Hello, and welcome to this lecture on Severe Stroke, Subarachnoid Hemorrhage, and Intracerebral Hemorrhage with me, Andrew Naik. I have a few disclosures related to grant support from the National Institutes of Health. Most types of strokes are ischemic strokes in North America. Large vessel occlusion, the kind treated in endovascular therapy, is about as common as ruptured brain aneurysms, subarachnoid hemorrhage, or SAH. Stroke is a common and leading cause of disability in the United States, a kind that will grow more common as an aging America has more cerebrovascular disease. In general, all of these types of stroke have hypertension as a predominant risk factor. Dysphagia is common, may lead to pneumonia, and swelling evaluations should be performed prior to oral feedings to reduce this risk. The prototypical severe stroke is occlusion of a large vessel, such as the middle cerebral artery or the internal carotid artery. Oftentimes, the type of symptoms related to a proximal internal carotid artery or middle cerebral artery stroke include gaze preference towards the side of the stroke. For example, eyes looking to the left for a left-sided stroke. Weakness on the other side of the body, right-sided weakness for a left-sided stroke. Left-sided strokes often have aphasia, the inability to speak or understand commands. Right-handed strokes are more likely to have trouble with visuospatial orientation. This is more challenging to discover on exam, and consequently, such patients tend to go longer before the stroke is discovered and have a lower NIH Stroke Scale score and are less likely to receive fibrinolytic therapy. A variety of acute stroke therapies are in wide use. The classic fibrinolytic is tissue plasminogen activator, released within four and a half hours of symptom onset. Many systems are replacing TPA with tenecteplase, which seems to be a little safer. In general, endovascular therapy is indicated for large vessel occlusions. The indications for endovascular therapy continue to expand based upon emerging clinical trial reports. In general, all patients with acute ischemic stroke should have a vessel imaging study performed immediately at the time of the initial evaluation, such as CT-ANGIO or MR-ANGIO, and an endovascular consultation to see if an endovascular procedure for reperfusion might be appropriate. Hemicraniectomy is considered for patients where large vessel artery goes on to occlude and have a large volume of infarction that cannot be reperfused. The cerebral edema results from large infarction, typically to herniation in two to five days. A hemicraniectomy removes the bone flap before this edema midline shift and herniation occurs. This technique improves survival, although moderately severe disability is the usual result. As an indication, neurosurgery should also be involved in patients who may require hemicraniectomy before edema and midline shift occur. This is one example from a typical patient. This patient presented with clot in the middle circularity, seen here in the left-sided picture. You can see the bright signal highlighted by the arrow in the CT scan, a hyperdense MCA sign showing the acute thrombus. Despite reperfusion therapy, this patient had an evolving infarction in most of the middle cerebral artery territory, as seen in the middle scan. And on the right-sided scan, you can see a bone flap has been removed. Although there's some edema and there's some effacement of the frontal horn of the lateral ventricle, in general, there's no substantial midline shift. This patient, as a complication of the hospital course, had a deep venous thrombosis, received Warfarin, had two years follow-up, was alert, awake, interactive, and had some mobility with a wheelchair. The diagnosis of subarachnoid hemorrhage is heralded as the worst headache of one's life and often the first headache like this. Patients who complain of the worst headache of their life or the first headache they've had like this typically should have neuroimaging followed by a lumbar puncture. It is when the diagnosis is most in question that the lumbar puncture is most helpful. Five to 10% of patients with subarachnoid hemorrhage are initially given the wrong diagnosis and discharged from the emergency room without the diagnosis being discovered. The most common mistake is not to obtain neuroimaging followed by not doing a lumbar puncture. Misdiagnosis increases the likelihood of poor outcome and aneurysm rebleeding. The second most common misdiagnosis is atypical migraine, mistaken for subarachnoid hemorrhage. Patients who have migraine can also have a subarachnoid hemorrhage. Patients will typically say the subarachnoid hemorrhage is qualitatively different and substantially worse. For patients with aneurysm and subarachnoid hemorrhage, the lumbar puncture will typically have tens of thousands of red blood cells. If the lumbar puncture is traumatic, you can perform a centrifuge immediately before red cells lyse and see if there's xanthochromia. You may also repeat the lumbar puncture at a higher spinal level as the cerebrospinal fluid washes down and CSF at a higher level is unlikely to be contaminated. Vasospasm is a bit of a misnomer. It is the narrow luminal angiography, reducing blood flow to the brain, that commonly occurs three to 14 days after subarachnoid hemorrhage. The severity of vasospasm is heralded by altered consciousness, new motor weakness. It may lead to preventable cerebral infarction, potentially preventable. It has variable location and variable severity. Vasospasm is most likely to occur in the large vessels and tends to occur when there is more subarachnoid blood in proximate to the vessel. The traditional treatment in the ICU for vasospasm often goes by the acronym HHH, induced hypertension, hypervolemia, and hemodilution. As it turns out, of these three, the induced hypertension is far and away the most helpful. The hemodilution may actually be harmful, as the anemia may reduce cerebral oxygen delivery. You should not do induced hypertension