EVD and Hyperventilation Question

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scotchnwater

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Quick question from last night on-call for Trauma Surgery:

My TBI pt suddenly has their ICP shoot up to the high 30s, neurosurgery isn't sure if this is a real number or the drain is malfunctioning due to being clogged up. She's got a hematoma and some contusions, coags had been slowly drifting up, so it is definitely possible she is bleeding.

They're waiting for the Neurosurg chief to come in - as well as the scanner to open up - before deciding what to do about it (still not knowing if the ICP really is much higher, or the drain isn't working right). Her baseline exam is pretty much nothing (per report) as a result of her injury, so we can't use that as an indication.

My suggestion (I was on-call for the primary service with Neurosurge consulting) was to briefly hyperventilate her (she was intubated) and see if her ICP changed accordingly. Not as any sort of therapeutic measure, but as a brief diagnostic measure. I know you don't use hyperventilation as mainstay therapy with high ICP, but my question to you is twofold:

1) Would you cause harm by doing brief hyperventilation down to a PC02 of 20-25 on a TBI patient?

2) Would this theoretically give us the information we're looking for (i.e. differentiate between a clogged drain and a new acute process causing increased ICP)?

My thinking was that it was important to distinguish this because one is a problem that we can deal with later (change/flush the drain) and the other needs to be dealt with more urgently (intervention for the high ICP).

The ICU nurse was 😱 HORRIFIED 😱 that I would suggest anything that wasn't on the 5"x7" TBI protocol card (she used my favorite excuse of "we don't do that here" - LOVE IT 😍), and the neurosurgery intern had his hands kind of tied until his Chief got there. I, of course, was impotent to act as well, but am just curious as to if this line of thinking is totally wacky or not.
 
You have the patient intubated, right?

I personally don't see anything wrong with mild hyperventilation in this case. As Osler once said, each patient is his own bedside laboratory. At worst, you might've caused some transient global ischemia secondary to vasoconstriction caused by this maneuver. Big deal.

This is precisely the kind of critical and "outside the box" thinking that is routinely **** upon our current "everyone has a say" and "protocol driven" culture we practice in.

Personally, I think it was a brilliant idea. You would've had an answer fairly quickly if the shunt tubing was clogged using this simple, thoughtful understanding of human physiology. But, I don't think you'd have to get her down all the way to 20-25. Probably around 28-30 would've sufficed. That you even had this idea is impressive. You're the kind of doctor that I'd like to practice with.

I'm sorry you were shut down. This seems par for the course lately. Get used to it.

-copro
 
couple of points to acknowledge

- monitors are only valuable when you can trust the result and when it affects your management

- Congratulations on thinking like a physician (using knowledge learned and applying to a situation you never thought to previously)

- How would have managing the patient as if the values were true harmed the patient versus the potential harm from doing nothing? I would have likely done what i could to decrease ICP and increase CPP until someone told me it was spurious.
 
Quick question from last night on-call for Trauma Surgery:

My TBI pt suddenly has their ICP shoot up to the high 30s, neurosurgery isn't sure if this is a real number or the drain is malfunctioning due to being clogged up. She's got a hematoma and some contusions, coags had been slowly drifting up, so it is definitely possible she is bleeding.

They're waiting for the Neurosurg chief to come in - as well as the scanner to open up - before deciding what to do about it (still not knowing if the ICP really is much higher, or the drain isn't working right). Her baseline exam is pretty much nothing (per report) as a result of her injury, so we can't use that as an indication.

My suggestion (I was on-call for the primary service with Neurosurge consulting) was to briefly hyperventilate her (she was intubated) and see if her ICP changed accordingly. Not as any sort of therapeutic measure, but as a brief diagnostic measure. I know you don't use hyperventilation as mainstay therapy with high ICP, but my question to you is twofold:

1) Would you cause harm by doing brief hyperventilation down to a PC02 of 20-25 on a TBI patient?

2) Would this theoretically give us the information we're looking for (i.e. differentiate between a clogged drain and a new acute process causing increased ICP)?

My thinking was that it was important to distinguish this because one is a problem that we can deal with later (change/flush the drain) and the other needs to be dealt with more urgently (intervention for the high ICP).

The ICU nurse was 😱 HORRIFIED 😱 that I would suggest anything that wasn't on the 5"x7" TBI protocol card (she used my favorite excuse of "we don't do that here" - LOVE IT 😍), and the neurosurgery intern had his hands kind of tied until his Chief got there. I, of course, was impotent to act as well, but am just curious as to if this line of thinking is totally wacky or not.
You had a good point and it was worth trying.
 
........The ICU nurse was 😱 HORRIFIED 😱 that I would suggest anything that wasn't on the 5"x7" TBI protocol card (she used my favorite excuse of "we don't do that here" - LOVE IT 😍............
>
I'm not a physician, and I'll be the first to admit to only having a generic understanding of hyperventilating a Pt to reduce ICP. I have however had a number of neuro docs tell me that hyperventilation for that reason is really only effective 24 - 48 hours after the initial injury. I'm sure someone here can offer far more insight than I can. More importantly, the only suggestion you shoud've made to the nurse is to page RT.😀
 
I think a PaCO2 of about 30 is the ideal middle ground to decrease ICP while preventing ischemia...why not try that and see what happens? How did things turn out?
 
