Hi, I'm Aarti Sarwal. I'm a professor in neurology at Wake Forest School of Medicine, and I really appreciate this opportunity to be a part of this session on questioning should we use ultrasound for every patient with suspected cerebral edema? So bear with me as I make a case for basically trying to convince you that neuro ultrasound can be an extremely useful tool for using cerebral edema assessment. I have no relevant disclosures in relation to this talk that are commercial. I do participate as a faculty and director for several CME related activities centering around ultrasound sponsored by Society of Critical Care Medicine NCS and a couple of other organizations. So ultrasound as a tool for actually assessing cerebral perfusion. Why would you need ultrasound when we have CT scans, MRIs and other modalities? Well, have you taken care of a patient that looks like this in the ICU? Patients may have mobile CT scanners accessible to them, but they're not universally available. A patient may still be high risk for transport and patients medical and other comorbidities may not make the patient amenable to traditional invasive neuromonitoring devices. Patients on therapeutic anticoagulation that are very high risk for deterioration like cerebral venous sinus thrombosis where therapeutic anticoagulation is a part of the management but patient is very high risk for venous infarctions and edema. Hepatic encephalopathy is a classical example. And other patients that are limited in our neuroassessments because of their sedation and high equipment use, patients on ECMO, patients on HFO, aortic balloon pumps and renal replacement therapies. These patients may have a confounded exam from sedation. You may be able to transport them, but it's extremely high risk transport both from the faculty who is trying to do that and the patient's dislodgment of device perspective. So ultrasound being a easy handy point of care tool in the ICU and has been used extensively in cardiac, lung, abdomen and vascular applications, why not use neuroultrasound? So neuroultrasound obviously is made difficult by the fact that the skull impedes transmission of sound waves. But fortunately, in a majority of patients except 10 to 35 percent, depending on your race, ethnicity, and age, we have a part of the skull in the temporal bone that allows temporal windows. So we call them windows to the brain. And the skull is just thin enough where with the traditional echo probe placed in the temporal area with the index marker pointed towards the patient eyes, you can get a cross section of the brain looking through these temporal windows and you can see the opposite part of the skull and you can see a butterfly structure that looks like the midbrain and some bony landmarks, the sphenoid being the petrous part of the temporal bone. So in a significant number of patients, we have temporal windows that allow insonation of the brain, although it is limited in about 10 to 35 percent patients, elderly, Asians, African-Americans. So if you do use ultrasound, what can you use it to visualize? Well, you can use it to visualize a big intracranial hemorrhage. This is a rendition on a transcranial preset and an abdominal preset of what an intracranial blade looks like. What you're looking at here is the opposite skull and fox cerebrae in the center. This is transcranial preset, this is abdominal preset and a hyperechoic shadow that doesn't correspond to a known anatomical landmark. So in this particular case, you can see the CT scan corresponds to this and the temporal window insonation can show you a big intracranial hemorrhage in the opposite cerebral hemisphere. You can measure midline shift. People have shown correlation of ultrasound measured midline shift with CT scan measured midline shift. The caveat is the midline structure that you choose for midline measurements needs to be standardized across serial measurements. In this particular case, we're giving the example of posterior part of the fox cerebrae, which we're measuring on either side to calculate the midline shift. And this is another example of this is opposite skull and then your posterior part of the fox cerebrae in this particular case is being used as the marker for measuring the midline shift. Obviously, it depends on the patient's pathology. If the pathology is more frontal, you want the fox cerebrae. If the pathology is more posterior, you might want the pineal gland or if it's frontoparietal, you may be able to get away with septum pellucidum. It also is easier to measure this from the same window looking at the ipsilateral and the contralateral side. As you can see, it's difficult to sometimes extrapolate the right and the left temporal windows if done separately. So looking at perineum pathology, midline shift assessment, some people have also used ultrasound for hydrocephalus assessment. I have been a little underwhelmed by that, primarily because of the artifacts produced by dilated ventricles as well as the corot plexus. So the video here is a rendition of the lateral ventricles. You can kind of see the midline corot plexus and two on the sides and a Y-shaped structure coming around. That is the lateral ventricles. And there is nothing defining the ventricular margins itself. So it's really hard to assess lateral ventricular size. But the third ventricle size has been shown to correlate with CT measurements of third ventricle as well. The one caveat there is if the patient has instrumentation. So this is an example of a patient having an EVD. You have to be careful about the anatomical locations. Again, it can be a useful tool for a patient with a very dilated ventricle out in the field in an austere environment where CT scan is not available. But obviously, CT scan here is the gold standard. You can do ocular ultrasound as an extension of neuroultrasound