Hello, and thank you for listening to the session on severe stroke, subarachnoid hemorrhage, and intrascribral hemorrhage. I have some disclosures, including funding from the NIH. There are three main subtypes of spontaneous stroke in the United States. Ischemic stroke accounts for about 75 to 80 percent, intrascribral hemorrhage, spontaneous bleeding to brain tissue, about 15 percent, and ruptured brain aneurysm, subarachnoid hemorrhage, about 5 percent. Stroke is a common cause of disability. Documentation of the neurological severity of injury with validated scales is typically required documentation in stroke centers. For a patient with subarachnoid hemorrhage, the typical standard scale required by the Joint Commission is the Hunt and Hess scale. It's graded from 1 to 5, 1 being an awake patient, and 5 a deeply comatose patient. The World Federation of Neurological Surgeons' scores is similar. For patients with spontaneous intrascribral hemorrhage, the most common severity of injury scoring system is the ICH score. It measures older age, large hematoma volume, presence of intraventricular hemorrhage, infratentorial location, and Glasgow Coma Scale. For patients with ischemic stroke, the NIH Stroke Scale score is typically required. It is a standardized neurological examination with 0, a normal exam, being the best possible score. Scores of 8 are considered moderately severe presentation. You will typically see the Modified Rankin Scale, a global functional outcomes score from 0, no symptoms, to 6, death. A quote, unquote, good modified outcome, a quote, unquote, good Modified Rankin Scale depends upon the disease process. Independence with a device for better, Rankin score of 3, is typically considered a good outcome for patients with intrascribral hemorrhage and subarachnoid hemorrhage. For patients with acute ischemic stroke, Modified Rankin Scales of 0 or 1 are typically considered good outcome, although this may vary from trial to trial. For all subtypes of stroke, the most predominant risk factor is hypertension. For all types of stroke, dysphagia is common and may lead to aspiration pneumonia. So standard swallow evaluations should be performed prior to initiating oral feedings. And patients should typically be fed with feeding tubes until that is done. The prototypical severe stroke is occlusion of the middle cerebral artery or the internal carotid, which includes the middle and anterior cerebral arteries. Typical presentations include a gaze preference toward the side of the stroke, because the frontal eye field is what drives the eye to the contralateral side. So in a large left-sided stroke, the eyes would typically have a forced deviation to the left. There would typically be contralateral weakness, say, right-sided weakness for left-sided stroke. Patients with left-sided stroke would typically have aphasia, an inability to speak or follow commands. People with right-sided strokes can be more challenging to diagnose, because there's trouble with visual-spatial orientation. They're more likely to be misdiagnosed and are less likely to receive acute treatment. Acute stroke treatments include intravenous tissue plasmination activator, CP or alteplase, approved for use in the United States within four and a half hours of symptom onset, endovascular treatment of large vascular occlusion to score and imaging, or a mismatch in diffusion and perfusion, how much brain is already infarcted and how much brain is at risk. The evaluation, imaging, procedures, and approach for endovascular treatment of stroke are changing quickly as the technology gets better and as we decide which patients are most likely to benefit with new trials. For patients with large artery infarction, where perfusion cannot be restored, hemicraniectomy is an option. Focal cerebral edema will typically lead to brain herniation, usually two to five days after the index stroke. Hemicraniectomy is removal of the skull on that side, typically performed within 48 hours. This allows brain to swell out of the surgical defect, minimizing midline shift and brain stem compression. Hemicraniectomy improves survival, typically with moderately severe deficits that follow up for one year. For patients with large ischemic stroke, early neurosurgical consultation is appropriate to determine if hemicraniectomy might be appropriate in this case. This is an example of one patient. You see there's bright signal on the left in the middle cerebral artery, a so-called dense MCA sign. This has led in the center panel to evolving infarction with low density and not yet much midline shift. In the right panel, one can see that there's been hemicraniectomy with a large removal of a flap of bone. There's minimal midline shift from the infarction on the left to the patient's