Acute stroke (ischemic or hemorrhagic) or TIA: Clinical sciences

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Introduction 0:00–0:36

Acute stroke can be hemorrhagic, which occurs due to vessel rupture and subsequent impaired blood flow, or ischemic, which occurs due to narrowing or blockage of an artery.
On the flip side, a temporary interruption of blood flow that results in transient neurologic symptoms with no infarction on imaging is called transient ischemic attack, or TIA.
Now, if your patient presents with chief concerns suggesting acute stroke or TIA, perform an ABCDE assessment to determine if they are unstable or stable.

Unstable Patient 0:36–1:25

If unstable, stabilize the airway, breathing, and circulation. At this point, you might even have to intubate the patient and start mechanical ventilation.
Next, obtain IV access, consider starting IV fluids, and don’t forget to put your patient on continuous vital signs monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry.
Finally, you might need to manage high intracranial pressure, especially in individuals with hemorrhagic stroke! Alright, now, let’s go back to the ABCDE assessment and take a look at stable patients.

Stable Patient 1:25–3:47

First, obtain a focused history and physical exam, and fingerstick glucose because hypoglycemia can mimic stroke symptoms.
Your patient will report a sudden onset of neurologic symptoms, such as weakness, numbness, incoordination, but also facial droop, slurred speech, and language difficulties.
Some patients will also report changes in vision, including visual field defects, or they might report a “thunderclap” headache, which is suggestive of subarachnoid hemorrhage!
Next, history might reveal risk factors, such as tobacco use, diabetes, hyperlipidemia, hypertension, and cardiovascular conditions, like carotid artery disease and atrial fibrillation.
Keep in mind that risk factors like tobacco use, diabetes, hyperlipidemia, and hypertension are associated with both hemorrhagic and ischemic strokes!
Some individuals could also present with hypercoagulable conditions, including antiphospholipid syndrome, or report substance use, such as cocaine and amphetamines.
On exam, you might find focal neurologic deficits, including facial droop, limb weakness or numbness, aphasia, or ataxia.
Finally, in most cases, the fingerstick glucose will be normal. With these findings...you should suspect stroke or TIA, so immediately proceed with a head CT.
Now, here’s a clinical pearl to keep in mind! In addition to head CT, standard tests to determine the stroke etiology include vessel imaging, echocardiography, and cardiac telemetry.
Also, you should check the patient’s lipid panel and hemoglobin A1c. Let’s first look at hemorrhagic and ischemic strokes.
If you identify a hemorrhagic lesion, which could be either in the brain parenchyma or in the subarachnoid space, diagnose hemorrhagic stroke.

Hemorrhagic Stroke 3:47–5:09

Hemorrhagic stroke can occur due to different causes, so be sure to consider the patient’s age, medical comorbidities, and stroke location.
This information will help you narrow down the hemorrhage etiology. For example, younger patients are more likely to have a bleed from a vascular abnormality, such as an arteriovenous malformation.
On the flip side, older patients are more likely to have a bleed from amyloid angiopathy and hypertension. Once you diagnose hemorrhagic stroke, proceed with management!
First, be sure to avoid hypertension and correct any coagulopathy. Next, consult your surgery team, specifically neurosurgery, for possible intracranial pressure monitoring, and CSF diversion with an external ventricular drain.
If there is an underlying vascular abnormality, such as an aneurysm or arteriovenous malformation, consult your neuro-interventional radiology team as well!
On the other hand, if you identify an ischemic lesion, diagnose ischemic stroke. Ischemic stroke can be associated with cardioembolism, such as from atrial fibrillation, but also hypercoagulable diseases and large vessel atherosclerotic disease.