for assessment of papilledema. So this is an ultrasound version of the optic disc bulging into the posterior chamber. And this crescent sign basically means patient has papilledema. It doesn't tell you whether this is old, whether this is new, acute or chronic. And we need more studies into the serial changes that occur in the crescent sign in acutely, critically ill patients with brain injuries. But another window to the brain, which is an ultrasound version of papilledema. Then you can use optic nerve sheath diameter. There are certain caveats to using optic nerve sheath diameter. We haven't quite found a universally applicable cutoff that can give us a good screening mechanism to look for ICP crisis. But when a patient does have a high optic nerve sheath diameter, it can definitely help us. The caveat has been, although we've standardized the measurement three millimeters behind the retina and more than about five to six millimeters across, has traditionally been known as a predictor of high ICP crisis. The two challenges are some people propagate measurements by imaging the optic nerve sheath in a longitudinal axis and then taking transverse measures. Some people propagate actually trying to image the transverse axis as a bullseye approach and then measuring it. The anatomical variations in the elasticity and the trajectory of the optic nerve sheath has been a challenge. The other challenge is that sometimes the optic nerve sheath gets excluded at the base of the brain because of a sudden ICP increase. And the egress of CSF from the base of the brain to the anterior trabecular part where you will see the widened optic nerve sheath diameter actually doesn't happen. And that's why a sudden increase in the ICPs can sometimes abnormal optic nerve sheath diameters as some of us have seen in practice. I personally propagate and use point-of-care transcranial Doppler. So you can insonate the circle of Willis. This is your B-mode ultrasound with opposite skull visible. You can see midbrain or the butterfly in the center and using color Doppler you should be able to insonate in most patients the circle of Willis. It may not be visible in one single section as this picture shows you but by insulating at slight angle changes you can pretty much interrogate the whole circle of Willis in majority of patients. The typical waveforms that you get on spectral Doppler patterns are low resistance waveforms. So here we are looking at the midbrain and we're looking at the middle cerebral artery, the distal part of it as you can see by the depth and the spectral waveforms have systole, diastole, very robust flow throughout the cardiac cycle, rapid upstroke, stepwise deacceleration and a diastolic flow that is a third to half of the systole. That is classical of low resistance waveforms characteristic of vital organs compared to peripheral vasculature where you see high resistance waveforms. The high resistance waveforms have a rapid upstroke but a very rapid downstroke as well sometimes triphasic systole and the diastolic component is minimal absent in most of the peripheral vasculature with high resistance circulation. The fun part is that the resistance of a organ can change with the disease processes. So a normal low resistance vascular bed as seen in the cerebral circulation can change to a high resistance bed say by a global increase in intracranial pressure, global vasospasm, multifocal stenosis. So the transition of these waveforms can sometimes help you in figuring out if the distal vascular resistance is changing in that vascular bed. So normal cerebral hemodynamics, this is high resistance where the diastole is present but very low compared to the systole and this is extremely high resistance where diastolic component is minimal almost zero at some parts of the diastole. So if you see a patient that you have a poor exam say a poor grade subarachnoid hemorrhage that is being monitored for vasospasm, you're looking at their mean flow velocities, you're looking at their waveforms, this is a low resistance waveform and if you see changing that to a high resistance waveform the diastole is dropping and the downstroke of the systolic part is also dropping that tells you that this patient has a change in distal vascular resistance which in this particular case happened because of a global increase in the intracranial pressure. Quantitatively you can measure it by what we call as pulsatility index where Pi is peak minus end diastolic velocity divided by patient's mean flow velocity and this can be a marker of showing you that the patient's distal resistance has increased. So in this particular case Pi changed from 0.7 to 1.8 but both qualitative and quantitative assessments can corroborate that this patient has increased distal resistance in this particular case by global increase in ICP and we have demonstrated this phenomena on a multitude of studies that cerebral perfusion as it changes in patients with increasing ICPs will manifest qualitatively in these changes in the waveforms. So when the patient's ICP is gradually increasing the normal cerebral waveforms that you see at the top here will gradually change to high resistance waveforms where the diastolic component will start dropping and the systolic component will become sharper on the upstroke as well as the downstroke. So these high resistance waveforms will have high Pis. Eventually when the ICPs continue to ascend untreated or not responding to treatment and your diastolic component of blood pressure has been overcome by the patient's intracranial pressure you will have forward flow from the heart to the brain during systole but during diastole the flow is actually coming backwards from the brain to the heart because the ICPs are much higher than the diastole. This classical pattern in this case is called the oscillating to and fro