Stroke Overview and Ischemic Stroke Pathophysiology

Stroke Overview

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

Ischemic Stroke Pathophysiology

• Ischemic stroke (87% of all strokes) results from the occlusion of a cerebral artery.
• Occlusion is caused by either local thrombus formation or emboli from a distant site.
• Atherosclerosis of large intracranial or extracranial arteries, or small artery disease, can cause ischemic stroke.
• Emboli can originate from the heart in patients with atrial fibrillation, valvular heart disease, or other prothrombotic heart problems, causing about 25% of ischemic strokes.

Ischemic Stroke Pathophysiology (Continued)

• Insufficient oxygen supply leads to ATP depletion, lactate buildup, intracellular Na and water accumulation, ultimately 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 prostaglandins, leukotrienes, and reactive oxygen species (ROS).
• These processes typically occur within 2-3 hours of ischemia, leading to cellular apoptosis and necrosis.

Ischemic Stroke Pathophysiology (Continued)

• Decreased cerebral blood flow leads to infarction of the cerebral tissue.
• The surrounding area, called the ischemic penumbra, may maintain membrane integrity and be potentially salvageable with urgent interventions.

Hemorrhagic Stroke Pathophysiology

• Hemorrhagic strokes (13% of strokes) include subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH).
• Early hematoma expansion within 3 hours of the onset worsens functional outcome and increases mortality.
• Secondary injury mechanisms include inflammation, cerebral edema, and damage from blood product degradation.

Clinical Presentation

• Symptoms include unilateral weakness, inability to speak, loss of vision, vertigo, or falling.
• Ischemic strokes are usually painless, though some complain of headaches.
• Pain and headaches are more common and severe in hemorrhagic strokes.
• Neurologic deficits depend on the affected brain area (e.g., hemiparesis, monoparesis, hemisensory deficits, vertigo, diplopia, aphasia, altered consciousness).

Diagnosis

• General blood glucose, platelet count, and coagulation parameters.
• CT and MRI head scans to detect hemorrhages and infarcts.
• Computed tomography angiography (CTA) is recommended for patients needing endovascular treatment.
• Carotid Doppler (CD), ECG, transthoracic echocardiography (TTE), and transcranial Doppler (TCD) studies provide valuable diagnostic information.

Goals of Stroke Treatment

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

Non-Pharmacologic Treatment (Ischemic Stroke)

• Endovascular intervention (thrombectomy with retrievable stents) is strongly recommended within 6 hours of symptom onset for anterior circulation occlusions, and may be considered in select patients up to 24 hours after onset.
• Benefits of mechanical thrombectomy are less clear in posterior circulation occlusions, and individual assessment is necessary.
• Decompressive hemicraniectomy (brain surgery to remove a portion of the skull) can reduce mortality and improve functional outcome in select patients.
• Carotid endarterectomy is an effective procedure to remove plaque buildup in stenotic carotid arteries, reducing stroke incidence and recurrence in appropriate patients.

Non-Pharmacologic Treatment (Hemorrhagic Stroke)

• Early intervention with surgical clipping or endovascular coiling of the bleeding vascular abnormality to reduce mortality from rebleeding.
• Early surgical intervention and hematoma removal are recommended for patients with cerebellar hemorrhage and neurologic deterioration. Cases of brainstem compression, and hydrocephalus warrant priority consideration.

Temperature Management

• Fever negatively impacts outcomes in both hemorrhagic and ischemic strokes.
• Identifying the source of fever and managing it pharmacologically or nonpharmacologically to maintain normothermia is critical.

Pharmacologic Treatment (Ischemic Stroke)

• Adherence to a guideline-recommended protocol is crucial for positive outcomes.
• Immediate protocol steps include activating the stroke team, obtaining CT scan to rule out hemorrhage, treatment within 4.5 hours of symptom onset, and meeting all inclusion/exclusion criteria.
• Administer alteplase (tissue plasminogen activator) 0.9 mg/kg IV within the guidelines and under supervision, with 10% as an initial bolus.
• Avoid anticoagulants and antiplatelet therapy for 24 hours after alteplase administration. Closely monitor BP, neurologic status, and for hemorrhages.
• Aspirin 160–325 mg/day started within 24–48 hours of symptom onset, or an alternate antiplatelet agent, improves long-term outcomes.

Pharmacologic Treatment (Ischemic Stroke) (cont.)

• Patients with high blood pressure (BP) and eligibility for alteplase treatment must have BP lowered before thrombolytic administration.
• Early BP reduction (220/120) in Non-alteplase cases is not indicated. Long-term antithrombotic therapy includes antiplatelet agents (e.g., aspirin, extended-release dipyridamole plus aspirin, clopidogrel) for non-cardioembolic strokes.
• Patients with atrial fibrillation and cardioembolic stroke require oral anticoagulation therapy, preferably with warfarin, apixaban, dabigatran, edoxaban, or rivaroxaban.
• Statin therapy is recommended for stroke prevention in all patients.

Pharmacologic Treatment (Hemorrhagic Stroke)

• Pharmacotherapy usefulness in spontaneous intracerebral hemorrhage (ICH) is limited; but if systolic BP is above 220 mmHg, ongoing aggressive blood pressure reduction should be initiated with continuous IV infusion medications.
• A goal systolic BP of 140 mmHg is safe and may improve functional outcome.
• For patients with subarachnoid hemorrhage (SAH) due to aneurysm rupture, keep systolic BP below 160 mmHg for symptom onset through aneurysm obliteration.
• Consider reversing anticoagulants if intracranial hemorrhage occurs in patients on these treatments.

Evaluation of Therapeutic Outcomes

• For patients receiving alteplase, monitor for bleeding with neurologic exam and blood pressure (BP)
• every 15 minutes for the first hour
• every 30 minutes for the next 6 hours
• every hour for the next 17 hours, then once per shift
• Daily evaluation of blood tests (e.g., PT/INR, hemoglobin/hematocrit) for anticoagulant patients.

This quiz covers the basic overview of strokes, including their types and characteristics. Additionally, it delves into the pathophysiology of ischemic stroke, detailing the mechanisms behind occlusions and their effects on the brain. Test your knowledge on this crucial medical topic!