Questions and Answers
What is a significant consequence of global hypoperfusion in acute ischemic stroke?
Which of the following is NOT a major cause of global hypoperfusion leading to acute ischemic stroke?
Which type of embolic cause is associated with clots that form in the heart?
What condition is a risk factor for thrombotic causes of ischemic stroke?
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In the context of ischemic stroke, what defines a paradoxical embolus?
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Which of the following arteries is commonly associated with large vessel thrombi in acute ischemic stroke?
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Which clinical feature is least likely to result from ischemic damage in anterior cerebral artery syndrome?
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What factor directly limits blood flow in cases of carotid stenosis related to acute ischemic stroke?
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Which of the following conditions can lead to acute strokes if critical stenosis is present?
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What is a primary effect of insufficient blood supply in watershed areas during acute ischemic stroke?
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What is the preferred time window for administering tissue plasminogen activator (tPA) after the last known normal?
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What should blood pressure be before administering tPA?
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What is a key consideration before performing a mechanical thrombectomy?
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Which laboratory test is essential for assessing stroke-related complications prior to tPA administration?
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In what situation should anticoagulation be avoided immediately after a large MCA infarct?
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What is the maximum dose of tPA for a patient weighing 70 kg?
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What follows the administration of tPA in terms of blood pressure management in the first 24 hours?
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What component distinguishes the penumbra from the infarct core?
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What is the NIHSS score threshold indicating eligibility for tPA administration?
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What is a complication that must be monitored for post-tPA administration?
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What factor contributes to watershed infarcts during acute ischemic stroke?
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Which of the following is NOT a common risk factor for thrombotic causes of acute ischemic stroke?
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What best describes the cause of a paradoxical embolus?
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Which artery is least likely to be involved in embolic causes of acute ischemic stroke?
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How does acute respiratory failure contribute to ischemic stroke?
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Which type of thrombi is primarily associated with lenticulostriate arteries?
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What is a primary difference between large vessel and small vessel thrombi in acute ischemic stroke?
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Which condition most directly results from carotid stenosis?
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Which of the following correctly represents a consequence of global hypoperfusion?
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What is a typical clinical feature related to middle cerebral artery syndromes?
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What is the primary purpose of obtaining a CT scan within 24 hours post-tPA administration?
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What is the significance of the penumbra in the context of acute ischemic stroke?
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Which condition would directly contraindicate the use of tPA in a patient suspected of having an acute ischemic stroke?
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What is the maximum systolic blood pressure allowed before tPA can be administered?
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In patients with carotid stenosis greater than 70%, which intervention is most appropriate?
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Post-tPA, monitoring blood pressure closely is important. What is the anticipated threshold for the first 24 hours?
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What lab tests should be prioritized before administering tPA to a stroke patient?
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What is the total dose of tPA for a patient weighing 70 kg?
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What is the primary goal of airway management in acute ischemic stroke patients?
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What could indicate a potential hemorrhagic complication following tPA administration?
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Which condition must be ruled out through imaging before administering tPA?
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What is the key time interval for tPA eligibility based on the last known normal?
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What NIH Stroke Scale (NIHSS) score suggests that a patient is eligible for tPA treatment?
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What is the critical blood pressure threshold that must be met prior to tPA administration?
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Which method is generally used for extracting clots during mechanical thrombectomy?
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What treatment strategy is recommended for patients with severe carotid stenosis exceeding 70%?
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What post-tPA monitoring should be prioritized for complications within the first 24 hours?
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What is the maximum allowable systolic blood pressure after tPA administration?
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What is the key purpose of using perfusion scans in the context of acute ischemic stroke?
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Which anticoagulation treatment should be avoided immediately following a large MCA infarct?
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Which of the following conditions is most likely to cause watershed infarcts in acute ischemic stroke?
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What mechanism defines embolic strokes associated with paradoxical embolism?
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Which small vessel thrombi are specifically associated with basal ganglia supply?
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Which of the following defines a major risk factor for thrombotic causes in acute ischemic stroke?
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What primary characteristic differentiates large vessel thrombi from small vessel thrombi in the context of acute ischemic stroke?
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In what situation does acute respiratory failure contribute to ischemic stroke risk?
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Which scenario best exemplifies a classic cause of arterial to arterial emboli?
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What is a primary factor influencing the risk of ischemic damage in watershed areas?
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What is the impact of carotid stenosis on cerebral blood flow?
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Which of the following is likely a rare cause of acute ischemic stroke?
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What is a primary risk factor for the development of large vessel thrombi in acute ischemic stroke?
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Which of the following correctly describes a paradoxical embolus in the context of acute ischemic stroke?
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How does carotid stenosis primarily contribute to acute ischemic stroke?
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What clinical feature is specifically associated with watershed infarcts in the context of acute ischemic stroke?
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Which type of acute ischemic stroke is most likely to result from a cardiac embolism?
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What is a distinguishing factor between small vessel thrombi and large vessel thrombi in acute ischemic stroke?
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What is the most significant implication of acute respiratory failure in the context of ischemic stroke?
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What characteristic distinguishes embolic strokes arising from arterial to arterial emboli?
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Which is the primary feature that differentiates the clinical manifestations of strokes based on the affected vascular territory?
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What is the primary reason for conducting a CT scan within 24 hours post-tPA administration?
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Which of the following conditions would likely lead to the discontinuation of tPA treatment?
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What is the primary goal of airway management in patients with acute ischemic stroke?
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Which blood pressure target should be maintained for the first 24 hours post-tPA treatment?
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What therapy is recommended for patients with severe carotid stenosis greater than 70%?