pattern where net forward flow during systole almost is negated by the net downward flow during diastole. This particular pattern if sustained and does not and if it does not respond to therapy it will progress to cerebral circulatory arrest and is one of the diagnostic criterias for PCD ancillary support for supporting a clinical suspicion of death by the logical criteria. Eventually the ICPs continue to ascend and now are close to your systolic pressure you will barely have systolic stumps eventually going on to complete cerebral circulatory arrest. You can't use this as a criteria for a cerebral circulatory arrest because this could be absence of temporal windows which can be seen in 10 to 35 percent of the patients depending on race ethnicity and age but if you showed windows and you see this progression that actually becomes a non-invasive way to look at patients ICPs and measure them in a non-invasive fashion. So say if you have a patient with a poor exam confounded by paralysis sedation or their medical comorbidities and you're concerned about the confounders to the exam and you perform a TCD seeing this oscillating pattern in multiple vessels all over where systolic flow is negated by the diastolic flow going backwards the oscillating pattern is sustained more than 30 minutes apart on two studies will basically support patient's progression to cerebral circulatory arrest. You can also use it to assess high-risk situations like a patient post-cabbage patient that had a brief cardiac arrest with significant cardiogenic shock resulting in need for in a balloon pump and impeller placement and in this particular case as you can see on the left the patient is on a significant amount of cardiac support and the big question is based on the pre-morbid status we don't know if this patient's brain is getting good supply or not. Now you can continue resuscitating this patient for a couple of days this patient is nowhere stable to even move for a mobile cd scanner transport but in case you had a TCD in this case the waveform is showing very oscillating waveforms and you're seeing two different systolic waveforms because of the balloon pump causing one waveform is coming from the balloon pump and one is actually coming from the patient's native impulse but this can give you an indicator that the patient's brain is not really perfusing well. Can this be a you know a goal directed target for you to titrate your therapy? In this particular case we had already maximized therapies for cardiogenic shock and the patient did progress to brain death eventually and passed but in other cases and that can actually help you figure out the efficacy of your therapies especially when significant cardiological support is being needed to make sure that the brain is actually getting good blood supply because neurological outcome is a it's a major part of that clinical paradigm. You can also use it to rule out malignant crisis so this is a patient on VA ECMO with exam significantly limited by paralysis and sedation and the question is that based on the other parameters things look okay but from the brain perspective does this patient have any signs of malignant cerebral edema? The insonation is limited obviously by the non-pulsatile nature of patient's circulation in this case but if you look at the left MCA or the right MCA you can see a pretty decent positive waveform with mean flow velocities because there's no possibility almost same as a normal person and in this particular case both in the right left are kind of in the same range with no gross asymmetry so at least that gives me a non-invasive way to say the patient seems to have intact cerebral perfusion bilaterally symmetrical with no concerns of significant impairment of CPP in all vessels. Does it say the patient does not have brain injury? Not really but at least it gives you a non-invasive surrogate that the hemodynamics and the plumbing is working from a brain perspective. We have used it in patients where other modalities failed us so this was a patient that had VA ECMO placed for influenza pneumonia this is pre-COVID patient and this is a four-year-old child that unfortunately had a small intracranial hemorrhage as a result of the anticoagulation an EVD monitor was placed and the patient was transitioning from VB ECMO to high frequency oscillator to avoid therapeutic anticoagulation. Now because of sedation paralysis there was a significant concern that we need to have a neuromonitoring paradigm in this particular patient but the EVD would not give us any meaningful data because of the oscillations. We were asked whether T-CDs could be amenable to providing us that information to support the patient's medical therapy going forward both from a cardiopulmonary perspective as well as a brain perspective. So in this particular case you can see the high frequency oscillator artifact but despite that we were able to get pretty decent meaningful information from all the vessels on the point of KTCD and all the vessels showed pretty normal waveforms a little higher resistance compared to what you would expect in a four-year-old and we used that to titrate patient osmotic therapy but it showed us that there was no malignant edema or progression of malignant cerebral edema on progressive studies. We used midline shift in this case as well which correlated to the last CT scan the patient had and we also performed some venous ultrasound. So over the next few days we used transplant adopters as a non-invasive marker of patient's cerebral edema progression which antiquated osmotic therapy and all this time EVD was actually not able to give information. Eventually patient got weaned off the high frequency and did relatively well for a patient that had an intracranial hemorrhage but a better outcome than kind of going blind and not titrating therapy. This