I hope I know what I'm talking about. But I've learned a lot today so hopefully I can share as much. Alright so I'm gonna go over a little bit of the procedural aspects the vessel identification and intonation windows. Um Some about waveform reporting interpretation of human dynamic findings and then I picked three obvious clinical examples. Subarachnoid hemorrhage monitoring is the vast majority of the utility of T. C. D. But it's got particular usefulness in intracranial stenosis and as an ancillary test for brain death as well. So T. C. D. Was actually uh first identified in the 19 eighties the very low frequency two megahertz pulsed Doppler. And remember this is transcranial Doppler. So there is no B. Mode imaging. This is all a Doppler study. So it's a blind study In the 1980s. It was introduced in the us as the first noninvasive study for the inter cranial circulation. When I first started learning this my technician who was training me basically told me to close my eyes and do it all by listening because it is blind. So there really isn't anything to look at except for the buttons on the machine. And so it really is a very auditory learning the way forms the pitches the frequencies that really give you a lot of that information advantages. It's a noninvasive study. It's pretty painless in most situations. It's a very safe study and can be used in any hospital environment. So the T. C. D. Machine comes to the patient in the I. C. U. S. And then we send only stable or outpatients um down to the downstairs laboratory. It is used really to think about cerebral blood flow but it can also give information about cerebral embolization. And it's particularly useful as a surrogate for measuring the physiologic changes of increased intracranial pressure Um challenges. It is a Doppler only examination. So the vessels are blindly identified and since the skull reflects 90% of the ultrasound waves um you really are dealing with a very small sample sizes. It's very technically challenging. And particularly so when there's a job related hyper est assis because those skull windows that we're trying to use um to incinerate into the intracranial circulation um may be hampered by that. So the most commonly used window is the trans temporal window. You know this is one of the reasons why baseball hitters where that helmet with the flap that comes down over the temporal bone. It's because it's one of the thinnest bones in the skull and we capitalize on that by using that as an ultrasound window. Uh So um knowledge of the intracranial vascular anatomy. You know the middle cerebral artery is going to be the first vessel that you incinerate and then increasing the depth of the sample volume so that you're tracking the M. C. A. Back intracranial E. Um a little bit angled downward to get the terminal. I see a back up further along into the anterior cerebral artery. And then when you start getting that bidirectional flow. You know that you're looking at both anterior cerebral arteries. One of them coming toward the probe, one of them going away from the probe. So it's partially um knowing your depth of signal, knowing how big heads are and so that you generally know where you are and really looking at the signals and the sound of the signals to identify where you are. You can look at these wave forms and these are not abnormal wave forms. These are the high diastolic wave forms of an auto regulated organ. So having high diastolic flow is normal in the intracranial circulation and it's really what you're looking for because they wave form like you've been seeing previously is distinctly abnormal. So hyper prosthesis limits uh somewhat anywhere between five and 12%. It's more common in elderly women. You know why our hips get thinner but our skulls get thicker is you know beyond me. Um And it's more an african american women. So it's definitely aged and race related. Um Here's an example of that M. C. A. A. C. A. Juncture where you're seeing the uh middle cerebral artery above the probe. The anterior cerebral artery going away from the probe that occurs at about six centimeters of death and that bi directional flow. Mhm. So that's the typical kind of noise that you're listening for in the sub occipital window at the base of the skull. Uh this requires neck flexion. And so as we're monitoring patients with subarachnoid hemorrhage getting them to really flex their neck when they have a chemical meningitis from subarachnoid hemorrhage can be very challenging. And the older people are with cervical spine disease. They may not have the ability to flex their neck. And so this is challenging for the technologists and sometimes for the patients. What we're insinuating here are the inter cranial vertebral arteries. The depth is between six and nine centimeters. And you know, it's that flow away from the probe. Um And then in the basal artery there's three segments, there's the proximal the mid and the distal segment Between eight cm and 12 cm. Um And you're trying to get all three of those segments and again flow away from the probe. And then there's the trans orbital window. And it's an important certainly aboard question for me that you know, when you're doing a trans orbital window, remember to turn the power down to 10%. This is a safety issue. To minimize risk to the ocular lens. Um So that that may well be something that's asked and the flow uh dynamics of the epidemic artery. Since it is a peripheral artery, it is the one vessel that you will see with the typical kind of high pulse. It till it e index. Um The very sort of peripheral ized waveform. But then the carotid siphon which is a little bit further in between six and 8 cm in if you're angling up a little bit um you make it flow away from the probe and it's that kind of c shape of the siphon. So depending upon where the flow is, you may get an idea about where you are in the siphon and looking for those flow uh directional