Thank you so much for this opportunity to present at the Society of Critical Care Medicine's Neurocritical Care board review course. We will be talking about the interpretation of critical findings on CT. So there are no relevant disclosures related to my presentation today. Our objectives for part one of our imaging presentations will be specifically focusing on CT. And I'll also talk a little bit about format resources for lifelong learning. The basics of MRI and geography, differences between contrast agents will be covered by Dr. Aarti Sarwal in the part two of the imaging presentation. These are just some format resources for you to continue your learning after you've seen some of these basics in our presentation today. So let's take a look at a case. Our patient is a 48-year-old male with no known stroke risk factors. And he presents with a left MCA territory stroke. His NIH stroke scale is 16. As part of his stroke code, he undergoes a CT head and a CT angiogram head and neck. And he's found to have a left MCA occlusion. He receives both thrombolytics and a thrombectomy and will go over his post-thrombectomy non-contrast CT head. And he eventually needs a hemicrane. So when you look at this CT head, the first thing to do to make sure that if you're seeing asymmetry between the left and the right side, that it is true asymmetry, you can take a look at where the eyes are oriented. And if they are in the same plane, then it's likely that the head is straight in the gantry. And any asymmetry that you see between the left and the right is true asymmetry. Here we're beginning to see some hyper densities. We also see some hypodensities. We also see some hyper densities in the subarycnoid space as well as the intraparenchymal space. This could be both contrast extravasation or hemorrhagic transformation or both contrast plus hemorrhagic transformation. So another cut of the same CT head, you're beginning to see some subtle signs of hypodensity of this evolving wedge shaped infarct in the left MCA territory, along with some intraparenchymal hyperdensity, some subarycnoid hyperdensity. And when we look at the post-hemicranial scan, you see this generous removal of the bone flap. You see the effacement of the left lateral ventricle. There's some hyperdensity along with a lot of that hypodensity. So there's hemorrhagic transformation of that acute ischemic stroke. A teaching point here, how do we distinguish between contrast and blood? On the first or second CT head, it's difficult. So one way to do it is you get serial CTs, contrast will clear up on subsequent CTs, blood will continue to linger on. Another way to do this, and only a few centers may have access to this, is a dual energy spectral CT. Hounsfield units, the only thing I want you to remember from this slide, bone is plus 1,000, air is negative 1,000, CSF of water is going to be zero. So when we talk about densities, we're really referring to these Hounsfield units. So bone is hyperdense, air is hypodense, CSF is hypodense, and with respect to, or relative to brain parenchyma. When we try to read CT heads, just like every other imaging modality or EKG, chest X-ray, we just want to be very systematic. On CT, we talk about densities, on MRI, eye for intensity, so MRI, we talk about intensity. We want to be systematic. If you have prior images, then compare them with the prior images, and what you could do, just like you do for a chest X-ray or EKG, you just have a systematic way of reading your CT head. For me, I tend to prefer the inside-out method. I look at the brain parenchyma first. Am I seeing any mass effect? Am I seeing any hyperdensity suggestive of hemorrhage? Am I seeing anything suggestive of edema? What's going on with the gray-white matter differentiation? The ventricles, do they appear normal? Do they appear enlarged? Is there any mass effect? Do they have any blood or hyperdensities that are filling up the ventricles? Regarding the extra axial spaces, what's going on with the subarycnoid space, subdural, epidural spaces? What is going on with the orbits? Are we seeing any orbital fractures or hyperdensities suggestive of bleeding in the orbits? Then examine the superficial soft tissue, bones, don't forget the bony window, and looking at the sinuses, asteroid air cells. This is a good website, Radiology Masterclass, for you to quiz yourself on different cuts of the CT head. There are images that are unlabeled, and then when you click on the images, you'll get a revelation of the labels, so you can quiz yourself on what you're seeing. For example, here we're seeing our gray matter that appears more hyperdense as compared to the white matter that appears more hyponous. Here we are just going to take a look at a couple of important sulci. This is the central sulcus, which can appear like that inverted omega, the Greek letter omega. Why is this important? This also helps you distinguish between the frontal lobe and the parietal lobe, as well as identifying the pre-central sulcus and the post-central sulcus. The pre-central sulcus that sits in the frontal lobe is your motor strip, your sensory cortex or primary sensory cortex is the post-central sulcus. Reviewing the images, of course, always look at the images, not just in one plane, but at least two planes. Most places will perform CT heads in the axial, coronal, sagittal planes. Don't forget to review the bone windows, not just for the bones, but also for drains, BP shunts, EVDs. You'll be able to see the location of these different devices more clearly on a bony window and always bear prior images, particularly if they're available. When we look at, now just let's examine some classic cuts of CT heads and learn how to identify some common anatomical structures. So this Mickey Mouse-like structure with two ears is our midbrain. These are the cerebral