I will keep them on time. On time is really important. Yeah, I got some grants. That's why I got to stay at Northwestern. There are three of the three major types of stroke, ischemic stroke, intubal hemorrhage, bleeding into brain tissue, and subarachnoid hemorrhage. Ischemic stroke is the most common, loss of blood flow to some brain tissue. That's about three quarters of strokes in the United States. Very common, one of the most prominent causes of disability in the United States, and in the Western world, actually. For all the three major types of stroke, subarachnoid hemorrhage, ruptured brain aneurysms, intubal hemorrhage, and severe ischemic stroke, the number one risk factor for these is hypertension. Treating high blood pressure, preventing high blood pressure, treating it when it occurs in the medicine clinic is the most common risk factor. If you stop high blood pressure, the rate of stroke goes way, way down. Communities that have much more effective primary medical care have much, much lower rates of stroke, but you're all intensivists, so that's not what you do. Dysphagia is very common in all these types of stroke, and often leads to trouble swallowing and aspiration pneumonia. Pneumonia is very common with these patients. If you work in a place that's a stroke center, you will almost certainly have a protocol and part of it is a speech pathologist or a nurse-led swallowing screen for all of these types of patients. Dysphagia is very common, leads to pneumonia. Before you give patients PO feeds, they should have a swallow screen. These are typically done by the nurses to ensure that oral feeding is safe. They will want you to recognize the prototypical types of severe stroke, occlusion of the internal carotid artery, often intracranially, and occlusion of the middle cerebral artery. They want you to recognize these because, one, when they occur, they are very, very disabling, often leading to hemiplegia or hemiparesis on the other side of the brain. If it's on the left side in almost everyone, that will lead to global aphasia, the inability to understand or interpret language. If it's on the right side, patients have tremendous visuospatial problems. These are the ones where they had you draw clocks, they put all the numbers on one side of the clock because they neglect the other side of space. If you are left-handed by me, like me, good news, if you have a right-sided stroke, you are more likely to retain language. Bad news, you're more likely to have a mix of visuospatial problems as well as aphasia with stroke in any part of the brain. These right-sided strokes are more likely to be misdiagnosed. The visuospatial things and the paying attention are often harder to pick up in a bedside exam, the harder to pick up in the NIH Stroke Scale Score. They're more likely to be misdiagnosed, they present later, they're less likely to be offered life-saving therapy, although they are just as disabling at follow-up. There are effective rapid treatments available for large vessel stroke. Everyone who drives a catheter has had a great run of about 15 years. For the first 15 years, none of it worked, and the last 15 years, all the catheter-based treatment trials for stroke are all coming up roses. So your endovascular colleagues are looking for patients with large vessel occlusions to take them all to the cath lab, and it actually works. They will want you to know about TPA for stroke. This is now about 30, 40 years old. It works for all stroke subtypes. Many hospitals are replacing TPA with tenecteplase. Anyone notice their hospital doing that yet? It seems to be about as effective. It seems to have a lower risk of bleeding. Most places are moving their protocols to tenecteplase. You should not have to remember the complicated dosing regimens. There will be a protocol with a pharmacist that will tell you how to do it, but they might want to say give tenecteplase. And there will be rapidly expanding indications for endovascular therapy. I'll show you a couple of cool pictures, often done with AI neuroimaging. Basically, if you see a large part of the brain is not yet dead and not getting perfused, the endovascular guys will want to take that patient to the angiosuites, balloon catheters, They will want you to know about hemicraniectomy, literally taking off part of the skull for patients who cannot get fibrinolytic therapy or have a large infarction. When cerebral edema occurs, that part of the brain swells. It will cause midline shift, herniate the brain to the other side of the skull. If you do a hemicraniectomy, that part of the brain herniates out where the hemicraniectomy is, doesn't crush the brains on the other side. It markedly increases the rate of survival with moderately severe disability. What does that usually mean? It usually means a Rankin scale of four, which means able to interact, often alert, works with family, but not independent for daily living, often needing a wheelchair. This is what a hemicraniectomy looks like. This patient has a left MCA infarction. You see there's a bright MCA sign here of acute clot in the MCA. They're unlikely to ask you to identify that on the critical care board, but they might on the neurocritical care board. This person could not get fibrinolysis. You see there's a large developing infarction here. I ignore that. And now you see a hemicraniectomy has been done. You see the bright bone here has been removed. You see there's still some edema here, but there's hardly any midline shift. There's a little bit of blusher. That's a little bit of hemorrhagic conversion. That's okay. And this patient had a very typical course. This person turned out to have a deep venous thrombosis, received warfarin for it, went to rehabilitation. Other than Amy Whitehouse, everybody loves rehab. At two years, this patient needed some help with daily living, was a rank and four, went to the park in a wheelchair with grandchildren. If that's an acceptable outcome, then you should do a hemicraniectomy. If the family says this patient would have wanted to be normal or dead, don't do that, and that'll be also one of the two outcomes that