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What is a critical imaging finding that would contraindicate tPA administration?
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What defines the penumbra in relation to acute ischemic stroke?
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What is the maximum time allowed for mechanical thrombectomy after the last known well?
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When should anticoagulation therapy be avoided to prevent complications after a large MCA infarct?
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What criteria must a patient meet to be eligible for tPA administration based on NIH Stroke Scale scores?
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What mechanism does global hypoperfusion primarily utilize to affect brain tissue in acute ischemic stroke?
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Which of the following characterizes arterial to arterial emboli in the context of acute ischemic stroke?
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Which risk factor is specifically associated with the development of thrombotic strokes?
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What is a significant clinical feature that may be observed in watershed areas during an acute ischemic stroke?
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In cases of carotid stenosis, what is the primary factor that limits blood flow to the brain?
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Which description best differentiates small vessel thrombi from large vessel thrombi?
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Which of the following scenarios most likely leads to a paradoxical embolus?
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What primary impact does acute respiratory failure have in the context of ischemic stroke?
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Which of the following conditions is least likely to contribute to thrombosis formation in acute ischemic stroke?
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What blood pressure reading must be achieved before administering tissue plasminogen activator (tPA)?
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Which imaging modality is most sensitive for detecting infarcts in acute ischemic stroke?
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What condition should be ruled out before administering tPA?
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Which anticoagulation treatment is appropriate for managing cardioembolic causes after an acute ischemic stroke?
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What is the recommended threshold for blood pressure during the first 24 hours after administering tPA?
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In acute ischemic stroke management, how is mechanical thrombectomy ideally conducted?
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Which of the following is a modifiable risk factor for ischemic stroke management?
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What NIH Stroke Scale (NIHSS) score indicates eligibility for tPA administration?
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What is the main role of the penumbra in acute ischemic stroke?
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What timeframe is critical for the administration of mechanical thrombectomy after the onset of symptoms?
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What mechanism primarily leads to watershed infarcts during acute ischemic stroke?
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Which statement about paradoxical emboli is true?
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Which of the following factors is least likely to contribute to thrombotic causes of acute ischemic stroke?
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Which of the following is a primary characteristic of embolic strokes compared to thrombotic strokes?
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What common condition can lead to ischemia due to inadequate oxygen delivery despite normal blood flow?
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Study Notes
Acute Ischemic Stroke Overview
- Acute ischemic stroke occurs when blood flow to the brain is obstructed, leading to brain tissue damage.
- Causes can be categorized into global hypoperfusion, thrombotic, embolic, and rare causes.
Causes of Acute Ischemic Stroke
Global Hypoperfusion
- Results in watershed infarcts due to insufficient blood supply.
- Major causes include:
- Cardiac Arrest: Leads to very low cardiac output and mean arterial pressure, impairing brain perfusion.
- Acute Respiratory Failure: Low oxygen delivery can cause ischemia, regardless of blood flow.
- Carotid Stenosis: Narrowing of carotid arteries limits blood flow, especially when exacerbated by low blood pressure.
- Cardiac Surgeries: Can lead to acute strokes if critical stenosis is present.
Thrombotic Causes
- Commonly occur due to the formation of clots in large and small vessels:
- Large Vessel Thrombi: Internal carotid artery (ICA), middle cerebral artery (MCA), and vertebral/basilar arteries.
- Small Vessel Thrombi: Lenticulostriate arteries (supply basal ganglia) and small pontine branches.
- Risk factors include hypertension, diabetes, hyperlipidemia, smoking, and obesity.
Embolic Causes
- Breakdown into three categories:
- Arterial to Arterial Emboli: Plaque ruptures in major vessels (e.g., ICA or aortic arch) and travels to cerebral vessels.
- Cardiac Emboli: Clots can form in the heart, particularly in the left atrium (often due to atrial fibrillation), valves, or left ventricle post-myocardial infarction.
- Paradoxical Embolus: Occurs due to atrial septal defects, allowing clots from the venous system to bypass the lungs and lodge in cerebral vessels.
Clinical Features
- Symptoms depend on the affected vascular territory (anterior cerebral artery, middle cerebral artery, and posterior cerebral artery syndromes).
- Watershed Areas: Regions between major arterial supplies that can be vulnerable during global hypoperfusion.
Diagnosis
- Initial Imaging: Non-contrast CT scan to rule out hemorrhagic stroke (intracerebral or subarachnoid).
- Possible findings include hyperdense signs indicating fresh clots or hypodense areas showing infarction.
- Follow-up imaging may include CTA to localize occlusion and MRI for sensitivity in detecting infarcts.
- Key Labs: Blood glucose levels, coagulation studies (INR), complete blood count (CBC), and possibly thyroid function tests for hyperthyroidism-related arrhythmias.
Treatment
-
TPA Administration: Tissue plasminogen activator (tPA) is used to dissolve clots:
- Must confirm neuro deficits, rule out hemorrhage, and assess eligibility based on time since last known normal (preferably within 3-4.5 hours).
- Contraindications include active bleeding, significant hypertension, and recent surgeries.
Indications for tPA
- Presence of neuro deficits with an NIH Stroke Scale (NIHSS) score ≥4.
- Negative imaging for bleeding or other contraindicated conditions.
- Strict criteria if the last known well was between three to four and a half hours prior.
Conclusion
- Recognizing acute ischemic strokes involves understanding the underlying causes, symptoms, and therapeutic approaches to ensure swift and effective management.### Blood Pressure Control and tPA Administration
- Blood pressure must be less than 185/110 mmHg before administering tissue plasminogen activator (tPA).
