Stroke Overview and Ischemic Pathophysiology

Stroke involves the abrupt onset of focal neurologic dysfunction lasting at least 24 hours.
Stroke can be ischemic or hemorrhagic.
Transient ischemic attacks (TIAs) are focal ischemic neurologic deficits lasting less than 24 hours and typically less than 30 minutes.

Accounts for 87% of all strokes.
Results from the occlusion of a cerebral artery.
Causes can be local thrombus formation or emboli from a distant site.
Atherosclerosis in large intracranial or extracranial arteries, or small artery disease can lead to ischemic stroke.
Emboli originating from the heart (e.g., atrial fibrillation, valvular heart disease, prothrombotic heart conditions) cause approximately 25% of ischemic strokes.

Insufficient oxygen supply leads to ATP depletion, lactate buildup, and intracellular accumulation of sodium and water, causing cytotoxic edema and cell lysis.
Calcium influx activates lipases and proteases.
Release of excitatory amino acids (e.g., glutamate, aspartate) damages neurons and produces damaging substances like prostaglandins (PGs), leukotrienes, and reactive oxygen species (ROS).
These processes occur within 2-3 hours of ischemia, culminating in cellular apoptosis and necrosis.

Decreased cerebral blood flow can lead to cerebral tissue infarction, with a surrounding ischemic area that might maintain membrane integrity.
This "ischemic penumbra" is potentially salvageable tissue with timely intervention.

Accounts for 13% of strokes, including subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH).
Early hematoma expansion within 3 hours of onset worsens functional outcomes and increases mortality.
Secondary injury mechanisms involve inflammation, cerebral edema, and blood product degradation.

Symptoms include unilateral weakness, inability to speak, vision loss, vertigo, or falls.
Ischemic stroke is often not painful, though some patients experience headaches.
Pain and headaches are more common and severe in hemorrhagic stroke.
Neurological deficits (e.g., hemiparesis, hemisensory deficits) depend on the affected brain area.
Patients with posterior circulation involvement may exhibit vertigo and diplopia.
Anterior circulation strokes can lead to aphasia and altered levels of consciousness.

General blood glucose, platelet count, and coagulation parameters.
Computed tomography (CT) and magnetic resonance imaging (MRI) scans identify areas of hemorrhage and infarction.
Computed tomography angiography (CTA), carotid Doppler (CD), electrocardiogram (ECG), transthoracic echocardiogram (TTE), and transcranial Doppler (TCD) provide further diagnostic information.

Reduce ongoing neurologic injury acutely to decrease mortality and long-term disability.
Prevent complications from immobility and neurologic dysfunction.
Prevent stroke recurrence.

Endovascular intervention and thrombectomy with retrievable stents are strongly recommended for anterior circulation occlusions within 6 hours of symptom onset. For some cases, this may be considered up to 6-24 hours.
Benefit of mechanical thrombectomy is less clear for posterior circulation occlusions and should be considered on a case-by-case basis.
Decompressive hemicraniectomy (brain surgery to remove a portion of the skull) may reduce mortality and improve functional outcomes in select patients.
Carotid endarterectomy (surgery to remove plaque buildup in a stenotic carotid artery) can reduce stroke risk and recurrence in appropriate patients.

In subarachnoid hemorrhage (SAH), early surgical clipping or endovascular coiling of the vascular abnormality is crucial to reduce mortality from rebleeding.
Early surgical intervention and hematoma removal is recommended for patients with cerebellar hemorrhage, neurologic deterioration, brainstem compression, or hydrocephalus due to ventricular obstruction.

Fever worsens outcomes in both hemorrhagic and ischemic stroke.
Identifying the source of fever and using pharmacologic and/or non-pharmacologic interventions to maintain normothermia is crucial.

Aspirin (160-325mg/day) started within 24-48 hours (and 24 hours after alteplase) reduces long-term death and disability in ischemic stroke.
Consider alternate antiplatelet agents in cases of aspirin allergy or contraindications.
Prioritize blood pressure control to <185/110 mmHg before thrombolytic administration in patients with elevated blood pressure who are eligible for alteplase.
Patients not requiring IV thrombolysis or endovascular intervention may have BP allowed to rise to 220/120 mmHg for the first 48-72 hours; early BP reduction does not prevent death or improve dependency.
Determine appropriate long-term antithrombotic therapy based on cause of ischemic stroke (e.g., aspirin, extended-release dipyridamole with aspirin, or clopidogrel for non-cardioembolic strokes; anticoagulation (e.g., warfarin, apixaban, dabigatran, edoxaban, or rivaroxaban) for cardioembolic strokes; statin therapy to prevent stroke recurrence.)

Usefulness of pharmacotherapy is limited in spontaneous intracerebral hemorrhage (ICH).
Patients with a systolic blood pressure >220 mmHg should receive aggressive blood pressure lowering with continuous IV medications.
Goal to lower systolic BP to 140 mmHg is safe and can improve functional outcome.
For patients with subarachnoid hemorrhage (SAH) from an aneurysm rupture, control blood pressure to at least a systolic BP of <160 mmHg in the period from symptom onset to aneurysm obliteration.
Treat coagulation issues in patients on anticoagulants.

Monitor for bleeding, neurological changes, and blood pressure every 15-60 minutes in the 1st hour, half-hourly for 6 hours, hourly for 17 hours, and then once per shift thereafter, in patients on alteplase.
Monitor daily for bleeding with aspirin/clopidogrel, extended-release dipyridamole, aspirin, warfarin, and other oral anticoagulants.
Monitor PT/INR and hemoglobin/hematocrit daily in patients on warfarin.