changes pretty much tells you that you're in the siphon. So one of the useful things is that the ophthalmic artery is often cannibalized as a collateral in the setting of a carotid occlusion. So when you see that ophthalmic artery waveform be cerebral. Ized looking with that high diastolic flow and reversed. That's basically giving you physiologic information that that ophthalmic artery, the flow is reversed. The flow is going into the inter cranial circulation and it's part of a collateral. And even if you're doing a. T. C. D. And you're not doing the cervical, you should make a comment that you know this is likely either a hemo dynamically significant for occluded internal carotid artery. Um Signal optimization. So since this is blind. Uh you can have an abnormal study that under reads the velocity because of the angle of incineration. So low velocities may not necessarily represent low flow or pre occlusion. They may be technical error. Um So you're always looking for the highest velocity vessels. Um that you can here because the high velocities are not going to be falsely over red. They're going to be what is really um Him dynamically what you're looking for. And and so here is a small tape of as the angle of incineration decreases from 50 to 60° aligns more to the direction of the flow in the vessel. That you can have a big difference in the mean flow velocity that's being reported. So you're always looking for you know kind of those micro movements of the probe to really get that highest velocity. Um So we think of mean flow velocities as kind of a measure of cerebral blood flow. For many of the things that have been said before. You know velocities are not synonymous with flow but we sort of think of it that way. And the pulse it till it E. Index is something that's really important in in transcranial Doppler because it gives you an idea about the vascular resistance and it's a combination of the mean flow velocity and the pulse civility index. That gives you a range of interpretations for the for the vessels. So here's a couple of wave forms. You know very much like what you've seen before. A normal vessel flow on the right 60 centimeters per second in the M. C. A. Uh greater than 50% stenosis. Here's 100 and 54 centimeters per second in the M. C. A. And then to the very left a very dampened low waveform. Um That is a either occlusion or a or a pre exclusive vessel. So when you're looking at the pulse it till it E indices. Uh the uh that's high spiky or short um high frequency wave forms. Uh There's a whole range of interpretations. If you do T. C. D. S. In young patients where you're monitoring for velocities that are indicative of sickle cell related disease. Uh They have very very low pulse. It till it ease. You know they're sort of their brain is kind of like a giant A. VM lots of flow as you get older and older you get those stain attic high resistance vessels like you do in other end organ disease related to hypertension and the like. And so those pulse it phillipe indices will go up. It will also go up with hypertension. The hypertensive therapy that we use our presser therapies that we use in the ICU. It goes up in intracranial pressure as the increasing that distal resistance by tissue pressure. Um High cardio output states and importantly hyperventilation which it is actually used in a reserve test. Low pulse it till it e indices. So again young age when you've got a proximal stenosis or occlusion and your maximally visa Dilated distantly to try to maintain distal cerebral blood flow, abnormal communications a VMS and a. V fistulas where it's abnormal increased flow. Um Alternatively vaso dilator therapies uh and heart failure sepsis. Other things that really drop your peripheral resistance can also be visualized in the brain. Um and breath holding. Um. Again so this is part of our our testing for cerebrovascular reserve. So when the brain is auto regulated it dampens a lot of these changes. But when a brain is dis auto regulated the PCO two is actually a very powerful manipulator of the peripheral resistance and therefore the flow velocities. So um I remember you know I ran into michaela here and I remember her calling me once about a patient that she was doing in the in the in the I. C. U. And it's like the meaningful velocities are all over the place. They're high they're low they're high low which one am I supposed to take and take a snapshot of. And and it was actually a patient with profound chain Stokes respirations. And so when they went through their hyperventilation phase they would become very high resistance clamped down and their blood flow would go down. And when they were in their ethnic phases they would retain C. 02 and the vessels would expand and they would have high flows. So you know think about this in your you know chain Stokes patients when you hyperventilate um grab your stomach and you know squat down you're likely to faint. You know that crazy thing that some kids do on the playground that's because it's cerebral um global cerebral ischemia. Um And when uh sleep apnea patients wake up with these bad morning headaches it's because of their several visa dilation and literally their increased I. C. P. Headaches in the morning. So you know this is something that is sometimes very apparent and particularly important to us. Um When we have patients on ventilators with cerebral ischemia. Brain hemorrhages, increased intracranial pressure and the like. And so it's something that you can manage um by looking at the T. C. D. So I said that subarachnoid hemorrhage this is what we use the bulk of monitoring for. Um It's 5% of all the strokes but they're the highest risk of poor outcome. Uh First related to re bleeding and hemorrhage and then second related to cerebral Visa spasm which causes this delayed cerebral ischemia and infarction. Um and leads to the morbidity of patients fortunately you know Visa spasm is