- tPA dosing is 0.9 mg/kg, with 10% given as a bolus and the remainder over 60 minutes.
- Post-tPA, monitor blood pressure closely, aiming for specific thresholds (185/110 mmHg or 180/105 mmHg) for the first 24 hours.
- After 24 hours, blood pressure goals can be modulated; maintain under 220 mmHg systolic if no tPA is given.
Neurological Assessment and Imaging
- Assess for neurological deficits and confirm no intracranial bleeding or hemorrhage before treatment.
- Obtain a CT scan within 24 hours post-tPA to monitor for potential complications, like hemorrhage.
Mechanical Thrombectomy
- Indicated for patients with neurological deficits and large vessel occlusions (e.g., MCA, ICA, vertebrobasilar) even beyond the standard 4.5-hour tPA window.
- Effective up to 24 hours after the last known well; quicker interventions are preferred (ideally within 6 hours).
- The procedure can either retrieve the clot using a stent retriever or aspirate it via a catheter.
Penumbra Concept
- The penumbra is ischemic tissue surrounding an infarct core that may be salvageable if re-perfused quickly.
- Use perfusion scans to assess the extent of salvageable brain tissue.
Airway Management
- Maintain airway (ABCs) and consider intubation if Glasgow Coma Scale (GCS) is ≤8.
- Address airway issues, especially in cases of decreased consciousness due to stroke or aspiration.
Anticoagulation Methods
- Anticoagulate if there's a cardioembolic cause (e.g., atrial fibrillation, left ventricular aneurysm).
- Use heparin infusion for initial control, then switch to DOACs (e.g., apixaban, rivaroxaban) or warfarin as appropriate.
- Avoid anticoagulation immediately after a large MCA infarct to prevent conversion to hemorrhagic stroke.
Carotid Stenosis Management
- Severe carotid stenosis (>70%) requires intervention via carotid endarterectomy (CEA) or stenting.
- Maintain antiplatelet therapy post-intervention to prevent thrombus formation.
Modifiable Risk Factors
- Key factors include hypertension (optimize control), diabetes (enhanced insulin management), and hyperlipidemia (initiate statins, e.g., atorvastatin).
- Encourage smoking cessation and weight management.
Complications Post-tPA
- Monitor for changes in neurological status; sudden neurological decline may indicate hemorrhage.
- If a bleed is detected post-tPA, discontinue tPA and consider fibrinogen replacement if levels are low (<180 mg/dL).
- Prompt imaging and intervention are critical if complications arise.### Management of tPA Reversal
- Administer Tranexamic Acid (TXA) as a 1 gram bolus, followed by another gram later; it helps in managing bleeding.
- Cryoprecipitate is important for providing fibrinogen, aiding in hemostasis.
- Platelet transfusions may also be considered based on protocols.
Post-tPA Complications: Angioedema
- Angioedema, although rare, can occur after tPA administration.
- Symptoms include hypoxia, difficulty breathing, and facial swelling.
- Treat with antihistamines (e.g., diphenhydramine), famotidine, and IV steroids (e.g., methylprednisolone 100 mg).
- Have a low threshold for intubation to manage airway edema.
Cerebral Edema Management
- Commonly associated with large hemispheric infarcts, especially Middle Cerebral Artery (MCA) strokes.
- Cytotoxic edema leads to cell rupture and water release, causing brain tissue swelling and potential midline shift.
- Treatment includes surgical intervention (hemicraniectomy) to relieve pressure and allow the swollen brain to expand.
- Medical management options include:
- 3% and 23.4% hypertonic saline to draw water from brain tissue.
- Mannitol as a common osmotic agent.
- Aim for a serum sodium level of 150-155 for hypertonic solutions.
Seizures Post-Infarct
- Seizures typically arise from cortical infarcts due to damaged neuron focus.
- Can lead to focal or generalized seizures; generalized seizures may present as tonic-clonic or non-convulsive status epilepticus.
- Treatment includes anti-epileptic drugs (AEDs) like valproate, phenytoin, and levetiracetam.
- In severe cases, consider anesthetic sedatives such as propofol.
Aspiration Pneumonia Risks
- Dysphagia can occur due to infarcts affecting swallowing control, leading to risk of aspiration and subsequent pneumonia.
- Conduct speech evaluations to assess swallowing ability; if dysphagia is present, alternative feeding methods (e.g., PEG tube or nasogastric tube) may be necessary.
- If aspiration pneumonia develops, treat with broad-spectrum antibiotics until culture results are obtained to narrow down therapy.
Acute Ischemic Stroke Overview
- Acute ischemic stroke results from obstructed blood flow to the brain, causing tissue damage.
- Main causes: global hypoperfusion, thrombotic events, embolic events, and rare causes.
Causes of Acute Ischemic Stroke
Global Hypoperfusion
- Leads to watershed infarcts from inadequate blood supply.
- Major causes include:
- Cardiac Arrest: Causes drastic drop in blood flow and pressure to the brain.
- Acute Respiratory Failure: Although blood flow may be present, low oxygen can cause ischemia.
- Carotid Stenosis: Narrowing of carotid arteries that limits blood flow, worsened by low blood pressure.
- Cardiac Surgeries: Risks acute strokes if significant arterial stenosis is pre-existing.
Thrombotic Causes
- Occur from clot formation in either large or small vessels.
- Large Vessel Thrombi: Affect arteries like internal carotid, middle cerebral, and vertebral/basilar arteries.
- Small Vessel Thrombi: Primarily impact lenticulostriate and pontine branches.