right. This patient had typical complication of hemicraniectomy, including a deep venous thrombosis, which was treated with Warfarin. The patient was discharged after about three weeks of rehabilitation. And a follow-up, the patient required help with daily living, was in a wheelchair but was sociable. Ruptured brain aneurysm, or cervical hemorrhage, classically presents with the worst headache of life or the first headache the patient has had, similar to the presentation. Typically worst and first headaches mandate a CT, and if negative, a lumbar puncture. MRI may also be helpful. About 5% to 10% of patients with cervical hemorrhage are initially misdiagnosed, with the most common mistake not obtaining brain imaging. Missing the diagnosis of cervical hemorrhage obviates the opportunity to obliterate the aneurysm before aneurysmal re-bleeding, which markedly increases the risk of poor outcome. With aneurysmal rupture, there are typically thousands to tens of thousands of red blood cells. If the lumbar puncture is traumatic, one can centrifuge to isolate out red blood cells from the traumatic LP and look for xanthochromia, a yellow tint in the cerebrospinal fluid. One could also repeat the LP at a higher level. Cervical hemorrhage should be graded from 1 to 5. This is required in stroke centers. A separate grading of neuroimaging by the Fisher grade, or modified, accounts for thick subarachnoid blood and bilateral intraventricular hemorrhage, which are better predictors of later delayed cerebral ischemia, or vasospasm, a misnomer. Vasospasm refers to the narrowed lumen on angiography, which indicates typically reduced blood flow to the brain. It's actually not spasm, it's proliferation of the media of the vessel, and typically occurs 3 to 14 days after subarachnoid hemorrhage onset. The symptoms of vasospasm are variable, including altered consciousness and pneumotobleakness. Vasospasm may lead to cerebral infarction with variable location and varying severity. The presence of any delayed cerebral ischemia increases the likelihood of poor outcome, and the more cerebral ischemia there is, the worse the patient's outcome is likely to be. The combination of the following medications reduces the risk of cerebral infarction after subarachnoid hemorrhage. And if you're counting on remembering this as the calcium channel blocker that begins with N, I have bad news for you. The best answer to this question is nemotopine. Vasospasm treatment in the intensive care unit typically includes three Hs, hypertension, hypervolemia, and hemodilution. As it turns out, not all of these are equal. Induced hypertension is likely to be far and away the most helpful of these three. Obviating hypovolemia is important, but actually inducing and sustaining hypervolemia turns out to be quite challenging and may be complicated by pulmonary edema. Hemodilution might be helpful in as much as the optimal blood viscosity is achieved with a hemoglobin of about 10 grams per deciliter. Further, hemodiluting patients may reduce cerebral oxygen delivery that has been associated with more delayed cerebral ischemia and worse outcomes. Hypervolemia increased the risk of spasm, delayed cerebral ischemia, and poor outcome. In general, patients should have hypovolemia avoided with the use of volume or colloid. There's some evidence that albumin might be more protective, and clinical research there is ongoing. Both the syndrome of an appropriate antidiuretic hormone secretion, SADH, and cerebral salt wasting are common. Distinguishing these two is between euvolema versus hypovolemia, although this is often clinically more challenging, as patients often have hypovolemia strictly avoided during the inpatient hospital stay, and effectively, masking some cerebral salt wasting is SADH. Without specific treatment, hyponatremia is common and may result in worse cerebral edema. Hypertonic saline is quite common in this condition, although there are other more elegant to avoid hyponatremia. Seizures occur in about 10% of patients. However, prophylactic seizure medications, although these are commonly used in traumatic brain injury, in general, have been shown to be deleterious in patients with subarachnoid hemorrhage. Universal prophylactic phenytoin has been independently associated with more complications such as fever, worse outcomes, and worse cognitive function. Patients with ultramental status should be considered for EEG monitoring. Note that a routine, quote-unquote, first-hour EEG only detects about half of patients who eventually turn out to have seizures on extended monitoring. Fever is common in subarachnoid hemorrhage, and most patients with subarachnoid hemorrhage end of fever do actually not have a bacterial infection. The fever is independently associated