peduncles. This area of hypodensity in the center, which looks like Mickey Mouse's nose, is our cerebral aqueduct. This is our sylveon, sorry, this is the supracellar cistern. And you begin to see the MCAs bilaterally and the quadrigeminal cistern. So there are some spaces, you know, which are CSFL spaces. In addition to our ventricles, you don't have to know the names of all the cisterns, but some cisterns are important to know, for example, the quadrigeminal cistern. This is the uncus, which is part of the temporal lobe. And when there is impending uncle herniation or uncle herniation occurs, there is pressure that goes from the uncus onto the cerebral peduncle and the quadrigeminal cistern gets effaced. So that gives you an idea of evolving mass effect. Now let's take a look at another classic cut. This is at the level of the basal ganglia. These two are our lateral ventricles. This is our basal ganglia, the thalami, so you've got the caudate, head of the caudate, you've got putamen and globus pallidus. And then there is a hypodense structure, this inverted L-shaped, which is our internal capsule. Anterior limb of the internal capsule, geno of the internal capsule, and posterior limb of the internal capsule. Another classic cut to look at, some blood vessels as well. So again, that Mickey Mouse-like structure, that's our midbrain. This is the occipital lobe. Here's where you will see the internal carotid artery. Right here, you begin to see the posterior cerebral artery. Just something to keep in mind, sometimes when blood vessels are calcified, you may be able to see them on non-contrast CT head. You always need CT angiography to take a look at these blood vessels on CT. The temporal horns are a good marker for detecting early hydrocephalus. Typically these horns are supposed to appear very small, slit-like. Once they begin to increase in size, that should suggest that there's hydrocephalus. So on CT, we talk about density. On MRI, we talk about intensity. You've got to be systematic, review prior images, and make sure you look at images in different planes. And don't forget about the bony windows. When we think about CT versus MRI, CTs are fast. Of course, there is exposure to radiation. And when we think about radiation and contrast exposure, there is the advantage of diagnosing. For example, when you're thinking about a stroke, a lot of centers will use a CT head and a CT angiogram head and neck as part of their acute stroke paradigm or acute stroke code. So something important to keep in mind, we do tend to prioritize neuron before nephron. Contrast-associated nephropathy is a risk. However, not recandlizing somebody who has a large vessel occlusion and meets other criteria for recandlization really, really supports this idea of neuron before nephron. It's not great. It's not great for posterior fossil lesions, but you could try to study them in the sagittal plane. And then always remember to review your own images and then compare your own read with what radiology has read. Now let's jump into looking at some common pathological features on CT head. First, let's start with cerebral edema and features suggestive of raised intracranial pressure. So starting from the left, moving to the right. So first we look at this CT head. We're seeing this hyper-density. It does not limit itself to any specific sulci, gyri. So it's a hollow hemispheric acute subdural hematoma causing mass effect and midline shift. And then we'll take a look at what global cerebral edema looks like. So normal CT head, now comparing it to this CT head where you see finger-like projections, it's almost as if these fingers are hugging the brain. So that's suggestive of global cerebral edema. Here, comparing a normal CT head to an abnormal CT head, comparing the left to the right side, you don't see sulci, gyri, again, suggestive of evolving cerebral edema in the right hemisphere. Right cerebral hemisphere, including the frontal as well as parietal lobes. In this CT head, we see some hyper-densities. We're also seeing some hypo-densities around the hyper-densities. In this patient, this is a right frontal contusion. We see some layering acute subdural hematoma in addition to that frontal contusion. This is a classic CT head of a patient with suspected aneurysmal subarycnoid hemorrhage. In the bilateral sylvian fissures, we see blood. There is expansion of the third ventricle with blood. There's blood in the quadrigeminal cistern. The frontal horns are rounded off. The third ventricle is enlarged. So there's also obstructive hydrocephalus. So this is a good slide to keep in mind for all signs, radiographic features of cerebral edema. And just going back, when you look at this appearance, this is a patient whose stroke is evolving over a few weeks now with hemorrhagic transformation. This is a patient with a stroke that happened perhaps months or years ago. The neuroradiology case library for University of Rochester is another good resource. They also go over CT findings case by case. Here is a CT head of a patient who is an IV drug user who has a cardioembolic stroke. You can see some hypodensities in the left frontoparietal region. You see further evolution in the frontoparietal region. And then around three months from presentation, you see how this hypodensity is becoming more well-established and some encephalomalacia as well. Let's go from anterior circulation strokes now to posterior circulation strokes. Here's a hyperdense basilar sign. You see a hypodensity in the right cerebellar hemisphere. And take a look at the evolution of that hypodensity in the right cerebellar hemisphere. We're beginning to see some effacement of the fourth ventricle. On this CT head, you are seeing evolution of hydrocephalus. The temple horns are increased in size. Remember, we were talking about how these temple horns should