- Risk factors include hypertension, diabetes, hyperlipidemia, smoking, and obesity.
Embolic Causes
- Three types of embolic sources:
- Arterial to Arterial Emboli: Plaque ruptures in major vessels, leading to obstruction in cerebral circulation.
- Cardiac Emboli: Form in the heart, especially in the left atrium due to atrial fibrillation or post-myocardial infarction.
- Paradoxical Embolus: Clots from the venous system enter the systemic circulation through an atrial septal defect.
Clinical Features
- Symptoms vary based on affected vascular territories: anterior, middle, or posterior cerebral arteries.
- Vulnerable areas include watershed regions between major arterial supplies during global hypoperfusion.
Diagnosis
- Initial Imaging: Start with non-contrast CT to exclude hemorrhagic stroke.
- Potential findings: hyperdense areas indicating fresh clots, hypodense areas showing infarction.
- Follow-up imaging may include CTA for occlusion localization and MRI for sensitivity in detecting infarcts.
- Key Labs: Blood glucose, INR, complete blood count (CBC), and thyroid function tests if hyperthyroidism is suspected.
Treatment
-
TPA Administration:
- Tissue plasminogen activator (tPA) dissolves clots.
- Eligibility requires confirming neurological deficits, ruling out hemorrhage, and time criteria (ideally within 3-4.5 hours).
- Contraindications include active bleeding, high blood pressure, and recent surgeries.
Indications for tPA
- NIH Stroke Scale (NIHSS) score ≥4 indicates neuro deficits.
- Imaging must rule out bleeding or other contraindications.
- Strict criteria apply for cases where the last known normal was between three and four and a half hours ago.
Blood Pressure Control and tPA Administration
- Blood pressure should be below 185/110 mmHg before tPA administration.
- tPA dosage is 0.9 mg/kg, with a 10% bolus and the remainder infused over 60 minutes.
- Post-administration monitoring targets blood pressure under 185/110 mmHg for the first 24 hours.
Neurological Assessment and Imaging
- Confirm no intracranial bleeding before tPA treatment.
- Perform CT scan within 24 hours post-tPA to detect complications like hemorrhage.
Mechanical Thrombectomy
- Suitable for patients with neurological deficits from large vessel occlusions despite being outside the standard tPA time window.
- Effective within 24 hours after the last known well, with optimal results when performed within 6 hours.
- Treatment methods include clot retrieval with a stent retriever or aspiration via catheter.
Penumbra Concept
- The penumbra represents ischemic tissue around the infarct core that can be salvaged if reperfusion occurs quickly.
- Perfusion scans assist in assessing salvageable brain tissue.
Airway Management
- Ensure airway protection (ABCs) and consider intubation for patients with Glasgow Coma Scale (GCS) ≤8.
- Address airway concerns in patients with reduced consciousness due to stroke or aspiration risk.
Anticoagulation Methods
- Initiate anticoagulation for cardioembolic causes (e.g., atrial fibrillation).
- Start with heparin infusion, transitioning to DOACs (e.g., apixaban, rivaroxaban) or warfarin later.
- Avoid anticoagulation after substantial MCA infarcts to prevent hemorrhagic transformation.
Carotid Stenosis Management
- Severe stenosis (>70%) necessitates carotid endarterectomy (CEA) or stenting.
- Continue antiplatelet therapy post-intervention to reduce thrombus risk.
Modifiable Risk Factors
- Focus on hypertension control, diabetes management, and hyperlipidemia through statin therapy (e.g., atorvastatin).
- Promote smoking cessation and maintaining a healthy weight.
Complications Post-tPA
- Monitor neurological status for any sudden decline indicating potential hemorrhage.
- Discontinue tPA if bleeding is detected and consider fibrinogen replacement if levels drop significantly.
Acute Ischemic Stroke Overview
- Acute ischemic stroke results from obstructed blood flow to the brain, causing tissue damage.
- Main causes: global hypoperfusion, thrombotic events, embolic events, and rare causes.
Causes of Acute Ischemic Stroke
Global Hypoperfusion
- Leads to watershed infarcts from inadequate blood supply.
- Major causes include:
- Cardiac Arrest: Causes drastic drop in blood flow and pressure to the brain.
- Acute Respiratory Failure: Although blood flow may be present, low oxygen can cause ischemia.
- Carotid Stenosis: Narrowing of carotid arteries that limits blood flow, worsened by low blood pressure.
- Cardiac Surgeries: Risks acute strokes if significant arterial stenosis is pre-existing.
Thrombotic Causes
- Occur from clot formation in either large or small vessels.
- Large Vessel Thrombi: Affect arteries like internal carotid, middle cerebral, and vertebral/basilar arteries.
- Small Vessel Thrombi: Primarily impact lenticulostriate and pontine branches.
- Risk factors include hypertension, diabetes, hyperlipidemia, smoking, and obesity.
Embolic Causes
- Three types of embolic sources:
- Arterial to Arterial Emboli: Plaque ruptures in major vessels, leading to obstruction in cerebral circulation.
- Cardiac Emboli: Form in the heart, especially in the left atrium due to atrial fibrillation or post-myocardial infarction.
- Paradoxical Embolus: Clots from the venous system enter the systemic circulation through an atrial septal defect.
Clinical Features
- Symptoms vary based on affected vascular territories: anterior, middle, or posterior cerebral arteries.
- Vulnerable areas include watershed regions between major arterial supplies during global hypoperfusion.
Diagnosis
- Initial Imaging: Start with non-contrast CT to exclude hemorrhagic stroke.