Thanks for all the comments - honestly, getting some of the feedback from you guys kind of makes up for the beat-down I get here when I have an idea that is quickly dismissed because I'm "just the intern". Thanks 🙂.

So the lady eventually went down to the scanner where she was found to have extension of her hematoma as well as new hemorrhages both intraventricular and intraparenchymal. When I left in the morning she was being transferred to neurosurgery (from the Trauma Surgery service I'm on).

As of tonight, looks like she's still not doing very well.... Not sure what the plan is from here.
 
Did you have a good pressure curve? if so the drain is probably functional
How much CSF were you draining? was there a counter pressure on the drainage?
 
>
I'm not a physician, and I'll be the first to admit to only having a generic understanding of hyperventilating a Pt to reduce ICP. I have however had a number of neuro docs tell me that hyperventilation for that reason is really only effective 24 - 48 hours after the initial injury. I'm sure someone here can offer far more insight than I can. More importantly, the only suggestion you shoud've made to the nurse is to page RT.😀

not sure why that would be because hyperventilation in the OR works to bring down the ICP but only for a few hours at a time. the system readjusts after 6 hours (i think) and then blowing off more CO2 does not lower the cerebral blood flow and thus doesn't touch the ICP. ask those guys why the relationship to time of injury is, i would be curious to know.
 
not sure why that would be because hyperventilation in the OR works to bring down the ICP but only for a few hours at a time. the system readjusts after 6 hours (i think) and then blowing off more CO2 does not lower the cerebral blood flow and thus doesn't touch the ICP. ask those guys why the relationship to time of injury is, i would be curious to know.

What you're talking about there is a separate issue than ICU treatment of TBI.

What we do in the OR is about shrinking the brain to assist in surgical exposure...allowing the surgeon to retract less for exposure, in THEORY, leading to less parenchymal brain injury.

What the OP is talking about is using this therapy to IMPROVE 30 day, 6 month, 1 year surivival in patients with TBI....and whether it works or not is not definitively proven....

2 complete different things.
 
Did you have a good pressure curve? if so the drain is probably functional
How much CSF were you draining? was there a counter pressure on the drainage?

I honestly don't know - I was not familiar with the monitors and set-up here, and my previous experience with such things had been a month in the Neuro ICU in medical school. I do know that the drain was set at 20 cm initially, although that was later adjusted once the Cheif came in and flushed it a few times. The pressure was still intermittently high as of last night.

What is "TBI"?

Yup....Traumatic Brain Injury.

What you're talking about there is a separate issue than ICU treatment of TBI.

What we do in the OR is about shrinking the brain to assist in surgical exposure...allowing the surgeon to retract less for exposure, in THEORY, leading to less parenchymal brain injury.

What the OP is talking about is using this therapy to IMPROVE 30 day, 6 month, 1 year surivival in patients with TBI....and whether it works or not is not definitively proven....

2 complete different things.

Mil, not sure if you're referring to me as the OP, but my question was not whether or not to use hyperventilation as treatment, but to use the same principles involved to aid in the diagnosisof a problem.
 
I honestly don't know - I was not familiar with the monitors and set-up here, and my previous experience with such things had been a month in the Neuro ICU in medical school. I do know that the drain was set at 20 cm initially, although that was later adjusted once the Cheif came in and flushed it a few times. The pressure was still intermittently high as of last night.



Yup....Traumatic Brain Injury.



Mil, not sure if you're referring to me as the OP, but my question was not whether or not to use hyperventilation as treatment, but to use the same principles involved to aid in the diagnosisof a problem.

mis read your post.....ventriculostomy....it should be draining CSF...if not it is not working...if it is draining, then it is working
 
First off great thinking and instincts.

Having managed a ton of these EVD's I can safely say that unless you have clear vigorous CSF flow into the EVD when you drop it below the level of the head, you have to interpret the pressure readings with caution.

I would like to suggest a great review article on Hyperventilation in Head Injury It does a great job of discussing the relevant aspects of hyperventilation and the associated pitfalls. Before you start your neuroanesthesia rotation (I know it seems like such a long way off now but it will come soon) Memorize pages one and two as well as the compliance and autoregulation curves. You will look like a star on your first day.

Given the clinical scenario you describe, brief hyperventilation as a way of troubleshooting the ICP monitor may be helpful. Hyperventilation results in arteriolar vasoconstriction which reduces cerebral blood volume and cerebral blood flow. Overaggressive hyperventilation can decrease cerebral blood flow to the point that the brain becomes ischemic. The consensus that I have found seems to target a PaCO2 of 30 as the lowest PaCO2 you should shoot for without SJO2 monitoring of cerebral oxygenation. (a whole other discussion there)

Per the Monroe-Kellie doctrine, there are 3 volume compartments in the cranium blood, csf, and parynchema. If you are high on the compliance curve, decreasing the volume of any one of these will result in a marked decrease in ICP.