appear slit-like. Here they are increased in size. You see the third ventricle. There is effacement of the fourth ventricle and some mass effect on the cerebral aqueduct, which is leading to some of this finding of obstructive hydrocephalus. In any patient who has undergone a life-saving surgery, a suboccipital decompression, you see some post-op surgical changes at the suboccipital cranial site and evolving cerebellar stroke. From strokes now, we'll move to hemorrhage. So now let's take a look at intracranial hemorrhage. So lots of different kinds of hemorrhages, both extra axial as well as parenchymal. So when we look at subdural hematomas, typically will happen because of rupture of bridging veins, subarycnoid hemorrhage, when you see high up cortical blood versus seeing blood in the sylvean fissures, in the supracellar cistern, is it aneurysmal or traumatic or non-aneurysmal will also be determined not only on the CT appearance, but of course, on the clinical history. Parenchymal blood could be traumatic, could be secondary to hypertension, could be because of an underlying mass lesion, vascular malformation such as an AVM, vasculitis, cerebral amyloidosis, or because of hemorrhagic transformation of an acute ischemic stroke. Epidural hematomas usually due to rupture of the middle meningeal artery, usually traumatic, can also be seen in patients who have sinus venous injury. So let's take a look at different kinds of parenchymal hematomas now. This is the patient who suffered from head trauma. You see a small lens-shaped hemorrhage, which is an epidural hematoma. You also see an intraparenchymal hemorrhage with some surrounding edema. This is a hemorrhagic contusion in the left temporal lobe. Here we see a hemorrhage that has some different densities, and there's a little bit of layering suggestive of an underlying coagulopathy. For this patient, this was a spontaneous ICH in a patient who had very severe thrombocytopenia, less than 10,000 platelets. Here's a patient who has an underlying history of colon cancer, and you see this hemorrhage in the left temporal lobe with a lot of surrounding edema, and this edema is out of proportion to what you would expect for this hematoma, suggestive of the possibility of an underlying hemorrhagic tumor. Here's a patient with a spontaneous ICH in a very classic basal ganglia location, second to hypertension. This is a good slide to keep in mind for your boards. Common areas for hypertensive intracerebral hemorrhages, 80% of them are going to be deep, so thalamus, cerebellum, pons, basal ganglia. 20% will be lobar. How do we calculate the volume of an ICH? It comes from the formula for the volume of an ellipsoid, ABC upon 2, where A is the widest diameter, B is perpendicular to A, and C is the total number of slices. Lobar hemorrhages, again, context matters. This same kind of hemorrhage could be seen in sinus venous thrombosis, could be seen in somebody with cerebral amyloidosis, could also be seen in somebody who has an underlying cancer, could be seen in hypertension or in trauma. Epidural versus subdural. Epidural hematomas tend to be length-shaped. As you can see here, subdural hematomas usually don't respect sutures. They will cross sutures and will be more crescent-shaped. For subarycnoid hemorrhage, we went over this. This is in the supracellar cistern area where the circular villus sits, suggestive of the possibility of an underlying aneurysm. Here's another CT that we've seen before with a patient who has blood in the sylvian fissures, third ventricle, quadrigeminal cisterns, obstructive hydrocephalus, parasagittal blood with an underlying ECOM aneurysm. These two hyperdensities that you end up seeing, this is secondary to bilateral EVDs that were placed to relieve obstructive hydrocephalus. The quantity of blood that is seen on the CT heads can be quantified if you have thin blood without bilateral intraventricular hemorrhage. That's modified fissure, grade 1, only 10% risk of developing vasospasm. If you see thin subarycnoid blood with bilateral intraventricular hemorrhage, about 20% risk of developing vasospasm with modified fissure 2. You have thick blood, but without bilateral intraventricular hemorrhage, modified fissure 3. For the ease of committing this to memory, you can remember 20 to 30% risk of vasospasm and then modified fissure 4, thick blood with bilateral intraventricular hemorrhage. So modified fissure 1, 2, 3, 4, and the risk of developing vasospasm 10, 20, 30, 40%. Now let's shift gears to tumors. Where is a tumor located? Is it extraxial? Is it intraaxial? These are some common extraxial tumors. The most common extraxial tumor happens to be a meningioma. If intraaxial, is this a metastatic tumor, 80% of the tumors that you see in adults are going to be metastatic. And the reverse is true for pediatrics, 80% of tumors that are seen on the CT head will be primary in pediatrics. Traumatic brain injury can show us a lot of different kinds of findings on CT head, including, for example, this layering subdural hematoma along the cerebellar fox. We see some effacement of the quadrigeminal cistern. We see this hollow hemispheric acute subdural hematoma causing mass effect and midline shift. And on another cut of the same CT, you see this hollow hemispheric subdural hematoma, layering of blood around the fox and mass effect from left to the right. Here's herniation of the brain through the bilateral frontal craniotomy sites. You see hypodensities and injury, evolving contusions, and you see herniation of the brain through the bifrontal craniotomy sites in this patient with trauma. So with that, I'd like to say thank you for this opportunity and good luck on your boards. I look forward to the Q&A session.

CT scans

anatomical structures

pathological features

hemorrhage

subarachnoid hemorrhage

traumatic brain injury