- Potential findings: hyperdense areas indicating fresh clots, hypodense areas showing infarction.
- Follow-up imaging may include CTA for occlusion localization and MRI for sensitivity in detecting infarcts.
- Key Labs: Blood glucose, INR, complete blood count (CBC), and thyroid function tests if hyperthyroidism is suspected.
Treatment
-
TPA Administration:
- Tissue plasminogen activator (tPA) dissolves clots.
- Eligibility requires confirming neurological deficits, ruling out hemorrhage, and time criteria (ideally within 3-4.5 hours).
- Contraindications include active bleeding, high blood pressure, and recent surgeries.
Indications for tPA
- NIH Stroke Scale (NIHSS) score ≥4 indicates neuro deficits.
- Imaging must rule out bleeding or other contraindications.
- Strict criteria apply for cases where the last known normal was between three and four and a half hours ago.
Blood Pressure Control and tPA Administration
- Blood pressure should be below 185/110 mmHg before tPA administration.
- tPA dosage is 0.9 mg/kg, with a 10% bolus and the remainder infused over 60 minutes.
- Post-administration monitoring targets blood pressure under 185/110 mmHg for the first 24 hours.
Neurological Assessment and Imaging
- Confirm no intracranial bleeding before tPA treatment.
- Perform CT scan within 24 hours post-tPA to detect complications like hemorrhage.
Mechanical Thrombectomy
- Suitable for patients with neurological deficits from large vessel occlusions despite being outside the standard tPA time window.
- Effective within 24 hours after the last known well, with optimal results when performed within 6 hours.
- Treatment methods include clot retrieval with a stent retriever or aspiration via catheter.
Penumbra Concept
- The penumbra represents ischemic tissue around the infarct core that can be salvaged if reperfusion occurs quickly.
- Perfusion scans assist in assessing salvageable brain tissue.
Airway Management
- Ensure airway protection (ABCs) and consider intubation for patients with Glasgow Coma Scale (GCS) ≤8.
- Address airway concerns in patients with reduced consciousness due to stroke or aspiration risk.
Anticoagulation Methods
- Initiate anticoagulation for cardioembolic causes (e.g., atrial fibrillation).
- Start with heparin infusion, transitioning to DOACs (e.g., apixaban, rivaroxaban) or warfarin later.
- Avoid anticoagulation after substantial MCA infarcts to prevent hemorrhagic transformation.
Carotid Stenosis Management
- Severe stenosis (>70%) necessitates carotid endarterectomy (CEA) or stenting.
- Continue antiplatelet therapy post-intervention to reduce thrombus risk.
Modifiable Risk Factors
- Focus on hypertension control, diabetes management, and hyperlipidemia through statin therapy (e.g., atorvastatin).
- Promote smoking cessation and maintaining a healthy weight.
Complications Post-tPA
- Monitor neurological status for any sudden decline indicating potential hemorrhage.
- Discontinue tPA if bleeding is detected and consider fibrinogen replacement if levels drop significantly.
Acute Ischemic Stroke Overview
- Acute ischemic stroke results from obstructed blood flow to the brain, causing tissue damage.
- Main causes: global hypoperfusion, thrombotic events, embolic events, and rare causes.
Causes of Acute Ischemic Stroke
Global Hypoperfusion
- Leads to watershed infarcts from inadequate blood supply.
- Major causes include:
- Cardiac Arrest: Causes drastic drop in blood flow and pressure to the brain.
- Acute Respiratory Failure: Although blood flow may be present, low oxygen can cause ischemia.
- Carotid Stenosis: Narrowing of carotid arteries that limits blood flow, worsened by low blood pressure.
- Cardiac Surgeries: Risks acute strokes if significant arterial stenosis is pre-existing.
Thrombotic Causes
- Occur from clot formation in either large or small vessels.
- Large Vessel Thrombi: Affect arteries like internal carotid, middle cerebral, and vertebral/basilar arteries.
- Small Vessel Thrombi: Primarily impact lenticulostriate and pontine branches.
- Risk factors include hypertension, diabetes, hyperlipidemia, smoking, and obesity.
Embolic Causes
- Three types of embolic sources:
- Arterial to Arterial Emboli: Plaque ruptures in major vessels, leading to obstruction in cerebral circulation.
- Cardiac Emboli: Form in the heart, especially in the left atrium due to atrial fibrillation or post-myocardial infarction.
- Paradoxical Embolus: Clots from the venous system enter the systemic circulation through an atrial septal defect.
Clinical Features
- Symptoms vary based on affected vascular territories: anterior, middle, or posterior cerebral arteries.
- Vulnerable areas include watershed regions between major arterial supplies during global hypoperfusion.
Diagnosis
- Initial Imaging: Start with non-contrast CT to exclude hemorrhagic stroke.
- Potential findings: hyperdense areas indicating fresh clots, hypodense areas showing infarction.
- Follow-up imaging may include CTA for occlusion localization and MRI for sensitivity in detecting infarcts.
- Key Labs: Blood glucose, INR, complete blood count (CBC), and thyroid function tests if hyperthyroidism is suspected.
Treatment
-
TPA Administration:
- Tissue plasminogen activator (tPA) dissolves clots.
- Eligibility requires confirming neurological deficits, ruling out hemorrhage, and time criteria (ideally within 3-4.5 hours).
- Contraindications include active bleeding, high blood pressure, and recent surgeries.
Indications for tPA
- NIH Stroke Scale (NIHSS) score ≥4 indicates neuro deficits.
- Imaging must rule out bleeding or other contraindications.
- Strict criteria apply for cases where the last known normal was between three and four and a half hours ago.