something that you can predict. It occurs in the vast majority of patients um either asymptomatic or symptomatic and it has a somewhat predictable time course of evolution. So doing these T. C. D. S every day and looking for pique vezo spasm which occurs Somewhere between several days in and a week or two. you can manage that visa spasm as it is evolving to try to prevent um distant infarction. Um So T. C. D. Criteria for moderate Visa spasm it's best in the middle cerebral artery in terms of our validations. Um 150 centimeters per second severe is 200 centimeters per second that's like panic value um in the basal artery there's pretty good data although the baseler is much harder to get greater than 90 centimeters. per second for moderate basal spasm and greater than 120 for severe basal spasm. And there are a number of clinical protocols that kick in when you're moderate when you're severe in terms of hyper polemic therapy, hypertensive therapy and the like you can predict Visa spasm based on how much blood is in the basal cisterns. And so we do this modified fisher scale on C. T. You know that blood layering in the basal cisterns bathing those cerebral vessels is what causes that internal inflammation and hyperplasia. That is the ideology of Visa spasm. And as you look here Visa spasm tends to be a gradual tubular. It involves large segments of the vessel. And and so it's a little bit easier to pick up on transcranial Doppler because it is present in numbers of segments as you march through the vessel. And so on the right is an angiogram picture of that significant Visa spasm. Uh Here's an example of moderate Visa spasm and just listen to the pitch intracranial artery stenosis. Can also pick up this kind of narrowing with T. C. D. Um Inter cranial disease. There's been a number of clinical trials that actually use T. C. D. Very much like crest does now for velocity criteria for entering people into the clinical trial. These are patients that typically have clusters of risk factors hypertension, diabetes hypercholesterolemia and it's much higher in certain races. Hispanics. Blacks. Blacks and asians um Like with extra cranial disease that typically occurs at branch points. Um So the I. C. A. Uh M. C. A. Bifurcation, the middle stem of the M. C. A. The basal artery. The severity of the stenosis is correlated with the risk of early recurrence. Um But the mechanisms can be many either you can have a plaque rupture causing artery to artery distal embolism. You can have plaque causing occlusion of those penetrating small vessels at the base of the skull. Um Or you can have stenosis that leads to a distal hemo dynamic insufficiency. So um regardless of the ideology of it it can cause um symptoms in very many ways. And um Derek I'm gonna have you help me out here uh Here's a patient with a normal M. C. A. Mean flow velocity run somewhere between 40 to 60 65. Okay. And the next example is someone with moderate M. C. A. Stenosis. Yeah and then the last is severe stenosis. Oops. And these criteria these T. C. D. Criteria were validated in a study called sonia which was a T. C. D. Sub study of a clinical trial that was looking at aspirin versus warfarin for the management of intracranial disease if you want the reference um detection of micro symbolic signals. This is something that you can always pick also pick up in the M. C. A. Listen for the squeak. There's one there's another one there's another one you can hear the chirps in there. There's been a lot of uh studies that have used micro symbolic signal monitoring uh monitoring, doing a carotid stent, inter operative monitoring of doing credit and our direct amis inter operative monitoring of doing an geographic procedures doing cardiac bypass surgeries. Much of the engineering improvements in bypass were actually uh guided by T. C. D. Monitoring during bypass surgeries. Um identifying that the aortic cross clamping was a big time for micro symbolic signals to the brain. Um There's been a number of studies the Department of Defense have used much of their ultrasound submarine um wisdom to try to define what are the nature of these signals. Are they capitation noises? Is it um aerosolized um Gaseous material is it particulate material? Um But there really isn't a good identification of exactly what the hits are with T. C. D. Um And then the last as an ancillary test for brain death evaluation. You know these these patients are critically ill. Um Looking for reductions in cerebral blood flow that would be consistent with cerebral circulatory arrest. And there's you know having a baseline study is very useful. Um A false positive absence of cerebral signal could be with hypothesis or other technical factors. So knowing that you had a T. C. D. Where you were able to inseminate these vessels. And now you have an absence of signal is very important, false negative preservations of flows when there truly is no functional cerebral blood flow can be seen in patients with strategies that decreased the intracranial pressure like DVDS or compressive hemi craniectomy. And so there's some false negative that the patient truly is brain dead. But you can actually see a wave forms on A. T. C. D. So be aware of those and there's a progression that is really related to the I. C. P. Low diastolic flows, absence of diastolic flow then that oscillating a reverberating flow. The very short systolic peaks and the absence of signal. So serial studies I think are very useful. And here's a sort of a a sequence as I. C. P progressively increases. You can see those pulse it till it ease go up 33.5 mean flow velocities are progressively going down, starting to get reverberating flow P. i. s. of five and 6. I mean these are incompatible with life, wow, wow, boom. And then eventually the very short systolic peaks until you have no flow at all. No, but all right, thank you very much.
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