Ischemic Stroke 5:09–10:33

Moreover, a major cause of ischemic stroke is internal carotid artery stenosis which can result in severe occlusion of the blood flow and ischemic stroke!
Another common etiology is the occlusion of small perforating arteries from long-standing hypertension, diabetes, and smoking.
This leads to small but high-impact strokes in deep brain structures, such as the basal ganglia and brainstem, known as lacunar strokes.
Next, if your patient reports neck pain after a recent trauma or chiropractic maneuvers, think of carotid artery dissection!
Finally, in young patients, another option to consider is a patent foramen ovale! Now, once you diagnose ischemic stroke, your next step is to assess for resolution of neurologic deficits.
If deficits have resolved, initiate blood pressure control. If blood pressure is greater than 220 over 120 millimeters of mercury, slowly initiate antihypertensives because sudden drops in blood pressure can result in hypoperfusion of the brain and recurrence of neurologic deficits.
The long-term goal is normotension! For secondary stroke prevention, start an antiplatelet agent such as aspirin, or anticoagulation, and depending on the stroke etiology, consider statins.
Keep in mind that patients with atrial fibrillation and hypercoagulable conditions require anticoagulation therapy as opposed to an antiplatelet agent!
However, if neurologic deficits are not resolved, proceed with two time-sensitive treatment decisions! First, determine if you can use an intravenous thrombolytic enzyme known as tissue plasminogen activator, or tPA, such as alteplase and tenecteplase.
Consider intravenous tPA only within the first 4.5 hours of stroke onset and if the patient’s blood pressure is less than 185 over 110 millimeters of mercury.
Also, avoid tPA in individuals with intracranial hemorrhage; a brain tumor; gastrointestinal malignancy or bleeding within 21 days; stroke, history of severe head trauma, or neurosurgery in the prior 3 months.
Finally, stay away from tPA if you identify coagulopathy, which is defined as INR greater than 1.7, activated PTT greater than 40 seconds, or a platelet count less than 100,000 per cubic millimeter.
The second time-sensitive treatment is mechanical thrombectomy of a clot, but only if your patient is presenting within 24 hours of stroke onset!
In this case, you need to obtain a CT or MR angiogram, and if you identify a large vessel occlusion, you could proceed with a thrombectomy.
Additionally, perfusion imaging can help you identify penumbra, which refers to the brain tissue surrounding the ischemic region that hasn’t yet been irreversibly affected.
If you identify penumbra, proceed with mechanical thrombectomy to save the viable tissue! Next, proceed with blood pressure control.
If the patient received tPA, maintain the blood pressure below 180 over 105 millimeters of mercury for 24 hours. However, if the patient underwent a thrombectomy, the blood pressure goal would depend on how successful the procedure was.
For example, if normal blood flow is restored, consider a lower blood pressure goal to prevent reperfusion injury. For those who got neither a tPA nor a thrombectomy, allow permissive hypertension up to 220 over 120 millimeters of mercury to maximize brain perfusion.
The long-term goal for all patients is normotension. Finally, don’t forget to initiate secondary stroke prevention.
In patients who received tPA, you should start antiplatelet or anticoagulation therapy 24 hours after administration due to bleeding risk.
If needed, consider statins. Next, let’s take a look at individuals with no hemorrhagic or ischemic lesions on initial CT.

No hemorrhagic/ischemic lesions 10:33–13:24

Now, here’s a clinical pearl! Stroke presentation depends on the affected vessel, so even with a normal initial head CT, you can guess the stroke location depending on the exam.
A middle cerebral artery stroke will cause contralateral weakness, numbness, and hemi- or quadrantanopsia, with aphasia or neglect depending on the affected hemisphere.
An anterior cerebral artery stroke will cause contralateral leg weakness, while a posterior cerebral artery stroke will cause contralateral hemianopsia.
Finally, lacunar strokes in the region of the internal capsule and thalamus will cause severe face and limb weakness and numbness.
Now, even if the CT imaging appears normal, you should not rule out an ischemic stroke yet! In this case, your first step is to assess for the resolution of neurologic deficits.
If deficits are resolved, obtain a brain MRI. If you identify infarction, diagnose ischemic stroke.
However, if the brain MRI reveals no findings suggestive of infarction, diagnose TIA. In both cases, start appropriate blood pressure control and provide secondary stroke prevention.
Now, here’s another clinical pearl! You can use the ABCD2 score to stratify stroke risk within the first 90 days after TIA.
The score is based on the patient’s age, blood pressure, type of symptoms, duration of symptoms, and presence of diabetes.
Finally, in individuals with no lesions on the initial head CT, with unresolved neurologic deficits, you should quickly determine the eligibility for intravenous tPA and thrombectomy.
Once time-sensitive treatment is completed, repeat head CT or brain MRI. If you identify an infarction, diagnose ischemic stroke, and if there is no infarction, diagnose TIA.
As before, maintain blood pressure control, taking into account whether the patient received tPA or thrombectomy, and provide secondary stroke prevention.
Alright, as a quick recap… If you suspect a stroke or TIA, first, obtain a head CT. If imaging reveals a hemorrhagic or ischemic lesion, diagnose hemorrhagic stroke or ischemic stroke, respectively.

Review 13:24–14:07

If the initial CT is normal, a brain MRI can help you differentiate ischemic stroke from TIA. Treatment for hemorrhagic stroke includes blood pressure control, correcting coagulopathy, and neurosurgical evaluation.
On the flip side, management of ischemic stroke includes intravenous tPA or thrombectomy, as well as secondary stroke prevention.