Blood Pressure Control and tPA Administration
- Blood pressure should be below 185/110 mmHg before tPA administration.
- tPA dosage is 0.9 mg/kg, with a 10% bolus and the remainder infused over 60 minutes.
- Post-administration monitoring targets blood pressure under 185/110 mmHg for the first 24 hours.
Neurological Assessment and Imaging
- Confirm no intracranial bleeding before tPA treatment.
- Perform CT scan within 24 hours post-tPA to detect complications like hemorrhage.
Mechanical Thrombectomy
- Suitable for patients with neurological deficits from large vessel occlusions despite being outside the standard tPA time window.
- Effective within 24 hours after the last known well, with optimal results when performed within 6 hours.
- Treatment methods include clot retrieval with a stent retriever or aspiration via catheter.
Penumbra Concept
- The penumbra represents ischemic tissue around the infarct core that can be salvaged if reperfusion occurs quickly.
- Perfusion scans assist in assessing salvageable brain tissue.
Airway Management
- Ensure airway protection (ABCs) and consider intubation for patients with Glasgow Coma Scale (GCS) ≤8.
- Address airway concerns in patients with reduced consciousness due to stroke or aspiration risk.
Anticoagulation Methods
- Initiate anticoagulation for cardioembolic causes (e.g., atrial fibrillation).
- Start with heparin infusion, transitioning to DOACs (e.g., apixaban, rivaroxaban) or warfarin later.
- Avoid anticoagulation after substantial MCA infarcts to prevent hemorrhagic transformation.
Carotid Stenosis Management
- Severe stenosis (>70%) necessitates carotid endarterectomy (CEA) or stenting.
- Continue antiplatelet therapy post-intervention to reduce thrombus risk.
Modifiable Risk Factors
- Focus on hypertension control, diabetes management, and hyperlipidemia through statin therapy (e.g., atorvastatin).
- Promote smoking cessation and maintaining a healthy weight.
Complications Post-tPA
- Monitor neurological status for any sudden decline indicating potential hemorrhage.
- Discontinue tPA if bleeding is detected and consider fibrinogen replacement if levels drop significantly.
Acute Ischemic Stroke Overview
- Acute ischemic stroke results from obstructed blood flow to the brain, causing tissue damage.
- Main causes: global hypoperfusion, thrombotic events, embolic events, and rare causes.
Causes of Acute Ischemic Stroke
Global Hypoperfusion
- Leads to watershed infarcts from inadequate blood supply.
- Major causes include:
- Cardiac Arrest: Causes drastic drop in blood flow and pressure to the brain.
- Acute Respiratory Failure: Although blood flow may be present, low oxygen can cause ischemia.
- Carotid Stenosis: Narrowing of carotid arteries that limits blood flow, worsened by low blood pressure.
- Cardiac Surgeries: Risks acute strokes if significant arterial stenosis is pre-existing.
Thrombotic Causes
- Occur from clot formation in either large or small vessels.
- Large Vessel Thrombi: Affect arteries like internal carotid, middle cerebral, and vertebral/basilar arteries.
- Small Vessel Thrombi: Primarily impact lenticulostriate and pontine branches.
- Risk factors include hypertension, diabetes, hyperlipidemia, smoking, and obesity.
Embolic Causes
- Three types of embolic sources:
- Arterial to Arterial Emboli: Plaque ruptures in major vessels, leading to obstruction in cerebral circulation.
- Cardiac Emboli: Form in the heart, especially in the left atrium due to atrial fibrillation or post-myocardial infarction.
- Paradoxical Embolus: Clots from the venous system enter the systemic circulation through an atrial septal defect.
Clinical Features
- Symptoms vary based on affected vascular territories: anterior, middle, or posterior cerebral arteries.
- Vulnerable areas include watershed regions between major arterial supplies during global hypoperfusion.
Diagnosis
- Initial Imaging: Start with non-contrast CT to exclude hemorrhagic stroke.
- Potential findings: hyperdense areas indicating fresh clots, hypodense areas showing infarction.
- Follow-up imaging may include CTA for occlusion localization and MRI for sensitivity in detecting infarcts.
- Key Labs: Blood glucose, INR, complete blood count (CBC), and thyroid function tests if hyperthyroidism is suspected.
Treatment
-
TPA Administration:
- Tissue plasminogen activator (tPA) dissolves clots.
- Eligibility requires confirming neurological deficits, ruling out hemorrhage, and time criteria (ideally within 3-4.5 hours).
- Contraindications include active bleeding, high blood pressure, and recent surgeries.
Indications for tPA
- NIH Stroke Scale (NIHSS) score ≥4 indicates neuro deficits.
- Imaging must rule out bleeding or other contraindications.
- Strict criteria apply for cases where the last known normal was between three and four and a half hours ago.
Blood Pressure Control and tPA Administration
- Blood pressure should be below 185/110 mmHg before tPA administration.
- tPA dosage is 0.9 mg/kg, with a 10% bolus and the remainder infused over 60 minutes.
- Post-administration monitoring targets blood pressure under 185/110 mmHg for the first 24 hours.
Neurological Assessment and Imaging
- Confirm no intracranial bleeding before tPA treatment.
- Perform CT scan within 24 hours post-tPA to detect complications like hemorrhage.
Mechanical Thrombectomy
- Suitable for patients with neurological deficits from large vessel occlusions despite being outside the standard tPA time window.
- Effective within 24 hours after the last known well, with optimal results when performed within 6 hours.
- Treatment methods include clot retrieval with a stent retriever or aspiration via catheter.