prophylactically. It is not effective and potentially dangerous. Patients with subarachnoid hemorrhage may become hypovolemic. Cerebral salt wasting and the syndrome of inappropriate antidirect hormone secretion, SADH, are both well-described. There are a variety of protocols, some using isotonic saline, some hypertonic saline, and some albumin, which may be neuroprotective to prevent the hypovolemia that often occurs in patients with subarachnoid hemorrhage. SADH markedly increases the risk of vasospasm and should be avoided. Both SADH and cerebral salt wasting are common. The distinction between the two is uvulemia, or SADH, versus hypovolemia in cerebral salt wasting. That being said, many patients would have cerebral salt wasting, but we prevent body depletion, and so we end up diagnosing as having SADH instead. In general, sodium serum of less than 130 are quite common, and resulting cerebral edema from the hyponatremia may worsen the neurological examination or lead to more cerebral edema. Hypertonic saline use is common, although you may also use VAP-TANs, although these have been less well-studied. Seizures occur in about 10% to 25% of patients. While it used to be recommended, prophylactic phenytoin is independently associated with worse outcomes, more fever, and worse cognition. Patients with altered mental status generally should go EEG monitoring to look for subclinical seizures. A routine hour-long EEG is not sufficient and will, in fact, pick up less than half of patients who do not have subclinical seizures. In general, 24 to 48 hours and consultation with an epileptologist interpreting the study is warranted. Subarachnoid hemorrhage should be graded. The standard Joint Commission Severity Injury Scale is the Hunt and Hess grade, from one no symptoms to five deep comatose. Fixed subarachnoid hemorrhaging or imaging increases the risk for basal spasm and delayed cerebral ischemia. You should try to prevent cerebral infarction from basal spasm with nemodipine, and if indicated, you should look for subclinical seizures with EEG, but you should not use prophylactic phenytoin. Intracerebral hemorrhage is also graded on severity for a simple scale. The ICH score assigns points for the lower Glasgow Coma Scale and infratentorial location, large intracranial hematoma volume, age at least 80 years, and intraventricular hemorrhage. However, the ICH score doesn't account for everything, such as hematoma expansion, which is more common in anticoagulant-coagulopathic patients and is a modifiable cause of poor outcome. In general, you should reverse anticoagulants quickly in patients with spontaneous intracerebral hematoma. For the novel or direct oral anticoagulants, you might use indexin and alpha, the daricizumab for dabicatran, or prothrombin complex concentrates. This area is in rapid evolution and clinical trials are still in the process of being published at the time of reporting. In general, you should reverse warfarin with vitamin K and prothrombin complex concentrate. You should not give platelet transfusion, which paradoxically worsened outcomes in a prospective randomized clinical trial of patients with ICH known to decasperate. DASMA precedent proves platelet activity but has not been shown to reduce hematoma expansion or improve outcomes. P2Y12 inhibitors also carry increased risk of more hematoma expansion. However, how to reverse this effect acutely is not clear at the time of recording. In general, you should lower the systolic blood pressure in patients with acute intracerebral hemorrhage from up to 220 to 140 milliliters of mercury. The usual first-line choice is nicardipine, but it does not have to be. There is controversy over how much to reduce blood pressure for patients who present with an isocystolic of greater than 220, with some lowering it to 1 foot quickly, some reducing it by 50 to 60 toward immediately, and then more the next day. Lower blood pressure reduction increases the risk of renal failure, which is independently associated with worse outcomes. Seizures and seizure medications in patients with intracerebral hemorrhage are similar to subarachnoid hemorrhage. While it used to be recommended, prophylactic phenytoin is independently associated with more fever and worse outcomes. The use of levotriparacetam does not seem to reduce functional outcomes, but does seem to induce worse cognitive function. There's a preliminary trial that suggests in high-risk patients it could reduce the risk of seizures. EEG monitoring should be considered particularly for patients with altered consciousness. Again, the first hour of routine EEG is not sensitive for the eventual diagnosis of subclinical seizures, and patients should undergo monitoring for 24 to 48 hours with discussion with an When they occur, seizures should be treated and do worse in outcome. Intracerebral hemorrhage in the cerebellum has a high risk of brain stem compression from the initial hematoma or from hematoma expansion. A colleague in neurosurgery should be involved in the care of all patients with cerebellar hematoma in case a decompressive posterior fossa craniotomy is indicated. Venous thrombosis is common after intracerebral hemorrhage, particularly in patients with weak limbs after endcoagulants are reversed or withheld. Mini-dose heparin, say 5,000 units Q12 to Q8, are generally indicated as safe if the hematoma is stable on CT. Most neurologists and neurointensivists tend to use unfractionated rather than low-molecule heparin because if there is more bleeding, it's easier to reverse, although more hematoma expansion in delayed fashion is quite uncommon. In general for intracerebral hemorrhage, you should grade its severity with the ICH score, reverse anticoagulant medications where patients have them if appropriate, reduce blood pressure quickly, avoid prophylactic phenytoin, and particularly for cerebellar intracerebral hemorrhage, early neurosurgical consultation.

stroke management

subarachnoid hemorrhage

intracerebral hemorrhage

hypertension

neuroimaging