is another patient that I'm exploring whether these waveforms and these information can actually serve as a goal to target for escalating therapy whether it's surgical or medical. So this is a postpartum patient that had a intracranial hemorrhage as a result of her aneurysm bleed but it was mostly parenchymal. She had a very good exam and was deemed a candidate for minimally invasive surgical evacuation of that particular bleed after the aneurysm was protected but in this particular case we had a good exam otherwise a candidate for surgical therapy. When I insulated her waveforms on the same site they were pretty non-compliant waveforms the same P1, P2, P3 non-compliant waveforms that you see on ICP monitors you can reproduce that on the TCDs as well. So we knew that she was very high risk of deteriorating even with small increments of ICP. We did not have an ICP monitor because she had a good exam she was able to follow commands. As her exam deteriorated over the day we were making decisions about taking her for surgery. I insulated her waveforms just as an academic inquiry and on the way to the surgery just prior to that her exam had kind of deteriorated to the point that she was taking more and more stimulus to give us the same exam but the decision had already been made to escalate surgery. I saw the waveforms progress from this non-compliant waveforms to very high resistance waveforms with reversed systole. So that gave me a pause whether this patient's ICPs were actually increasing and that corresponding to her decreasing mental status exam or the grossly the motor and the speech exam was the same. When the patient came back from surgery she actually ended up having a reversal of these waveforms which continued to be high resistance so we actually used these waveforms because there was still high resistance as a marker that her brain is still tight and continue to tight with osmotic therapy until she really got out of the cerebral edema window. Incidentally in her case her optic nerve shift diameter was also high at 6.4 millimeters and in this case the transverse venous ultrasound measurements were also helpful that are still very exploratory but I'm doing them in patients with potential cerebral edema crisis. The other place where actually measuring CPPs rather than calculating them based on ICP and systemic blood pressure can be helpful is diseases that cause ICP crisis that are not related to the brain compartment. This is an example of a patient from Columbia Presbyterian that basically was having ICP crisis and every time the ICP goes up you can see the oxygenation is going down it corresponds to blood flow going up. Now you can say maybe this is a Monroe this is a cushion response or a protective response and the patient's ICP goes up and the patient's blood flow is going up to maintain CPPs but in this particular case on the EEG electrodes patient was actually having seizures. So the seizures were causing the increased cerebral blood flow which was driving the patient's ICP. Now you can measure that invasively but you can also measure them non-invasively. In this particular ICP crisis if you were suspecting a low CPP and the ICP was caused by cerebral edema from the brain compartment you would see perfusion limiting waveforms as in the oscillating waveforms but in this particular patient if you had done the transcranial dopplers the normal TCD waveforms could actually support that this is hyperemic intracranial hypertension compared to the oligemic intracranial hypertension and this concept has been introduced by other people Kofke et al in the past as well and TCDs can really be a non-invasive way for you to distinguish these two disease processes. So processes where the perfusion is being limited by ICP crisis because it is the cerebral edema from brain compartment that is impairing patient's blood flow and these are the patients that are very high risk of passing on to cerebral cell quickly arrest. So oligemic intracranial hypertension distinguished from hyperemic intracranial hypertension where maybe it's the blood compartment that is excessive in the brain say in hypercarbia, reperfusion injury in a disorderly regulated brain, nitroglycerin causing cerebral vasodilation. So TCDs can be a great tool non-invasively to distinguish this hyperemic intracranial hypertension from oligemic intracranial hypertension. So I hope that a few of these arguments helped you at least see the value in using TCDs as a screening tool in conjunction with other modalities like the exam, neuroimaging for the presence of malignant cerebral edema, especially in cases where other imaging modalities may not be immediately available or the patient is high risk for that. I hope that you find some value in using transcranial Doppler to actually look at the patient's cerebral perfusion rather than just calculating it and especially distinguishing patients where the ICPs are being driven by the patient's perfusion as in hyperemic intracranial hypertension where the treatment is going to be very different. You will drop the patient's blood pressure goals or you will reduce the vasodilating agent or you will fix the patient's CO2 compared to patients where the ICPs are being caused by cerebral edema driving ICPs that are limiting the perfusion where the TCD waveforms can actually help you show that patient needs escalation of medical or surgical therapy to reduce that cerebral edema and maybe if future studies can show that TCDs could serve as a target in whole life therapy for cerebral edema. Thank you for your time and this opportunity and I hope to see you at one of our neuroultrasound offerings at the summer ultrasound courses in Illinois and I hope you practice neuroultrasound. Thank you.

neuro ultrasound

cerebral edema

imaging modalities

high-risk patients

skull

temporal windows