Penumbra Concept
- The penumbra represents ischemic tissue around the infarct core that can be salvaged if reperfusion occurs quickly.
- Perfusion scans assist in assessing salvageable brain tissue.
Airway Management
- Ensure airway protection (ABCs) and consider intubation for patients with Glasgow Coma Scale (GCS) ≤8.
- Address airway concerns in patients with reduced consciousness due to stroke or aspiration risk.
Anticoagulation Methods
- Initiate anticoagulation for cardioembolic causes (e.g., atrial fibrillation).
- Start with heparin infusion, transitioning to DOACs (e.g., apixaban, rivaroxaban) or warfarin later.
- Avoid anticoagulation after substantial MCA infarcts to prevent hemorrhagic transformation.
Carotid Stenosis Management
- Severe stenosis (>70%) necessitates carotid endarterectomy (CEA) or stenting.
- Continue antiplatelet therapy post-intervention to reduce thrombus risk.
Modifiable Risk Factors
- Focus on hypertension control, diabetes management, and hyperlipidemia through statin therapy (e.g., atorvastatin).
- Promote smoking cessation and maintaining a healthy weight.
Complications Post-tPA
- Monitor neurological status for any sudden decline indicating potential hemorrhage.
- Discontinue tPA if bleeding is detected and consider fibrinogen replacement if levels drop significantly.
Acute Ischemic Stroke Overview
- Acute ischemic stroke results from obstructed blood flow to the brain, causing tissue damage.
- Main causes: global hypoperfusion, thrombotic events, embolic events, and rare causes.
Causes of Acute Ischemic Stroke
Global Hypoperfusion
- Leads to watershed infarcts from inadequate blood supply.
- Major causes include:
- Cardiac Arrest: Causes drastic drop in blood flow and pressure to the brain.
- Acute Respiratory Failure: Although blood flow may be present, low oxygen can cause ischemia.
- Carotid Stenosis: Narrowing of carotid arteries that limits blood flow, worsened by low blood pressure.
- Cardiac Surgeries: Risks acute strokes if significant arterial stenosis is pre-existing.
Thrombotic Causes
- Occur from clot formation in either large or small vessels.
- Large Vessel Thrombi: Affect arteries like internal carotid, middle cerebral, and vertebral/basilar arteries.
- Small Vessel Thrombi: Primarily impact lenticulostriate and pontine branches.
- Risk factors include hypertension, diabetes, hyperlipidemia, smoking, and obesity.
Embolic Causes
- Three types of embolic sources:
- Arterial to Arterial Emboli: Plaque ruptures in major vessels, leading to obstruction in cerebral circulation.
- Cardiac Emboli: Form in the heart, especially in the left atrium due to atrial fibrillation or post-myocardial infarction.
- Paradoxical Embolus: Clots from the venous system enter the systemic circulation through an atrial septal defect.
Clinical Features
- Symptoms vary based on affected vascular territories: anterior, middle, or posterior cerebral arteries.
- Vulnerable areas include watershed regions between major arterial supplies during global hypoperfusion.
Diagnosis
- Initial Imaging: Start with non-contrast CT to exclude hemorrhagic stroke.
- Potential findings: hyperdense areas indicating fresh clots, hypodense areas showing infarction.
- Follow-up imaging may include CTA for occlusion localization and MRI for sensitivity in detecting infarcts.
- Key Labs: Blood glucose, INR, complete blood count (CBC), and thyroid function tests if hyperthyroidism is suspected.
Treatment
-
TPA Administration:
- Tissue plasminogen activator (tPA) dissolves clots.
- Eligibility requires confirming neurological deficits, ruling out hemorrhage, and time criteria (ideally within 3-4.5 hours).
- Contraindications include active bleeding, high blood pressure, and recent surgeries.
Indications for tPA
- NIH Stroke Scale (NIHSS) score ≥4 indicates neuro deficits.
- Imaging must rule out bleeding or other contraindications.
- Strict criteria apply for cases where the last known normal was between three and four and a half hours ago.
Blood Pressure Control and tPA Administration
- Blood pressure should be below 185/110 mmHg before tPA administration.
- tPA dosage is 0.9 mg/kg, with a 10% bolus and the remainder infused over 60 minutes.
- Post-administration monitoring targets blood pressure under 185/110 mmHg for the first 24 hours.
Neurological Assessment and Imaging
- Confirm no intracranial bleeding before tPA treatment.
- Perform CT scan within 24 hours post-tPA to detect complications like hemorrhage.
Mechanical Thrombectomy
- Suitable for patients with neurological deficits from large vessel occlusions despite being outside the standard tPA time window.
- Effective within 24 hours after the last known well, with optimal results when performed within 6 hours.
- Treatment methods include clot retrieval with a stent retriever or aspiration via catheter.
Penumbra Concept
- The penumbra represents ischemic tissue around the infarct core that can be salvaged if reperfusion occurs quickly.
- Perfusion scans assist in assessing salvageable brain tissue.
Airway Management
- Ensure airway protection (ABCs) and consider intubation for patients with Glasgow Coma Scale (GCS) ≤8.
- Address airway concerns in patients with reduced consciousness due to stroke or aspiration risk.
Anticoagulation Methods
- Initiate anticoagulation for cardioembolic causes (e.g., atrial fibrillation).
- Start with heparin infusion, transitioning to DOACs (e.g., apixaban, rivaroxaban) or warfarin later.
- Avoid anticoagulation after substantial MCA infarcts to prevent hemorrhagic transformation.
Carotid Stenosis Management
- Severe stenosis (>70%) necessitates carotid endarterectomy (CEA) or stenting.