For each mmHg drop in PaCO2 you can expect ~0.3-1 cc decrease in cerebral blood volume and for each 0.5cc drop in cerebral blood volume you can expect ~ a 1 mm Hg drop in ICP.

The drop in ICP will only last for 6-8 hours before the pH of the perivascular spaces normalize and the flows and thus the ICP resumes to the elevated state that you were modifying. More concerning, an abrupt return to normocarbia at this point will cause cerebral vasodilation and increased ICP above what you started with.

So what can you expect if you do this test of hyperventilation for 10-20 minutes (I have seen all of the following happen in the scenario you describe)

1: ICP measurement decreases then goes back up afterwards - in all likelyhood, the ICP measurements are correct, your EVD is working, and you need to find a more permanent solution to ICP reduction

2: ICP decreases and stays down even after resuming normocarbia - the EVD is working. With high ICP's, the bridging veins can become remarkably constricted and venous outflow can be markedly reduced leading to congestion and a self sustaining elevated ICP. By briefly decreasing the ICP through hyperventilation, the veins are allowed to drain and the cycle is broken. The ICP remains down until the next episode of agitation or other ICP elevating event which puts you back into the vicious cycle.

3: ICP Increases due to increased intrathoracic pressure and decreased venous return. Pressure returns to normal several hours after resuming normocarbia due to the bridging vein theory discussed in 2. EVD is likely working.

4 : No change in ICP: EVD is not working, or is not sensitive enough to pick up a subtle change.

5: Neurosurgery/ nursing/ RT comes in and screws everything up so the data is meaningless

6: Somebody accidentally extubates the patient and really louses up your day.


Go with your gut, hyperventilate for 10-20 minutes and you won't do any damage, and you may even learn something useful.
 
First off great thinking and instincts.

Having managed a ton of these EVD's I can safely say that unless you have clear vigorous CSF flow into the EVD when you drop it below the level of the head, you have to interpret the pressure readings with caution.

I would like to suggest a great review article on Hyperventilation in Head Injury It does a great job of discussing the relevant aspects of hyperventilation and the associated pitfalls. Before you start your neuroanesthesia rotation (I know it seems like such a long way off now but it will come soon) Memorize pages one and two as well as the compliance and autoregulation curves. You will look like a star on your first day.

Given the clinical scenario you describe, brief hyperventilation as a way of troubleshooting the ICP monitor may be helpful. Hyperventilation results in arteriolar vasoconstriction which reduces cerebral blood volume and cerebral blood flow. Overaggressive hyperventilation can decrease cerebral blood flow to the point that the brain becomes ischemic. The consensus that I have found seems to target a PaCO2 of 30 as the lowest PaCO2 you should shoot for without SJO2 monitoring of cerebral oxygenation. (a whole other discussion there)

Per the Monroe-Kellie doctrine, there are 3 volume compartments in the cranium blood, csf, and parynchema. If you are high on the compliance curve, decreasing the volume of any one of these will result in a marked decrease in ICP.

For each mmHg drop in PaCO2 you can expect ~0.3-1 cc decrease in cerebral blood volume and for each 0.5cc drop in cerebral blood volume you can expect ~ a 1 mm Hg drop in ICP.

The drop in ICP will only last for 6-8 hours before the pH of the perivascular spaces normalize and the flows and thus the ICP resumes to the elevated state that you were modifying. More concerning, an abrupt return to normocarbia at this point will cause cerebral vasodilation and increased ICP above what you started with.

So what can you expect if you do this test of hyperventilation for 10-20 minutes (I have seen all of the following happen in the scenario you describe)

1: ICP measurement decreases then goes back up afterwards - in all likelyhood, the ICP measurements are correct, your EVD is working, and you need to find a more permanent solution to ICP reduction

2: ICP decreases and stays down even after resuming normocarbia - the EVD is working. With high ICP's, the bridging veins can become remarkably constricted and venous outflow can be markedly reduced leading to congestion and a self sustaining elevated ICP. By briefly decreasing the ICP through hyperventilation, the veins are allowed to drain and the cycle is broken. The ICP remains down until the next episode of agitation or other ICP elevating event which puts you back into the vicious cycle.

3: ICP Increases due to increased intrathoracic pressure and decreased venous return. Pressure returns to normal several hours after resuming normocarbia due to the bridging vein theory discussed in 2. EVD is likely working.

4 : No change in ICP: EVD is not working, or is not sensitive enough to pick up a subtle change.

5: Neurosurgery/ nursing/ RT comes in and screws everything up so the data is meaningless

6: Somebody accidentally extubates the patient and really louses up your day.


Go with your gut, hyperventilate for 10-20 minutes and you won't do any damage, and you may even learn something useful.

Wow...very informative post. Thank you! 🙂
 
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