you're likely to get. That's fine. Aneurysmal subarachnoid hemorrhage, as opposed to traumatic subarachnoid hemorrhage, your head gets whacked so hard there's some bleeding in the subarachnoid space, spontaneous subarachnoid hemorrhage, worst headache of life, and first headache like this. If the patient says one of those things, they're getting a spinal tap and a CT scan. That's how it goes. The lumbar puncture is most helpful when the diagnosis is most in question, meaning I think it's the worst headache. I have migraines, but I've never had a migraine like this before. I've had some light-sensitive, but this is different. When the story is funny is when you most want to do the lumbar puncture, because 5% to 10% of patients with aneurysmal subarachnoid hemorrhage are misdiagnosed, sent out of the emergency department or sent out of the hospital. It is not defensible if that patient turns out to have a ruptured brain aneurysm. The most common mistake is not getting a CT. I'm always surprised by who does get a CT. It seems like random people walking on Michigan Avenue in Chicago will just get a CT. Sometimes people come with a headache and get discharged without a CT. I don't know how it happens, but 5% of the time it does. If you hear about one of these patients, if they say this is the first headache like this or the worst headache, they get a CT. If the CT is negative, they get an LP. If it's July or early in the academic year and the person in the LP botches it and it's a bloody tap, what do you do? Go one level higher because the CSF goes down, it will wash the blood down, try and get a cleaner tap. Or the anesthesia colleague can do these things in the neck, gives me the heebie-jeebies, but they can do neck punctures and get CSF that way too. They say it's really easy and they do it all the time. It gives me the creeps, but there you are. If there's subarachnoid hemorrhage, you should be familiar with something called vasospasm. This is a misnomer. It looks like spasm on angio. It's really an intimal medial proliferation of the muscles in the vessel wall such that they get bigger and then the lumen of the vessel gets narrower. Narrow vessels leads to ischemia, ischemia leads to stroke. That's bad. It's often heralded by altered consciousness, not typically delirium, and new focal motor weakness. Apparently, there was a pro wrestler called Triple H. If you don't follow pro wrestling, good for you. You don't typically want to do Triple H. Prophylactically, guidelines say don't do that. Of the three parts of this, inducing hypertension, making someone hypervolemic in human dilution, the best part is actually the induced hypertension, markedly increases cerebral perfusion. This is how you can walk in the neuro ICU and you'll see somebody with a systolic pressure of 200. The anesthesiologist will say, looks good and keeps going. They're doing that on purpose because induced hypertension for vasospasm after subarachnoid hemorrhage. You do not want to let the patients get hypovolemic. If patients with SH are hypovolemic, they're much more likely to have cerebral ischemia, vasospasm, cerebral infarction, and a poor outcome. In general, you want to make sure these patients do not become volume deplete. How you do that is quite variable. There's a variety of protocols abound. Some use isotonic saline, some use plasmolytes, some use 5% albumin. Don't tell the pharmacy. We actually got pharmacy approval to do that because there's still some question about that. Albumin might be neuroprotective. There's a clinical trial ongoing for that. Do not let the patient become dry. They will get vasospasm and infarct. Patients with subarachnoid hemorrhage will often become hyponatremic. It is probably the most common electrode abnormality after subarachnoid hemorrhage. They might want to ask you about distinguishing SIADH versus cerebral salt wasting. The distinction is hypovolemia between these two. Do we mask cerebral salt wasting by not letting the patient become hypovolemic? Maybe. But that will be the distinction you might show up on a standardized test. Both of these do exist. If left to their own devices and not looked after, we'll get cerebral salt waste, get hypovolemic. We probably make some of them look like SIADH because we don't let them become hypovolemic because you know bad things will happen. You can also use hypertonic saline for hyponatremia and cerebral salt wasting at the same time. There are all these very elegant decision trees of what it was. For a while we looked at VAP-TANs to lead to a pure free water diuresis. Because hypertonic saline is so cheap and so easy to use, when I was a fellow I put a line in everyone because hypertonic saline was central lines only. Now that we can give hypertonic saline, as it turns out, safe for peripheral IVs, everyone lost interest and we just give everybody 3%. Seizures occur between 10% to about a quarter of patients. For a while guidelines said you should give patients prophylactic phenytoin to prevent seizures. We were actually the group that found this actually to have been an extremely bad idea. It actually doesn't prevent that many seizures, has a lot of side effects, leads to fever, which is a very bad actor and worse outcomes. If the patient has blood in their head and altered mental status, they should get EEG monitored to look for subclinical seizures. More about that later in the hour. A routine EEG is not enough. It will only detect about half the patients who eventually have seizures. For subarachnoid hemorrhage, ruptured brain aneurysm, there's a severity grade 1 to 5. More subarachnoid blood means more vasospasm is likely. You want to prevent vasospasm after SH with nimodipine and you want to look for subclinical seizures with EEG. Any questions about subarachnoid hemorrhage before I talk about spontaneous intracerebral hemorrhage? Like subarachnoid hemorrhage, ICH has its own grading scale. If anybody works in a comprehensive stroke center, you will have to document something called the ICH score as a standard Joint Commission mandated measure of severity. This is really helpful. It reliably predicts