- Continue antiplatelet therapy post-intervention to reduce thrombus risk.
Modifiable Risk Factors
- Focus on hypertension control, diabetes management, and hyperlipidemia through statin therapy (e.g., atorvastatin).
- Promote smoking cessation and maintaining a healthy weight.
Complications Post-tPA
- Monitor neurological status for any sudden decline indicating potential hemorrhage.
- Discontinue tPA if bleeding is detected and consider fibrinogen replacement if levels drop significantly.
Acute Ischemic Stroke Overview
- Acute ischemic stroke results from obstructed blood flow to the brain, causing tissue damage.
- Main causes: global hypoperfusion, thrombotic events, embolic events, and rare causes.
Causes of Acute Ischemic Stroke
Global Hypoperfusion
- Leads to watershed infarcts from inadequate blood supply.
- Major causes include:
- Cardiac Arrest: Causes drastic drop in blood flow and pressure to the brain.
- Acute Respiratory Failure: Although blood flow may be present, low oxygen can cause ischemia.
- Carotid Stenosis: Narrowing of carotid arteries that limits blood flow, worsened by low blood pressure.
- Cardiac Surgeries: Risks acute strokes if significant arterial stenosis is pre-existing.
Thrombotic Causes
- Occur from clot formation in either large or small vessels.
- Large Vessel Thrombi: Affect arteries like internal carotid, middle cerebral, and vertebral/basilar arteries.
- Small Vessel Thrombi: Primarily impact lenticulostriate and pontine branches.
- Risk factors include hypertension, diabetes, hyperlipidemia, smoking, and obesity.
Embolic Causes
- Three types of embolic sources:
- Arterial to Arterial Emboli: Plaque ruptures in major vessels, leading to obstruction in cerebral circulation.
- Cardiac Emboli: Form in the heart, especially in the left atrium due to atrial fibrillation or post-myocardial infarction.
- Paradoxical Embolus: Clots from the venous system enter the systemic circulation through an atrial septal defect.
Clinical Features
- Symptoms vary based on affected vascular territories: anterior, middle, or posterior cerebral arteries.
- Vulnerable areas include watershed regions between major arterial supplies during global hypoperfusion.
Diagnosis
- Initial Imaging: Start with non-contrast CT to exclude hemorrhagic stroke.
- Potential findings: hyperdense areas indicating fresh clots, hypodense areas showing infarction.
- Follow-up imaging may include CTA for occlusion localization and MRI for sensitivity in detecting infarcts.
- Key Labs: Blood glucose, INR, complete blood count (CBC), and thyroid function tests if hyperthyroidism is suspected.
Treatment
-
TPA Administration:
- Tissue plasminogen activator (tPA) dissolves clots.
- Eligibility requires confirming neurological deficits, ruling out hemorrhage, and time criteria (ideally within 3-4.5 hours).
- Contraindications include active bleeding, high blood pressure, and recent surgeries.
Indications for tPA
- NIH Stroke Scale (NIHSS) score ≥4 indicates neuro deficits.
- Imaging must rule out bleeding or other contraindications.
- Strict criteria apply for cases where the last known normal was between three and four and a half hours ago.
Blood Pressure Control and tPA Administration
- Blood pressure should be below 185/110 mmHg before tPA administration.
- tPA dosage is 0.9 mg/kg, with a 10% bolus and the remainder infused over 60 minutes.
- Post-administration monitoring targets blood pressure under 185/110 mmHg for the first 24 hours.
Neurological Assessment and Imaging
- Confirm no intracranial bleeding before tPA treatment.
- Perform CT scan within 24 hours post-tPA to detect complications like hemorrhage.
Mechanical Thrombectomy
- Suitable for patients with neurological deficits from large vessel occlusions despite being outside the standard tPA time window.
- Effective within 24 hours after the last known well, with optimal results when performed within 6 hours.
- Treatment methods include clot retrieval with a stent retriever or aspiration via catheter.
Penumbra Concept
- The penumbra represents ischemic tissue around the infarct core that can be salvaged if reperfusion occurs quickly.
- Perfusion scans assist in assessing salvageable brain tissue.
Airway Management
- Ensure airway protection (ABCs) and consider intubation for patients with Glasgow Coma Scale (GCS) ≤8.
- Address airway concerns in patients with reduced consciousness due to stroke or aspiration risk.
Anticoagulation Methods
- Initiate anticoagulation for cardioembolic causes (e.g., atrial fibrillation).
- Start with heparin infusion, transitioning to DOACs (e.g., apixaban, rivaroxaban) or warfarin later.
- Avoid anticoagulation after substantial MCA infarcts to prevent hemorrhagic transformation.
Carotid Stenosis Management
- Severe stenosis (>70%) necessitates carotid endarterectomy (CEA) or stenting.
- Continue antiplatelet therapy post-intervention to reduce thrombus risk.
Modifiable Risk Factors
- Focus on hypertension control, diabetes management, and hyperlipidemia through statin therapy (e.g., atorvastatin).
- Promote smoking cessation and maintaining a healthy weight.
Complications Post-tPA
- Monitor neurological status for any sudden decline indicating potential hemorrhage.
- Discontinue tPA if bleeding is detected and consider fibrinogen replacement if levels drop significantly.
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Description
This quiz provides an overview of acute ischemic stroke, detailing its causes and types of obstructions to blood flow in the brain. It covers critical factors such as global hypoperfusion and thrombotic causes that lead to brain tissue damage. Test your understanding of the underlying mechanisms and risk factors associated with this medical condition.
