU and family was already mad. So I placed arterial line so nurses would react quickly to BP changes because otherwise I find they become extremely content with q30 cuff pressures.
Amazingly once SBP reached 180-200 mm Hg pt woke up and started talking. Now she is started on diet. I am curious should I repeat MRI to see if DWI changes are resolving ?

Well done

What is repeating MRI going to change? You have your answer.

 

[Nephro critical care]

Well done

What is repeating MRI going to change? You have your answer.

I am just curious if the DWI changes would be expected to resolve in a couple of days.

 

[sharkbaitwhohaha]

I am just curious if the DWI changes would be expected to resolve in a couple of days.

Me too. But this curiosity might cost the patient an extra house payment in medical bills. Just food for thought.

 

[Telamir]

I don't think it'll matter, both from a curiosity or clinical standpoint.

If the patient's clinical symptoms resolve/improve: Cool. If they don't, then you already know they had a watershed stroke. There's nothing to gain from the study.

 

[deathmerchant]

I had a recent case where a woman who is chronically uncontrolled hypertensive presented to ED with ‘hypertensive urgency’. Her BP was about 220 systolic. Pt got started on IV antihypertensives gtt and then SBP plummeted to 90s. She then became unresponsive.
Moved to ICU. MRI shows bilateral mutiple infarct anterior and posterior circulation. Thought embolic or watershed. SBP now 100s. Getting fluids and has AKI.
I am thinking watershed infarcts from hypotension. How aggressive would you be with this pts BP ?? I think she chronically runs 200s.

First, will need to see the size/shape/location of strokes and if any microhemorrages on SWI to determine the risk of reperfusion injury from increasing BP. Typically, after the first 48 hours there is no advantage of induced hypertension.
My recs if she is chronically >200. Day 1 BP at 140-180. Day 2 120-160 and Day 3 100-140.

The second variable is vascular anatomy on CTA or MRA. If there is carotid stenosis or other large vessel stenosis/occlusion, I would try to keep BP higher for longer. If vessels are open and/or there are great collaterals the above advice stands.
Avoid diuretics and vasodilators. Maintain good intravascular fluid volume. and obv anti-platelets.

Finally, if there is a reliable, frequent clinical neuro assessment by a neurologist, repeat imaging is not too helpful. Maybe a CTH if sudden change in status. If neurology is not available/reliable- repeat MRI can be helpful in determining final prognosis, how much long term deficits will be there and if needed, when to start anticoagulation.

 

[deathmerchant]

I am just curious if the DWI changes would be expected to resolve in a couple of days.

Typically it takes 3-4 weeks for ischemic DWI changes to resolve.

 

[Nephro critical care]

First, will need to see the size/shape/location of strokes and if any microhemorrages on SWI to determine the risk of reperfusion injury from increasing BP. Typically, after the first 48 hours there is no advantage of induced hypertension.
My recs if she is chronically >200. Day 1 BP at 140-180. Day 2 120-160 and Day 3 100-140.

The second variable is vascular anatomy on CTA or MRA. If there is carotid stenosis or other large vessel stenosis/occlusion, I would try to keep BP higher for longer. If vessels are open and/or there are great collaterals the above advice stands.
Avoid diuretics and vasodilators. Maintain good intravascular fluid volume. and obv anti-platelets.

Finally, if there is a reliable, frequent clinical neuro assessment by a neurologist, repeat imaging is not too helpful. Maybe a CTH if sudden change in status. If neurology is not available/reliable- repeat MRI can be helpful in determining final prognosis, how much long term deficits will be there and if needed, when to start anticoagulation.

Unfortunately we have no neuro in house. The facts were in the cerebellar hemispheres/occipital lobes suggesting posterior circulation although some in anterior circulation and higher cortices as well. She had AKI so could not get CTA but I will get MRA without contrast to look at basilar artery.
Is SWI going to get more info than DWI ?

 

[Telamir]

I mean. That description could also be seen with PRES.

SWI just shows you if there are micro hemorrhages.

 

[johnny_bananas]

I had a recent case where a woman who is chronically uncontrolled hypertensive presented to ED with ‘hypertensive urgency’. Her BP was about 220 systolic. Pt got started on IV antihypertensives gtt and then SBP plummeted to 90s. She then became unresponsive.
Moved to ICU. MRI shows bilateral mutiple infarct anterior and posterior circulation. Thought embolic or watershed. SBP now 100s. Getting fluids and has AKI.
I am thinking watershed infarcts from hypotension. How aggressive would you be with this pts BP ?? I think she chronically runs 200s.

Diagnosis?
I agree with you, the patient had a hypotensive stroke. Prior posters mentioned PRES - radiologically ischemic strokes are very different from PRES, the former has isolated cytotoxic edema and the latter mainly vasogenic. Also there was a temporal relationship with the patient worsening right after low BP, and improving with higher BP.

Further investigations?
I agree with other posters, there is limited value in repeating an MRI for the purposes of seeing if the cytoxic edema would improve, there is a known radiological progression of ischemic infarcts, and the changes will not rapidly disappear.

However, there is utility in obtaining an MRA of the head and neck. If the AKI is severe you can order a 'Time of Flight' (TOF) that does not require contrast, but TOF does over-estimate the degree of vessel stenosis. The value of an angiogram is that the patient may likely have severe extracranial or intracranial stenosis. Confirming that the patient has severe atherosclerosis has management implications, and you also want to rule out any thrombus. Watershed infarcts secondary to hypotension are difficult to differentiate from cardioembolism so I would get an Echo and 48 hr telemetry (at a minimum) while in hospital.

Management?
Cool case, and good for you that you had the fortitude to start pressers. I strongly disagree with other posters about BP goals, there is no benefit and possible harm targeting a BP less than 160, particularly if the patient has vessel stenosis. In patients with chronic hypertension they have cerebral autoregulatory dysfunction and lowering BP can impact cerebral perfusion pressure leading to ischemic infarcts - this is what happened to your patient. We also know that your patients brain likes pressures of 180-200, they got better when you started the pressers!
I would titrate off the pressers and if the patient worsens you would need to go back up. If your patient is off presssors and their BP is below 220, and systemically they are okay you do not need to acutely treat this. After 1 week, I would start a very low dose long acting anti-hypertensive that they will need to slowly titrate up.
If they have severe stenosis - I would start a high-dose statin, and they should be started on ASA 81mg OD.

Cool case thanks for sharing!

 

[Nephro critical care]

Diagnosis?
I agree with you, the patient had a hypotensive stroke. Prior posters mentioned PRES - radiologically ischemic strokes are very different from PRES, the former has isolated cytotoxic edema and the latter mainly vasogenic. Also there was a temporal relationship with the patient worsening right after low BP, and improving with higher BP.
Cool case thanks for sharing!

MRA turned out to be negative today. No hemorrhage noted on on imaging today. She is fully alert and oriented. On gross neuro exam she has no deficits other than dysdiachokinesia which goes along with cerebellar infarcts. Radiological pattern is watershed infarcts rather than PRES. I started ASA/plavix.


Thank you all for your input !

 

[Telamir]

Cool. Glad to hear it turned out well.