with worse clinical outcomes. However, interventions to control fever specifically have not improved clinical outcomes, although they are associated with an increase in interventions and complications such as pneumonia and deep venous thrombosis. In general, for subarachnoid hemorrhage, you should grade the severity with the Hunton-Heskell from 1 to 5. Thick subarachnoid blood on CT portends a high risk of vasospasm and delayed cerebral ischemia. You should reduce this likely risk with namodipine, and if indicated, consider EEG continuous monitoring. However, you should not use prophylactic phenytoin for all patients. You might consider its use when patients judge high risk to have a seizure or those for a comatose while the EEG is pending. Intracerebral hemorrhage is scored in severity with the ICH score, shown as calculated here, with points for Glasgow Coma Scale, infratentorial location in the cerebellum or brainstem, large volume, older age, and interventricular hematoma. Of note, the ICH score does not count for hematoma expansion after the diagnostic CT, which also independently worsens outcomes for patients and is more common in patients who are coagulopathic, say from warfarin or another anticoagulant. Hematoma expansion leads to worse outcome, and any detected coagulopathy should be quickly reversed. Novel or direct oral anticoagulants such as dabigatranviroxaban may be treated with a specific antibody such as adaracizumab for dabigatran or prothrombin complex concentrates or andexanet-alpha. Warfarin-associated intracranial hemorrhage should be treated with prothrombin complex concentrates, which leads to less hematoma expansion and faster normalization of the INR compared to fresh rows of plasma. For patients known to take aspirin of intracerebral hemorrhage, there's no clear therapy that's been shown to be helpful. A prospective randomized trial of platelet transfusion unexpectedly worsened outcomes, so platelet transfusion should not be given for patients with ICH on aspirin. Desmopressin reverses an aspirin effect and improves platelet activity, but there are no prospective trials of desmopressin's effect in hematoma expansion and outcomes. The best therapy for patients taking PHY12 inhibitors such as clopidogrel is not known. American Heart Association guidelines suggest that patients with acute hypertension up to a systolic of 220 should have their systolic blood pressure reduced to 140 torr. There is some controversy as to the best treatment for patients who present with a systolic blood pressure of greater than 220 in the sitting of the intracerebral hemorrhage. An updated version of American Heart Association guidelines for ICH is expected at the time of recording. Seizures occur in 5% to 10% of patients with spontaneous intracerebral hemorrhage. Prophylactic phenytoin is independently associated with more fever, worse outcomes in patients with ICH as an SAH. Prophylactic levodegastin has fewer side effects than phenytoin and does not seem to impact fever or dependence at follow-up. However, prophylactic levodegastin is associated with worse cognitive function at follow-up. EEG monitoring should be considered, particularly for a patient with altered consciousness. And of course, any clinical seizures should be treated. Seizures found in EEG monitoring should also be treated. Intracerebral hematoma in the cerebellum has a high risk of brain stem compression, and early neurosurgical consultation should be obtained for such patients. Deep venous thrombosis is common after intracerebral hemorrhage, particularly with weak or parotid limbs and the withholding of anticoagulants. In general, minidose heparin, say 5,000 units Q8 to Q12 hours for DVT chemoprophylaxis, is probably safe three to five days after spontaneous ICH if the hematoma is stable. Low-molecule heparin is used by some. However, in the event of delayed hematoma expansion, it's harder to reverse. Prophylactic administration of which of the following is most likely to improve outcomes at intracerebral hematoma? The answer here is D, minidose heparin, 5,000 units Q12 to Q8 hours, depending on the patient's weight. Therapeutic dose phenytoin is more likely to be associated with worse outcomes. Full-dose aspirin has not been shown to impact outcomes after cerebral hemorrhage. Salt tablets have no particular place in management. In summary for intracerebral hemorrhage, graded severity with the ICH score. Reverse any known coagulopathy as quickly as you can. Reduction of blood pressure is typically helpful to a goal systolic of 140. Avoid prophylactic phenytoin. And early neurosurgical consultation, particularly for patients with cerebral hemorrhage.

stroke

severe stroke

subarachnoid hemorrhage

intracerebral hemorrhage

validated scales