outcomes. It does not, however, account for the major preventable cause of poor outcome, hematoma expansion where the hematoma you see on the initial CT scan gets bigger over time. You might see on some standardized tests in the near future some question about how to reverse the anticoagulants. I'm not giving anything away at SCCM. They ask this for everything. If someone is taking a pre-ICH anticoagulant and they bleed into their brain, that's really bad. And the chance of hematoma expansion makes poor outcome much, much worse. So if the patient's taking some pre-ICH antithrombotic, you want to reverse that because if you do, the patients are less likely to have more bleeding in their head and less likely to be dead or disabled at follow-up. There is some controversy about the novel oral anticoagulants, I'm sorry, direct oral anticoagulants. They've been out for a year. They're not novel anymore. Other options include prothrombin complex concentrates and andexanet alpha. There's a paper in the Lincoln Journal over the summer that says there's less hematoma expansion but more thrombosis with andexanet alpha. They say they weren't powered to detect clinical outcomes. You know they were going for it. So it does improve outcome, does make hematoma expansion less likely. You should choose one of these. If the patient was taking warfarin prior to intrepid hemorrhage, the best answer to my knowledge is still prothrombin complex concentrates. It is better than fresh frozen plasma. For aspirin, early in my career I thought platelet transfusion would be a great treatment for patients who were taking aspirin then had an ICH. So I wrote a proposal to NHLBI to do a prelim clinical trial of platelet transfusion. The review I got back said, this guy really needs someone to teach him how to write a grant better. And he's too junior. I was so offended I didn't read the rest of the review. A couple years later I went back, read the proposal. One, it really wasn't a very well written grant and I did need to take a grant writing course and I did. Two, it turns out to be a very bad idea. The Europeans actually did it and platelet transfusion made outcomes worse. Didn't actually reduce hematoma expansion, led to worse outcomes because platelets as it turns out are dirtier than packed red cells. There's way more infection. There's way more fever. And if the people who were donating blood were taking aspirin themselves, their platelets still don't work when you give them to somebody else. So don't give platelet transfusion to reverse aspirin and acute ICH. It's worse than nothing. In terms of P2Y12 inhibitors, I got nothing. We actually just published a paper earlier this year that shows P2Y12 inhibitors, especially when combined with aspirin, markedly increase the risk of a lot of hematoma expansion. I don't know what to do for these patients yet. We're working on it. Most patients with intracerebral hemorrhage will show up with severe hypertension. In general, you should lower that and make them normotensive. Nicartapine is the usual first-line choice, but there's a variety of choices and drugs that are used worldwide. The more you reduce blood pressure, the higher the risk of acute renal failure, which also increases outcome, worsens, makes a poor outcome more likely, but not as much as hematoma expansion. How much you should reduce blood pressure patients with a blood pressure of more than 220 is not clear. In general, the goal of blood pressure should be systolic 140. There's someone in this room who wants to argue about whether we should follow systolic or mean arterial blood pressure. Don't be that person. For intracerebral hemorrhage, there's also a risk of spontaneous seizures. About 10 to 25% of people. There also used to be a guideline to say you should give everybody prophylactic phenytoin. Yes, we also showed that one was wrong and guidelines say don't do that. Everyone switched to levotiracetam. Good news is levotiracetam is less toxic than phenytoin. It only impairs cognitive outcome, and our group has shown that, in fact, if you look at patients who get prophylactic levotiracetam, their functional outcomes are no different, but it knocks about half the standard deviation off their cognitive quality of life. That's things like, can you understand medication administration? Can you manage your own money? Can you live independently? So you do not want to indiscriminately give prophylactic levotiracetam either. How do you tell which patients are definitely going to cease and only treat them with levotiracetam? We're working on that. Could you do a clinical trial of patients at high risk for seizures and randomize them to levotiracetam or not? We tried to get that, and the review of the acute group stroke center is, and I'm quoting here, meh, sideways thumb, didn't get funded. You should look for seizures on EEG, and if you find them, you should definitely treat those. You might get a question about cerebellar and cerebral hemorrhage. You should always make sure your neurosurgery buddies know about those. If those compress the brain stem, which is right in front of the cerebellum, they all get decompressed. They do really, really, really well. DVT is really, really common, especially in patients whose limbs don't move. After the hematoma is stable, typically 24 to 48 hours out, then you can use small-dose heparin 5,000q12, 5,000q8. Neurointensivists tend not to like to use low-molecule heparins because if there is more bleeding, it isn't reversible with protamine. So we tend to use regular and fractured heparin. We know it's old, but we know that if there's more bleeding or something else goes wrong, you can reverse it with protamine, and that's important to us. So to sum up, intracerebral hemorrhage, grade it with the ICH score, reverse coagulopathy, you should review those before the test, you want to reduce blood pressure, don't give prophylactic phenytoin or probably love terastatin either, and for cerebellar ICH, you want to ask your neurosurgery buddies to see the patient quickly.

stroke management

ischemic stroke

hypertension

dysphagia screening

intracerebral hemorrhage